Oral Medicine and Radiology, 2019

Oral Medicine and
Radiology
Abhay Suresh Kulkani MDS
Reader
Department of Oral Medicine and Radiology
PDU Dental College
Solapur
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Preface
I t gives me immense pleasure to write and publish this book. I do not claim the originality
and full completeness of the matter. In fact the book is based on various concepts laid down
in standard textbooks. This book was possible only because I had the advantage of authentic
literature provided by these authors.
Presently, there are many textbooks on oral medicine and radiology by various authors,
having appropriate coverage of the subject. The purpose of this book is to prepare the student
for examination, especially for competitive examination and viva voce. The book attempts to
highlight small aspects of the subject which have more value especially during seminars and
various postgraduate activities. I have tried to collect various subject materials important for
undergraduate and postgraduate curriculums from various books, so that different topics
will be briefed under one heading.
The question and answer format in fact is made so that the students can have a very simpler
approach towards the subject. Several attempts are made in this book to orient the subject and
make the subject easy to remember, recollect and reproduce. The book carries some clinical
tips too which will guide during clinical postings.
I am very much indebted to Dr Birangane RS, Principal, Professor and Head, Department
of Oral Medicine and Radiology, PDU Dental College, Solapur, for his constant support in
writing this book. His stand and dynamic leadership before and during the write up was a
great source of inspiration.
I am thankful to Dr Sanjeev Onkar, Professor, Oral Medicine and Radiology, PDU Dental
College, Solapur, for his contribution in collecting, analyzing and editing the matter. The
enthusiasm shown by him during this project was really encouraging.
I am also thankful to Dr Swapnali Chowdhary, Ex-Faculty (Reader), Oral Medicine and
Radiology, PDU Dental College, for her open-handed contribution in writing this book. The
prompt response and inclination towards this project shown by her was simply incredible.
I am pleased for the support provided by Dr Rohan Chowdhary, Senior Lecturer, Oral
Medicine and Radiology, PDU Dental College, for his every single assistance and valuable
hints for completeness of this project.
I also express my gratitude to Dr Pratik Parkarwar, Senior Lecturer, Oral Medicine and
Radiology, PDU Dental College, for his reinforcement and guidance during this project.
I would also like to thank Dr Shailesh Lele and Dr Micheal Glick, for their valuable
suggestions and feedback.
I am really indebted to Dr Sumeet P Shah for his zeal, interest and meaningful contribution
to this project.
Dr Abdulla Kazi, PG student of Oral Medicine and Radiology, PDU Dental College, has a
great role in this project. The disciplined approach, the regularity, punctuality and inclination
towards the subject was amazing. His overall role as writer and editor was vital.
vi Oral Medicine and Radiology
I am grateful to Ramesh Krishnammachari and all team members of CBS Publishers &
Distributors for the support shown by them for this project.
I will be ever indebted and grateful to my wife Dr Priya, my children Atharva and Ayushi
and all my family members for their constant support during the project. This book would
never have been possible without their support.
I am thankful to my teachers for their valuable guidance.
Last but not least is the Almighty to whom I will be highly abide to whatever he has created
in this world and directions he is giving us to run on.
My special thanks to Mr YN Arjuna (Senior Vice President Publishing, Editorial and Publicity),
Mrs Ritu Chawla (AGM Production), Mr Prasenjit Paul, Mr Parmod Kumar and Mr Rohan Prasad,
for their skilful service and immense help in editing and preparing illustrations of this book.
Abhay Suresh Kulkani
Contents vii
Contents
Preface v
Section 1 ORAL MEDICINE

1. Vesiculobullous, Red and White, Vascular, Reactive and Oral Cavity Lesions 3
2. Orofacial Pain and Disorders of Temporomandibular Joints 48
3. Benign Lesions of Oral Cavity 77
4. Infections and Autoimmune Disorders of Oral Cavity 101
5. Potentially Malignant Disorders of Oral Cavity and Oral Cancers 109
6. Diseases of Salivary Glands, Pigmented Lesions of Oral Cavity 118
7. Developmental Disturbances, Physical and Chemical Injuries to the

Oral Cavity 131
8. Systemic Manifestations in Oral Cavity and Traumatic Lesion 141
Section 2 RADIOLOGY
9. Radiology—Part 1 159
10. Radiology—Part 2 210
Suggested Reading 247

Index 249
Section 1
Oral Medicine
1. Vesiculobullous, Red and White, Vascular, Reactive and Oral Cavity
Lesions
2. Orofacial Pain and Disorders of Temporomandibular Joints
3. Benign Lesions of Oral Cavity
4. Infections and Autoimmune Disorders of Oral Cavity
5. Potentially Malignant Disorders of Oral Cavity and Oral Cancers
6. Diseases of Salivary Glands, Pigmented Lesions of Oral Cavity
7. Developmental Disturbances, Physical and Chemical Injuries to the
Oral Cavity
8. Systemic Manifestations in Oral Cavity and Traumatic Lesion
1 Vesiculobullous, Red and White,
Vascular, Reactive and Oral Cavity
Lesions
1. What is lesion? What are primary and eventually regress. Reactive enlargements
secondary lesions? are often, but not always, tender or painful
Lesion: An abnormal change in structure of an and usually have a more rapid growth rate
organ or part due to injury or disease, especi- (measured in hours to weeks) than tumors.
ally one that is circumscribed and well defined. Some reactive enlargements begin as a
• Primary lesions: These are physical changes diffuse lesion and become more localized
in the skin considered to be caused directly with time. Sometimes reactive lesions are
by the disease. associated with tender lymph nodes and
systemic manifestations, such as fever and
• Secondary lesions: These are those lesions
malaise. Once it is decided that a soft tissue
that are characteristically brought about by
enlargement is reactive, the next step is to
modification of the primary lesion either by
determine what the lesion is reacting to,
the individual with the lesion or through
such as bacterial, viral, or fungal infections
the natural evolution of the lesion in the
or chemical or physical injury.
environment.
Soft tissue tumors are characterized by being
2. What is the decision tree of oral mucosal persistent and progressive; they do not resolve
lesions? without treatment. They are usually not
The decision tree can be simplified as: painful early in their development, and the
A. Soft tissue enlargements are characterized growth rate varies from weeks to years.
by being persistent and progressive; they Tumors—benign and malignant
do not resolve without treatment. They are • Benign tumors are typically better defined
usually not painful early in their develop- or circumscribed and have a slower
ment, and the growth rate varies from growth rate, measured in months and
weeks to years. These include tumor/cysts/ years, than malignant neoplasms.
neoplasm and reactive. • Malignant neoplasms are more likely to be
Reactive soft tissue enlargements may increase painful and cause ulceration of the over-
and decrease (fluctuate) in size and usually lying epithelium than benign lesions.
3
4 Oral Medicine and Radiology
Since malignant neoplasms invade or • Bulla is elevated blister containing clear

infiltrate surrounding muscle, nerve, fluid more than 1 cm in diameter.
blood vessels, and connective tissue, they Vesicle and bulla both are primary lesions
are fixed or adherent to surrounding by definition. One primary lesion cannot turn
structures during palpation. Some into other, if it happens it is secondary lesion.
benign tumors are also fixed to surroun- Vesicle cannot change into bulla. However, in
ding structures, while other benign some diseases the smaller vesicles may
tumors are surrounded by a fibrous coalesce to form larger vesicles which may
connective tissue capsule, which may clinically appear as bullae. These larger and
allow the lesion to be moved within the fused vesicles may be called coalesced vesicles
tissue independent of surrounding or larger vesicles.
structures.
B. Surface lesions of oral mucosa consist of 4. Enumerate the vesiculobullous lesions
lesions that involve the epithelium and which present predominantly as bullous
superficial connective tissue of mucosa and lesions.
skin. They do not exceed 2–3 mm in thick- Pemphigus vulgaris, bullous pemphigoid,
ness. Clinically, the surface lesions are benign mucuous membrane pemphigoid,
slightly thickened or flat rather than swell- bullous lichen planus, erythema multiforme,
ings and enlargements. Surface lesions are Stevens-Johnson syndrome, epidermolysis
divided into three categories based on their bullosa, linear IgA disease.
clinical appearance: White, pigmented, and 5. Enumerate the vesiculobullous lesions
vesicular, ulcerated, erythematous. These predominantly presents as vesicular
include white pigmented, vesicular, lesion.
ulcerated and erythematous lesions.
Herpes simplex virus infection (primary
3. Define vesicle, bulla. Can vesicle turned herpetic gingiostomatitis), varicella (chicken-
into bulla? What are coalesced vesicles? pox), herpes zoster (shingles), hand-foot-and-
• Vesicle is elevated blister containing clear mouth disease, herpangina, dermatitis
fluid which is less than 1 cm in diameter. herpetiformis.
Vesiculobullous, Red and White, Vascular, Reactive and Oral Cavity Lesions 5
6. How the size of pemphigus bulla varies cancer-associated clinical syndromes caused
compared to other diseases? by biologic or humoral factors, including
As a general rule, the pemphigus bulla is hormones, cytokines, and immunoglobulins.
smaller than the bulla in benign mucous It may parallel the underlying malignancy
membrane pemphigoid and considerably and successful treatment of tumor may lead
larger than those seen in the viral diseases such to disappearance of syndrome. Sometimes
as herpes and hand-foot-and-mouth disease. may be the first sign of malignancy and its
In short viral disease bullae are smaller recognition may be critical for early detection
than pemphigus and pemphigus bullae are of cancer.
smaller than benign mucous membrane 1. Painful, progressive stomatitis, with pre-
pemphigoid. ferential involvement of tongue. The tongue
involvement is very much consistent.
7. What is Nikolsky’s sign? State all condi-
tions in which it is positive. 2. Histologically acnthatholysis/lichenoid/
interface dermatitits. Sometimes repeated
Gentle pressure on clinically unaffected
biopsies are necessary to detect acantholysis
mucosa and skin produces new lesion (in form
(even though it is readily detectable in oral
of vesicle/bullae/stripping of mucosa) in that
lesions) due to masking by necrosis and
area is Nikolsky’s sign.
secondary inflammation. Lesions on skin
It is positive in pemphigus, paraneoplastic sometimes are not detectable and some-
pemphigus, benign mucuous membrane times the lesions are lichenoid and erythema
pemphigoid, toxic epidermal necrolysis, multiforme like. Direct immunofluore-
burns, epidermolysis bullosa, bullous lichen scence (DIF) is negative frequently.
planus, bullous impetigo, staphylococcal
3. Antiplakin antibodies are seen.
scalded skin syndrome, mycosis fungoids and
the sign also allegedly occurred in a patient 4. Presence of underlying lymphoproliferative
with systemic sclerosis who developed neoplasm and two-thirds of cases are asso-
D-penicillamine-induced pemphigus vulgaris. ciated with malignant disease (Hodgkin’s
lymphoma, CLL) and others are associated
8. What are phenotypes of pemphigus? with Castleman’s disease, abdominal lym-
What are characteristics of pemphigus phoma, thymoma, retroperitoneal sarco-
lesions? mas. CT sacn may be used to detect.
Mucosal dominant and mucocutaneous
dominant. 10. Enumerate the conditions causing
As the antigen is located in epithelium palatal petechiae.
flaccid bulla may develop which will soon • Trauma from fellatio • Trauma from
rupture and form ulceration. (direct trauma and severe coughing
Oral lesions may be initial sign (80–90%) negative pressure)
and last to disappear. • Trauma from severe • Prodromal sign
Females are most commonly affected. vomiting of infectious
9. What is paraneoplastic syndrome? What mononucleosis
are diagnostic criteria of paraneoplastic • Prodromal sign of • Streptococcal
pemphigus? hemostatic disease pharyngitis
Paraneoplastic syndromes are a group of • Sometimes in child- • Sometimes in
clinical disorders associated with malignant ren from herpan- scarlet fever
diseases that are not directly related to the gina (early sign)
physical effects of primary or metastatic • In bulimia nervosa • Leukemia (early
tumor. Or paraneoplastic syndromes are trauma from finger sign)
11. State all categories under which lichen

planus can be classified and justify.
Why?
Lichen planus can be classified as:
a. Autoimmune disease: As clinically:
1. Female predilection.
2. Late occurrence of disease
3. Most of time bilateral occurrence
b. Potentially malignant disorder of oral
cavity: As the erosive variety has got malig-
nant potential
c. White lesion: It may exhibit as asympto-
matic white lesion, e.g. reticular lichen
planus
d. Red and white lesions: As it exhibits both
red and white components, e.g. atrophic
and erosive variety
e. Psychosomatic disorders affecting oral
cavity: Many authors stated that psycho-
logical intervention may be warranted
given the fact that level of anxiety and
salivary cortisol in oral lichen planus (OLP)
patients are high, supporting the relation-
ship of OLP with stress. The most frequent
conditions which may lead to lichen planus
are depression, anxiety and stress. Exacer-
bation of orallichen planus has been linked
to period of psychological stress and
anxiety.
f. Vesiculobullous lesions: As it has bullous
variety.
g. Mucocutaneous disorders: As it may same type of keratotic striae is seen in lupus
involve skin and oral mucosa simulta- erythematosus but these are more delicate and
neously. subtle than seen in lichen planus and show
12. What are Wickham’s striae? characteristic radiation from a central focus.
The term Wickham’s striae (WS) was coined by 13. What is fountain sign?
Louis Frédéric Wickham in the year 1895 and Hypertrophic lichen planus is most pruritic
corresponds to fine whitish points or grey lacy form of lichen planus and fountain sign is seen
lines or dots seen on the top of the popular rash during intralesional injections. Lesions of LPH
and oral mucosal lesions of lichen planus (LP). are characterized by hypertrophic verrucous
These resembles the lichen type moss that is plaques predominantly distributed over the
often seen on rocks. The Wickham’s striae are shins. While injecting these plaques with corti-
accentuated by immersion of oil on skin surface. costeroids by a 26 G needle, it has been often
The pathogenesis of Wickham’s striae is found that the medicine comes out through
believed to be thickening of granular layer. The the follicular openings in a jet mimicking a
“fountain”. This phenomenon is mostly seen

in LPH lesions of less than 2 years duration.
14. What are syndromes associated with
lichen planus?
• Vulvovagina gingival syndrome: The
involvement of vulva, vagina and gingiva
with lichen planus is called vulvovagina
gingival syndrome. The erosive type is most
frequent type.
• Grinspan syndrome: This is the triad of oral
lichen planus, diabetes mellitus, and
hypertension. Because drug therapy for
diabetes mellitus and hypertension is
capable of producing lichenoid reactions of
the oral mucosa, the question arises as to
whether Grinspan’s syndrome is an longitudinally, and split lateral edges angle
iatrogenically induced syndrome. forward to give a pup-tent appearance. This
• Graham Little syndrome (Graham Little- has been referred to as pup-tent sign. The
Piccardi-Lassueur syndrome): This consists “tenting” or “pup-tent” sign is observed as a
of LPP of scalp, non-cicatrical pubic/axillary result of nail bed involvement that elevates
hair loss, follicular keratotic papules the nail plate and may cause longitudinal
resembling keratotis pilaris on limb, trunk splitting.
and retroauricular areas and typical cuta- 16. Why do you get white lesions of oral
neous or mucosal lichen planus. This is a cavity?
rare syndrome. Mucosal lesions clinically appear white
15. What is pup-tent sign? because of many reasons:
Discrete red or violaceous papules in the nail 1. Increased thickness of epithelium as a result
bed may lift and split the overlying nail plate of increased number of constituent cells
(hyperplasia/acanthosis), e.g. frictional
keratosis
2. Increased and abnormal production of
keratin (hyperkeratosis), e.g. frictional kera-
tosis, linea alba (physiological keratosis),
actinic keratosis, white sponge nevus
3. Imbibition of fluid by surface keratin/or
epithelial cells. This results in hydration and
oedema results in cloudy white lesions
4. Deposition of exogenous material like
material alba
5. Surface debris lesions associated with
necrosis of overlying epithelium. Formation
of pseudomembrane which is white that
results from necrosis which results from
coagulation of surface tissue. Removal of
pseudomembrane may leave raw mucosal
surface with tiny bleeding spots. These are 6. Potentially malignant disorders:
painful lesions, e.g. thermal burn, chemical a. Leukoplakia
burn, psuedomembranous candidiasis, b. Actinic cheilitis
fibrin clot
7. Neoplastic:
6. White lesions due to subepithelial change—
these have normal overlying epithelium, a. Squamous cell carcinoma
but changes in the connective tissue
partially mask blood vessels and cause the 18. Enumerate hereditary white lesions.
area to appear white, yellow or tan. These White sponge nevus, HBID (Witkop’s dis-
lesions have a smooth translucent surface, ease), follicular keratosis (Darrier’s disease).
do not rub off, and are not painful. Lack of
19. Enumerate the conditions causing bi-
vascularity in hyperplastic connective
lateral white lesions on buccal mucosa.
tissue. This is responsible for pale or opaque
appearance as seen in scar tissue. Oral Linea alba, oral submucuos fibrosis, white
submucous fibrosis, scarring (subepithelial sponge nevus, HBID, lichen planus, lichenoid
fibrosis) drug reaction, cheek chewing, lupus erythe-
matosus, candidiasis.
7. Submucosal deposits of sebaceous glands
give rise to yellowish granular appearance 20. What is Witkop’s disease?
(Fordyce’s granules).
It is rare, hereditary condition (autosomal
17. Classify white lesions of oral cavity. dominant), it is also called hereditary benign
1. Hereditary/developmental: intraepithelial dyskeratosis. Early onset of
a. Leukoedema bulbar conjunctivitis and oral white lesions
b. White spongy nevus (usually first year of life). Oral lesions are soft,
c. Hereditary benign intraepithelial dys- asymptomatic, white folds and plaques of
keratosis spongy mucosa.
d. Pachyonychia congenita 21. What is preleukoplakia?
e. Dyskeratosis congenita A preleukoplakia definite entity with specific
2. Reactive: diagnostic criteria and behaviour, it is charac-
a. Frictional keratosis terized by low-grade or mild reaction of
b. Morsicatio buccarum mucosa, conceived as a precursor stage of
c. Nicotine stomatitis leukoplakia. It is grey or greyish-white area
d. Tobacco pouch keratosis but never completely white lesion with
e. Chemical burn indistinct borders. It may have lobular pattern
3. Immunologic: and distinct borders. It describes a diffuse
a. Lichen planus white lesion of the oral mucosa, less dense and
b. Lichenoid mucositis less marked than leukoplakia. It is strongly
associated with tobacco smoking. This pre-
c. Discoid lupus erythematosus
leukoplakia terminology is been replaced by
d. Graft-versus-host disease
the terminology as thin, smooth leukoplakia.
4. Bacterial/viral/fungal: The prevalence in India varies from 0.5 to
a. Candidiasis 4.1%. Approximately 15% of preleukoplakia
b. Mucous patches in secondary syphilis progress to leukoplakia, 0.4% may progress
c. Oral hairy leukoplakia to oral cancers. Malignant transformation may
5. Systemic disease: occur from preleukoplakia and may convert
a. Uremic stomatitis to leukoplakia and then to malignancy.
22. Define leukoplakia. What are the clinical

types of leukoplakia?
Leukoplakia is defined as a white patch or
plaque that cannot be characterized clinically
or histologically as any other lesion.
Types of leukoplakia
• Homogeneous: Uniformly white patch
with slightly raised mucosa (cracked mud
appearance)
• Proliferative verrucous leukoplakia (PVL)
is an aggressive form of oral leukoplakia
that is persistant and refractory to treatment
with a high-risk of malignant transforma-
tion, begins as benign hyperkeratotic lesion
and often becomes multifocal.
• Nodular lesion: White lesion with granular

surface associated with candida infections.
• Speckled leukoplakia: Combined red and
white lesions with irregular surface.
• Reversible and irreversible leukoplakias:

Leukoplakia may also be divided into two
types according to whether it sponta-
neously disappears after the chronic irritant
has been eliminated. Lesions that disappear
are referred to as reversible leukoplakias, 28. Why leukoplakia of floor of mouth and
whereas the persistent lesions are termed ventrolateral surface of tongue are
irreversible leukoplakias. attributed to malignization?
23. Give classification of leukoplakia accord- The floor of mouth and ventrolateral tongue
ing to malignant change and prognosis. with extension back into the lateral soft palate
and tonsillar area forms high-risk zone. There
In 2002 WHO has given this classification
are two major factors that explain this as high-
• Phase I: Thin, smooth leukoplakia—better risk zone.
prognosis 1. These sites are easily bathed by carcinogens,
• Phase II: Thick, fissured leukoplakia as any carcinogens will mix with saliva and
• Phase III: Proliferative verrucous leuko- get pooled in this region.
plakia (PVL)—higher malignant transfor- 2. These lesions of mouth are covered by
mation rate thinner, non-keratinized mucosa which
• Phase IV: Erythroleukoplakia—poor prog- offers less protection.
nosis. 29. What are the high-risk leukoplakia?
24. Name the systemic condition associated • Red component
with leukoplakia. • Raised component
Dyskeratosis congenita, syphilis • Presence in high-risk oval
• Tobacco and alcohol use
25. What is stippled leukoplakia? • Nonsmoker and unknown etiology of
Leukoplakic lesions as a white patch with lesion
red dots of thin mucosa within it are called • Non-reversible type
stippled leukoplakia. These are different from • Microscopic atypia
erythroleukoplakia as mixture of white and • The malignant potential is low in homo-
red patches. genous leukoplakia, higher in verrucous
leukoplakia and highest in speckled leuko-
26. What are thin, thick and granular
plakia.
leukoplakias?
30. What is erythroplakia? What are the
Thin (early) leukoplakia is subtle white patch types of erythroplakia?
may show epithelial dysplasia on biopsy.
Erythroplakia can be defined as a persistent
Thick leukoplakia is thick white lesion may velvety red patch that cannot be identified
show epithelial dysplasia. as any other specific red lesion such as inflam-
Granular leukoplakia, a small leukoplakic matory erythemas or those produced by blood
lesion with a rough, granular surface. The
biopsy may show dysplasia. Such a lesion
would be easily missed during examination.
27. What are the variants of homogenous
and non-homogenous leukoplakias?
Homogenous: Lesion that was uniformly
white and unscrapable. Flat, corrugated,
wrinkled, pumice like.
Non-homogenous: Lesion predominantly
white and speckled with red verrucous,
ulcerated, nodular, erythroleukoplakia.
7. Pan (betel quid) stain

8. Pan encrustration
9. Lichenoid reactions.
32. What is differentiating point between
erythroplakia and pseudomembranous
candidiasis?
Erythroplakia has a sharper border while
lesions of acute and chronic pseudomemb-
ranous candidiasis has got diffuse border.
33. Define oral submucous fibrosis (OSF).
Why is it classified as potentially malig-
nant disorder?
It is defined as slowly progressive chronic
fibrotic disese of oral cavity and oropharynx
characterized by fibroelastic change and
inflammation of the mucosa, leading to a pro-
gressive inability to open the mouth, swallow
or speak.
Pinderberg (1972) given criteria that consi-
dered this as potentially malignant disorder:
1. Higher occurrence of OSF in oral cancer
patients
2. Higher incidence of squamous cell carci-
noma in patients with OSF
3. Histological diagnosis of cancer without
any clinical suspicion in OSF
vessel anomalies or infection. Three different 4. High frequency of epithelial dysplasia
clinical appearances were described by Shear 5. Higher prevalence of leukoplakia among
1. The homogeneous form, which is completely OSF.
red in appearance,
34. What are the initial clinical symptoms
2. Patches of EP and leukoplakia occurring and signs suggestive of oral submucous
together, and fibrosis?
3. Speckled EP, in which small leukoplakic
Symptoms: The most common feature of sub-
specks are scattered over an area of EP.
mucous fibrosis is burning sensation of mouth
31. Enumerate the tobacco associated lesions aggravated by spicy food (42%) followed by
less likely to become cancers. either hypersalivation or dryness of mouth
These lesions have not shown excess risk for (25%).
malignant transformation. Signs: The common sign is blanching, i.e.
1. Preleukoplakia marble-like appearance of oral mucosa. It may
2. Leukoedema be localized, diffuse or reticular. The patient
3. Smokers palate with localized blanching who chew only areca
4. Palatal erythema nut the incubation period is short, while betel
5. Palatal erythema with papillary hyperplasia, quid chewers it is long. Reticular blanching
6. Tobacco pouch keratosis (tobacco-lime (lace-like) consist of blanched areas with
users lesion) intervening, clinically normal mucosa giving
it lace-like appearance. Over the time one type

of blanching may change to other type.
35. What is elliptical rima oris?
In oral submucous fibrosis when lips are
involved, the connective tissue and muscle
bands in the lips run around the rima oris
like a thin band. In severe labial involvement,
the opening of mouth is altered to an elliptical
shape.
Heavy curtain like appearance
Heavy curtain and shrunken uvula appearance
36. What is heavy curtain like appearance

and hockey stick like appearance and
bud-shaped uvula?
Involvement of soft palate in submucous
fibrosis is marked by fibrotic change and a
clear delineation of soft palate from the hard
palate as if a “heavy curtain‘ is hanging from
the hard palate.
Hockey stick uvula: The uvula in submucous Heavy curtain like appearance and bud-shaped
fibrosis is sunked and hooked up like a hockey uvula
stick due to fibrosis and is called hockey stick in the form of greyish-white to dramatic
uvula (turned to one side). wrinkled, fissured surface texture, numer-
Bud-shaped uvula: The uvula in submucous ous erythematous spots may distributed
fibrosis is shrunken and small is called bud or the diffuse blanching and the multi-
shaped (it is not tuned to one side). nodular appearance of the hard palate. The
37. Mention the conditions considered for orifices of the palatal minor salivary glands
differential diagnosis of oral submucous can be appreciated as minute, red spots.
fibrosis. 2. Palatal erythema associated with the
palatal excrescences in individuals in heavy
In early stages anemia because of pale mucosa
smokers. The elevated red areas are the
may be mistaken for blanching. In severe
orifices of the palatal minor salivary glands.
anemic condition, the oral mucosa is pale and
hyperpigmented, the tongue is depapillated
and buccal mucosa is coarse, the criteria of
palpable bands is diagnostic.
Scleroderma (oral manifestation) is another
entity to be considered. It is generalized. The
occurrence of scleroderma is rare and rarer is
still oral involvement. Sometimes the blan-
ching is well-circumscribed, i.e. localised can
be mistaken for leukoplakia in the absence of
other features of oral submucous fibrosis.
38. Name the various disorders of oral mu-
cosa associated with smokeless tobacco.
Excessive use of tobacco has been associated
with several lesions in the oral cavity, which
include tooth stain (brown to black mainly on
lingual aspects of molars), tobacco-related
blanching of mucosa seen in chewers (gene-
rally palate), palatal erosions, tobacco-induced
pigmentation (greyish white), lichenoid type
of reactions, sometimes areas of depigmen-
tation intermingled with pigmentation.
Gingivitis, gingival recession, periodontal
conditions, acute necrotizing ulcerative
gingivitis. Abrasions, tobacco excrescence,
burns, hyperkeratotic lesions mainly on lateral
border of tongue, hairy tongue, tobacco pouch
keratosis and leukoplakia. Verrucous carci-
noma if present shows adjacent tobacco pouch
keratosis (ST mucosal lesions), squamous cell
carcinoma and oral field cancerization.
39. Name the lesions associated with tobacco
smoking.
The lesions are as follows:
1. Nicotinic stomatitits (smoker’s palate):
Hard palate shows characteristic changes
3. Palatal white patches in reverse smoking:

The combustion product of tobacco and
extreme heat responsible for palatal
changes which range from white to
erythematous patches.
4. Smokers melanosis: Common condition in
dark-skinned ethinic group. It presents as
diffuse, brown, pigmented patch. Anterior
gingivae, buccal mucosa common site while
tongue may be involved. Smoker’s melano-
sis is caused by stimulation of melanin
production by melanocytes due to chemical
substances in cigarette smoke.
7. Smoker’s patch: This condition describes

altered condition of epithelium due to
smoking, most of lesions are in the midline
or one side. Patch or roughly oval-shaped
area. It is small in size roughly oval in
shape. The surface of patch may be smooth
and not ulcerate or exociarated and after-
wards it may become covered by yellowish
5. Cigarette smoker’s lip: It is a localized, material, sometimes red and crusted area,
usually well-defined, flat or slightly elevated not tender.
lesion of the lips that corresponds to the 8. Preleukoplakia: Greyish-white patch
area where the patient holds cigarettes. The
lesion usually begins as a reddened area but 40. What are the changes in palate due to
becomes whiter with time. smoking?
These changes are as follows:
1. Keratosis: Diffuse whitening of entire
palatal mucosa.
2. Excrescences: 1–3 mm elevated nodules
often with red spots which represent initial
palatal reaction and are transient.
3. Patches: Well-defined elevated white
plaques.
4. Red areas: Well-defined reddening of
palatal mucosa.
6. Central papillary atrophy of the tongue: 5. Ulcerated areas: Crater-like areas covered
This is noted in the bidi smokers. This is by fibrin.
reduced spontaneously once the habit 6. Non-pigmented areas: Palatal mucosa
cessation occurs. devoid of pigmentation.
41. What are the palatal changes associated

with reverse smoking?
Palatal mucosal changes in reverse smokers
were of varying degrees ranging from adap-
tive changes to potentially malignant lesions
and ulcerations. The adaptive changes are
hyperpigmentation and excrescence. Depig-
mented areas are the transition regions
between the adaptive and potentially malig-
nant lesions. Potentially malignant lesions
were leukoplakia and erythroplakia.
Keratosis: May be independently or co-exist
with other components. Account for 55% of
component. Reverse dhumti smoker’s lesion: Mostly in
Goa, lesion is less severe than by reverse
chutta smoking.
Excrescences: It is present in severe form in Patches: Same as leukoplakia, but differ

reverse smokers. Account 46% of palatal histologically, account for 12% of component.
components. Leukoplakia seen in areas of depigmentation.
Hyperpigmentation: It presents melanin pig-

Red areas: Indistinguishable from erythro- mentation in spotted, linear, patchy, diffuse
plakia and account for 2% of palatal com- and reticular types.
ponents.
Ulcerated areas: They represent burn type of Non-pigmentated areas: Clinically devoid of
reaction, ulcers and account for 2% of palatal melanin pigmentation and are surrounded by
components. hyperpigmentation.
42. What are multimorphic lesions in palate

due to smoking?
Keratosis and excrescences co-exist more
frequently, then excrescences and patches, red
areas and patches. The co-existent changes
with non-palatal changes include leukoplakia
on dorsum of tongue which is an otherwise
uncommon location for it and may progress
to malignancy (0.3%). This indicates that
deleterious habit of reverse smoking may
extend to other locations that are in close
proximity to the lightened end of chutta.
43. What is geographic tongue? What is

etiology and types of it?
Benign migratory glossitis also known as
geographic tongue is a recurrent condition of
unknown etiology characterized by loss of
epithelium particularly of the filiform papillae

on the dorsum of the tongue. Clinically the
appearance is of multifocal, circinate, irregular
erythematous patches bounded by slightly
elevated, white colored keratotic bands.
The etiology and pathogenesis remains obs-

cure. Many risk factors have been proposed
including hormonal disturbances, oral contra-
ceptive use, juvenile diabetes mellitus,
pustular psoriasis, allergic conditions such as
atopy, hay fever and rhinitis, fissured tongue,
Robinow’s syndrome, Reiter’s syndrome,
Down’s syndrome, psychological factors,
nutritional deficiencies, lithium therapy,
familial predisposition, fetal hydantoin syn-
drome and Aarskog’s syndrome.
• Type I: Lesions confined to tongue in both
active and remission phases. No other
lesions in oral cavity.
• Type II: Same as type I with similar lesions
in other areas of oral cavity.
• Type III: Lesions on the tongue that are not
typical and accompanied by lesions in other
areas of oral cavity. It has got two forms
fixed and abortive.
– Fixed: A few areas of tongue affected, no
movements of lesion seen. They may dis-
appear and reappear on the same location.
– Aborative: The initial lesion is yellowish-
white patches. These disappear before
acquiring the typical appearance of geo-
graphic tongue.
• Type IV: No tongue lesions but the mig-
ratory lesions are present elsewhere in the
oral cavity (erythema circinata).
44. What is kissing lesion?
Median rhomboid glossitis (MRG) is con-
comitant with a palatal inflammation corres-
ponding to contact with the involved area on
the tongue, it is called ‘kissing lesion’ and this Some authors quote that furred tongue is
finding may suggest the prolonged contact an uncommon disease which is occurring
between the Candida-infected dorsum of the during febrile diseases appear as thick or
tongue and the hard palate. In these patients thickish white yellow coating on dorsal
immunosuppression should be suspected and surface of tongue. This lesion is due to
investigated and it has been considered as a lengthening of filiform papillae by 3–4 mm
marker of HIV infection. and accumulation of food debris and bacteria.
It disappears shortly.
45. What is furred tongue?
It is also called hairy tongue. It is defined as 46. What are the varices of tongue?
thickened surface of tongue with color It is also called sublingual varices. It is defined
change from black to white. It results from as tortuous veins undersurface of tongue
hypertrophy of filiform papillae and the des- bilaterally. The other presentation is multiple
quamated epithelium is trapped into it resul- blue purple or elevated pappular blebs on
ting in large plaque. It is seen in febrile illness ventral/lateral surface of tongue. The reason
and smokers. The patients with soft diet show is vasodilation and venous ectasia with aging,
furred tongue and the patients who are not which is due to loss of connective tissue tone
having diet high in roughage and fibre. The supporting vessels. Occasionally, a single
associated findings are xerostomia and pala- varix may be noted with soft purple papule
titis nicotina in mouth breathers and smokers
respectively. Proper brushing and diet modifi-
cation are necessary.
Hairy tongue and furred tongue

which intends with firm palpation. Lips and broad spectrum antibiotics), e.g. mucor-
buccal mucosa are the other areas where it is mycosis and aspergillosis. Other risk factors
present. The lesions are asymptomatic except are organ transplants patients, variety of
where secondary thrombosis occurs. systemic/immunological disorders (systemic
lupus erythematosus), alcohol/IV drug abuse.
47. What is cheilocandidiasis? Recipients of previous treatment with cortico-
A diffuse form of chronic candidiasis charac- steroids, cytotoxic agents, prolonged antibiotic
terized by pain, swelling, erythema with focal therapy.
ulcerations, and crusting is called cheilocandi-
diasis. It represents a secondary candidal 50. What are types of oral candidiasis?
infection superimposed on areas of trauma These are primary and secondary.
from mechanical or solar factors. Primary infections are limited to oral and
perioral sites, e.g. acute erythematous, acute
48. What is superficial and deep fungal pseudomembranous, chronic erythematous,
infections? chronic psuedomembranous and chronic
Superficial fungal infections have an affinity hyperplastic, chronic plaque like, and nodular
for keratin and epidermis and adnexal candidiasis. Candida associated lesions are
structures. These usually have a characteristic denture stomatitis, angular cheilitis, and
clinical finding (none to a painful burning median rhomboid glossitis.
sensation causing dysphagia) and diagnosis
Secondary infections are accompanied by
is done on clinical findings, e.g. candidiasis.
systemic mucocutaneous manifestations, e.g.
These are managed with topical antifungal
familial chronic mucocutaneous candidiasis,
agents. The superficial infections have incuba-
diffuse chronic mucocutaneous candidiasis,
tion period relatively short, the onset of dis-
candidiasis endocrinopathy syndrome,
ease is sudden and the symptoms are initially
familial mucocutaneous candidiasis, severe
severe but decrease in severity with time, so
combined immunodeficiency, DiGeorge
that spontaneous healing may occur.
syndrome, chronic granulomatous disease
Deep fungal infections are less common and and AIDS.
affect deeper structures, internal organs. These
affect sites other than oral cavity and may be 51. Which is the painful candidiasis type?
an indicator of systemic diseases. These are Acute atrophic or erythematosus variety.
commonly noted in immunosuppressed
individuals (HIV, AIDS and malignancies). 52. Which type of candidiasis may show
These are more dangerous than superficial. malignant transformation?
Diagnosis is confirmed by biopsy, e.g. Hyperplastic type which is refractory to
aspergillosis, histoplasmosis deep infections, treatment.
on the other hand, have a protracted incu- 53. What are the host factors associated with
bation period, the symptoms are insidious in candidiasis?
their onset, and the course of disease becomes
increasingly severe. These factors are divided into local and
systemic in nature.
49. What is opportunistic fungal infections? Local causes are inhaled corticosteroids cause
The opportunistic fungal infections are those erythematous candidiasis. They suppress
which affect mostly immunocompromised localized cellular immunity and phagocytosis
patients and debilited patients (AIDS, promotes establishment of candida. Impaired
leukemia/lymphoma, particularly during salivary flow, as salivary flow serves to dilute
chemotherapy and in patients who are and remove potential pathogenic microorga-
receiving immunosuppressive agents and nisms.
Systemic causes are medications causing

xerostomia antihistaminics, tricyclic anti-
depressants, some antihypertensives, hypno-
tics and sedatives. Broad spectrum antibiotics
increase susceptibility to Candida infection by
altering local flora that naturally inhibit
candidal growth. Other medications are anti-
neoplastic agents, immunosuppressive agents
(azathioprine and glucocorticoids), anticho-
linergic medications. Smoking, DM, endo-
crinopathies, immunosuppressive conditions,
malignancies and nutritional disorders. Cottage cheese appearance
54. Enumerate various drugs used for treat-
ment of fungal infections. Reddened bald appearance: This is seen in
erythematous candidiasis. It shows painful
1. Azoles-imidazoles (clotrimazole, micona-
reddened mucosa with a little or no white
zole, ketoconazole), triazoles (fluconazole,
component. In acute form the dorsal surface
itraconazole)
of tongue will usually show diffuse loss of
2. Polyenes (amphotericin and nystatin) filiform papillae resulting in reddened bald
3. Echinocandins (caspofungin) appearance. This is also accompanied by
4. Pyrimidines (flucytosine) burning sensation. It typically follows a course
55. What is curdled milk appearance and of broad spectrum antibiotics. Patient often
reddened bald appearance? complains that mouth feels as if hot beverage
Oral lesions of pseudomembranous candi- has scalded it.
diasis (thrush). It is characterized by the
presence of adherent white plaques. This is
also called cottage cheese appearance. These
can be easily wiped off leaving either
erythematous area or normal mucosa which
can easily bleed. It is often seen in baby’s
mouth or lips. It occurs in newborns and
infants. It may be passed from mother to baby
if the delivering mother has yeast infection.
This is also called cottage cheese appearance

(curdled milk appearance)
56. What is id reaction? and extremities, even on palms and fingers the
Occasionally, a papular/pustular wide- lesions are seen. No specific therapy is
spread cutaneous eruption appears (occasion- required.
ally vesicles) after the commencement of
systemic antifungal treatment—this is so 57. Enumerate the differentiating points
called id reaction. This is immunological between hemangioma and vascular
response (autosensitization) and not an malformation.
adverse drug reaction. It is a distant skin Differentiating points between hemangioma
manifestation of an established fungal infec- and vascular malformation is shown in
tion. The most common location is on trunk Table 1.1.
Table 1.1: Characteristic differences between hemangioma and vascular malformation

Hemangioma Vascular malformations
Definition Hemangiomas are noncancerous “Vascular malformation” is a gene-
growths that form due to an abnor- ralized term used to describe a
mal collection of blood vessels. group of lesions, present at birth,
formed by an anomaly of angio-
vascular or lymphovascular
structures
Description Proliferation of abnormal Development of abnormal blood
endothelial cell vessels occurs
Elements Capillaries are increased in A mix of arteries, veins and capil-
numbers laries (A-V shunt)
Growth pattern Congenitally rapid growth It grows with patient
F:M ratio 3–5:1 and severe cases 7:1 1:1
Boundaries Often circumscribed Poorly circumscribed
Bone involvement Rarely affects bone (distortion May affect bone (distortion,
but no invasion) thinning, underdevelopment,
hypertrophy, invasion, destruction
and rarely lytic lesions)
The vibrations and Not associated with thrill May be associated with thrill or
abnormal sounds or bruit bruit
Involution Spontaneous involution is Does not involute
possible
Radiology Doppler sonography: Doppler ultrasonography:
Fast flow lesion Slow-fast flow
MRI—tumoral mass with MRI—hyperintense signal (slow)
low voids Flow-voids (fast)
Arteriogram—lobular tumor Arteriogram—A-V shunting
Immunohistochemistry High expression of PCNA, VEGF Lack of expression
Hematology No coagulopathy Risk of bleeding (disseminated
intravascular coagulation)
Resection Persistent lesions are resectable Difficult to resect; surgical
hemorrhage
Recurrence Recurrence uncommon Recurrence common
Contd...
Table 1.1: Characteristic differences between hemangioma and vascular malformation (Contd.)
Hemangioma Vascular malformations
Clinical presentation
58. What are the complications of AVH?

The two most common AVH-related emer-
gencies that the oral and maxillofacial
specialist may need to manage are a life-
threatening bleed and a rapid proliferation of
the AVH that may obstruct the airway.
59. Enumerate the extravascular blood
lesions.
Extravascular blood lesions are due to the Ecchymosis on soft palate and on hard palate,
presence of blood outside of blood vessels. subconjunctival ecchymosis
They do not blanch and typically resolve
A hematoma is the result of hemorrhage with
within a month. The patient often has a history
pooling of blood in the connective tissue. A
of trauma or bleeding problem.
Ecchymosis is a bruise. It occurs due to
hemorrhage and accumulation of blood in the
connective tissue. It is usually the result of
trauma, but may also be secondary to defi-
ciency of platelets and/or clotting factors and
viral infections. An ecchymosis is typically flat
and red, purple, or blue in color. If the ecchy-
mosis is due to trauma, then it will resolve
spontaneously and no treatment is necessary.
If it is secondary to a systemic disease, then
further work-up is indicated.
Hematoma on right buccal mucosa

hematoma causes thickening or enlargement rubber nipple or rubber skin. Identical

of the mucosa. It is purple to black in color. lesions appear in various locations in the
No treatment is necessary once a diagnosis is gastrointestinal tract, primarily the small
made. A hematoma will resolve sponta- intestines.
neously in several weeks to over a month. 61. What are angiomatous syndromes?
Petechiae are round, red, pinpoint areas of Enumerate it.
hemorrhage. Petechiae are usually caused by These are associated with vascular malfor-
trauma, viral infection, or a bleeding problem. mations. The list includes:
They resolve over a few weeks. Petechiae do 1. Hereditary hemorrhagic telangiectasia
not require treatment. Investigation of the (Osler-Weber-Rendu syndrome): It is an
cause of petechiae may be indicated. uncommon autosomal dominant disease.
This multisystem disorder can affect the
nose, skin, gastrointestinal tract, lungs, liver
and brain. Epitaxis is the most common
presenting problem. Patients with HHT
have abnormal blood vessel development
that manifests as telangiectasias and
arteriovenous malformations (AVMs).
2. Blue rubber bleb nevus syndrome (BRBNS):
It is a rare vascular anomaly syndrome
consisting of multifocal venous malfor-
mations (VM). The malformations are most
prominent in the skin, soft tissues, and
gastrointestinal (GI) tract, but may occur in
any tissue. These patients develop anemia
and requires lifelong supplementation of
iron and blood transfusions.
3. Bannayan-Zonana syndrome: It is a rare
hamartomatous disorder, characterized by
macrocephaly, multiple lipomas, and heman-
giomas. Inheritance is by autosomal domi-
nant transmission with male predominance.
4. Sturge-Weber syndrome (encephalotrige-
minal angiomatosis): It has a vast spectrum
60. Name syndromes associated with caver- of cutaneous, neurologic and ophthalmic
nous hemangioma. manifestations which may or may not be
1. Kasabach-Merritt syndrome: In this syn- associated with one another. The oral
drome, a large cavernous or arteriovenous manifestations include ipsilateral port-wine
hemangioma is complicated by thrombo- stains of oral mucosa along with the
cytopenic purpura. hypervascular changes and angiomatous
2. Maffucci’s syndrome: Multiple hemangiomas lesion of gingiva. Gingival hyperplasia can
and enchondromas. also be attributed to anticonvulsant medi-
3. Blue-rubber bleb nevus syndromes: This cation and secondary to poor oral hygiene
rare syndrome, an autosomal-dominant in mentally retarded patients. Macroglossia
trait, produces a peculiar blue hemangioma and maxillary bone hypertrophy have also
that has the appearance and texture of a been reported in a few cases.
62. What is acquired hemangioma?

A majority of hemangiomas are congenital, but
some are acquired later in life. Some of the
acquired capillary hemangiomas of the oral
cavity may develop from infantile heman-
giomas (IH) mostly on the gingivae. The
conditions may be right for certain IH lesions
with many patent capillaries to develop
significant blood flow during the IH stage.
Such capillary systems remain after the
irritant has been eliminated and the inflam-
mation subsides. The resultant lesion is
usually nodular and bluish-red, usually bleeds
easily, and may blanch on pressure. Indicated
treatment is sclerosis, excision, or perhaps
a combination of these modalities after deter-
mination of the blood supply to the lesion.
63. Why central hemangiomas are called
great imitators?
These lesions of bone have been referred to as
the great imitators because they can produce
so many different radiographic images. It is
not pathognomonic and can stimulate many
other lesions. Worth et al. have prepared an
5. Klippel-Trénaunay syndrome (Klippel- excellent and thorough review of the various
Trénaunay-Weber syndrome; Angio-osteo- radiographic appearances.
hypertrophy): It is characterized by the
In about 50% of cases a multilocular appea-
triad of vascular malformation (capillary
rance can be detected, small (honeycomb) and
hemangioma or port wine stain), venous
large (soap bubble) loculations.
varicosity and soft tissue and/or bony
Another form these lesions can take reveals
hypertrophy.
coarse, linear trabeculae that appear to radiate
6. Servelle-Martorell syndrome: It is a conge- from an approximate centre of the lesion.
nital vascular malformation associated with Small, angular, linear trabeculae of varying
soft tissue hypertrophy and bony hypo- shapes are seen; however, the general outline
plasia. is round (cartwheel appearance) and some-
7. von Hippel-Lindau syndrome (vHL times the trabaculae are right angles to surface
syndrome): It is caused by a gene mutation (sunburst appearance).
which frequently induces both non-malig- A third appearance that may be observed
nant tumors and malignant tumors (or is a cyst-like radiolucency with an empty
cancers) that can spread to other organs cavity and sometimes a hyperostotic border.
(become metastatic). Many of the tumors The radiographic margins of these images
may involve abnormal growth of blood may be well or poorly defined. Resorption of
vessels. roots of the involved teeth occurs with some
8. Maffucci’s syndrome: This syndrome is frequency, and calcifications (phleboliths)
non-hereditary and is characterized by appearing as radiopaque rings are occasion-
multiple enchondromas and hemangiomas. ally seen.
Central hemangioma is a great mimicker,

as it resembles:
1. Osteosarcoma;
2. Fibrous dysplasia;
3. Central giant cell granuloma;
4. Ameloblastoma;
5. Multiple myeloma;
6. Dentigerous cyst; and
7. Odontogenic cyst radiographically. It also
may clinically mimic: (i) A central arteriovenous
fistula; (ii) Aneurysms; or (iii) A shunt.
64. What is erosion and ulcer?
An erosion has been defined as a shallow crater Erosion on palatal gingival
in the epithelial surface that appears on clinical
examination as a very shallow erythematous
area and implies only superficial damage.
Ulcer has been defined as a deeper crater
that extends through the entire thickness of
surface epithelium and involves the under-
lying connective tissue and associated with
underlying molecular necrosis.
65. What are short-term and persistent
ulcers?
Short-term ulcers (those that persist no longer
than 3 weeks and regress spontaneously or as
a result of non-surgical treatment). The majority
of traumatic ulcers, recurrent aphthous ulcers
(RAUs) (except major aphthae), recurrent
intraoral herpetic ulcers, and chancres fall into
the category of short-term ulcers, and persistent
ulcers (those that last for weeks and months).
Occasionally, traumatic ulcers, major
aphthae, and ulcers from odontogenic infec-
tion, malignant ulcers, gummas, and ulcers
secondary to debilitating systemic disease are
classified as persistent ulcers and may remain Ulcer on left buccal mucosa and lower lip
for months and even years. Persistent ulcers
should be considered malignant until proved aphtha (HA), recurrent erythema multiforme,
otherwise. Behçet’s syndrome.
66. Name the conditions causing recurrent 67. Enumerate the syndromes associated
ulcers. with aphthous stomatitis.
Recurrent aphthous stomatitis (RAS), recurrent- Behçet’s syndrome: It is characterized by
intraoral herpes simplex (RIHS), major recurring oral ulcers, recurring genital ulcers
aphthous ulcer (major AU), and herpetiform and eye lesions.
Magic syndrome: Mouth and genital ulcers orogenital ulcerations. In 1937, Hulusi Behçet
and polychondritis. defined the disease with classic triad of
Marshall’s syndrome (PFAPA): Periodic aphthous ulcerations, genital ulcerations and
fever, aphthous stomatitis, pharyngitis and uveitis. Other less common lesions are
cervical adenitis. cutaneous involvement, arthritis, thrombo-
phlebitis, gastrointestinal manifestations and
HIV/AIDS: Recurrent aphthous stomatitis
CNS involvement.
(RAS) is one of the common oral manifesta-
tions of HIV/AIDS. In this condition, the ulcers 69. What is pathergy test?
are similar to those of non-infected group but It is a clinical test done to diagnose Behçet’s
are long lasting and are less responsive to disease (BD). Skin lesions resembling erythema
routine medications. In many patients, major nodosum or large pustular lesions occur in
aphthae are found and are associated with ad- over 50% of patients with BD. These lesions
vanced HIV infection (CD4+ counts less than may be precipitated by trauma, and it is com-
50/mm3) which suggests that immune common for patients with BD to have a cutaneous
promise is a factor predisposing to aphthous hyper-reactivity to intracutaneous injection or
stomatitis. a needle stick (pathergy).
Sweet syndrome (SS): It is characterized by a One of the most important skin manifesta-
constellation of clinical symptoms, physical tions is the presence of positive pathergy. One
features, and pathologic findings which in- or two days after the injection of an inert
clude fever, neutrophilia, tender erythematous substance (e.g. sterile saline) using a 20 gauge
skin lesions (papules, nodules, and plaques), needle, a tuberculin-like skin reaction or sterile
and a diffuse infiltrate consisting predomi- pustule develops. This hyper-reactivity
nantly of mature neutrophils that are typically appears to be unique to BD and is seen in
located in the upper dermis. Sweet syndrome 40–88 per cent of patients with this disease.
is classified in three main types: Classical,
paraneoplastic and drug induced. Classical 70. What are the features of atypical RIHS?
type is more common in women between the • RIHS of gingival papilla
ages of 30 and 50 years, is often preceded by • Persistent infection of gingivae
upper respiratory tract infection and may be • Persistent enlarged ulcers
associated with inflammatory bowel disease
• RIHS in immunoincompetence
and pregnancy. The paraneoplastic type is
associated commonly with hematogenous 71. What are the sites of recurrent herpes
malignancy mainly acute myelogenous leuke- infections?
mia. The commonly associated solid tumors Recurrent herpes lesions may begin with a
are those of genitourinary organs, breast and prodrome of burning, tingling, or pain without
of gastrointestinal tract. Drug-induced Sweet a visible lesion. Next, a vesicle may appear that
syndrome most commonly occurs in patients will soon rupture into a moist ulcer, or an ulcer
who have been treated with granulocyte will emerge directly. Such secondary lesions
colony stimulating factor, however, other have a predisposition for the vermilion and
medications may also be associated.
vermilion-skin edge of the lips (recurrent
68. What is Adamantiades syndrome? herpes labialis).
It is also called Behçet’s syndrome or Behçet’s The lesions otherwise have a predisposition
disease. Benedict Adamantiades described in for the keratinized surfaces of the palate and
1931 as chronic ocular inflammation and gingiva.
Recurrent intraoral herpes on palate and gingiva

72. Enumerate the differentiating points of erythema multiforme and herpes infection.
Erythema multiforme Herpes infection
Age Young adults Children
Size Large ulcers Small ulcers
Vesicles Thin walled, generally at
mucocutaneous junction
Location Oral/lip ulcers Oral/perioral ulcers
Skin lesions These are target lesions Skin ulcers
Severity Mild to severe Moderate to severe
Intraoral sites Buccal mucosa, tongue, lips, palate Gingiva and lips
Extraoral sites Extremities Perioral skin
Cause Hypersensitivity HSV
Treatment Symptomatic Antiviral drugs
73. Enumerate the differentiating points between aphthous ulcers and recurrent herpes
simplex infection.
Aphthous ulcers Herpes infection
Cause Immune dysfunction HSV 1
Triggers Stress, trauma, diet, hormones, Stress, trauma, depressed
depressed immunity, smoking immunity, UV light
Prodrome Little prodrome Prodromol symptoms
Clinical appearance No vesicles Vesicles precede ulcers
Single oval ulcers Multiple confluent ulcers
Microscopic appearance Non-specific Viral cytopathic changes
Sites Non-keratinized Keratinized
Treatment Corticosteroids, tetracycline Antiviral treatment
74. Name the conditions exhibiting oral produce minimal symptoms. Scarring, parti-
fissures. cularly of the conjunctiva, is the mechanism
1. Angular cheilosis, exfolative cheilitis of debilitation associated with cicatricial
2. Denture irritation hyperplasia, epulis pemphigoid (hence its name).
fissuratum As the disease continues, scar bands form
3. Congenital cleft, median rhomboid glos- between the bulbar conjunctiva (the conjunc-
sitis-fissured variety tiva over the globe) and the palpebral conjunc-
4. Fissured tongue, Melkersson-Rosenthal tiva (the conjunctiva over the inner eyelids),
syndrome called symblepharon. This scar band in
5. Squamous cell carcinoma—fissured variety particular contracts to invert usually the lower
6. Syphilitic rhagades, cheilitis granulomatosa lid eyelashes toward the cornea in a condition
called trichiasis. This, in turn, abrades the
7. Plasma cell gingivostomatitis
cornea, causing ulceration, which leads to
8. Riboflavin deficiency, Plummer-Vinson opacifications and even blindness in 15% of
syndrome cases. In severe cases, scar bands will connect
9. Crohn’s diseases, pyostomatitis vegetans, the upper and lower palpebral conjunctiva to
Down’s syndrome partially close the eye, a condition called
75. What is symblepharon? What is its ankyloblepharon.
further stage called? What are the other The other lesions are triachiasis and
ocular lesions of pemphigoid? entropion.
The ocular lesions of pemphigoid are symble- Entropion of the eyelid occurs when the lid
pharon, triachiasis and entropion. margin inverts or turns against the eyeball.
The condition is seen in cicatricial pemphi- Trichiasis is the eyelashes grow inward
goid. The conjunctiva will be reddened but will towards eye touching cornea or conjunctiva.
Entropion after epilation

76. What are the differentiating points of pemphigus and benign mucous membrane
pemphigoid?
Pemphigus Benign mucous membrane pemphigoid
Bulla location Intraepithelial Subepithelial
Antibodies are directed against Desmogleins Collagen proteins
Lesions distributed on Oral mucosa and skin Oral mucosa and eyes
Bulla Thin Thick
Rupture of bullae Easily Not easily
Prevalence Common Infrequent
Scarring Absent Present
Acantholysis Absent Present
77. How erythema multiforme differs from SJS and TEN?

Erythema multiforme (EM) SJS and TEN
Erythema multiforme (EM) is typically mild, self- SJS and TEN are less common and more severe
limiting and recurring mucocutaneous reaction condition
Immune mediated inflammatory reaction Hypersensitivity reaction
Common under 40 years of age, rarely seen Adults
under the age of 3 and over 50 years
Little gender difference Women are affected twice as men.
Seasonal clustering in spring Nothing
No hereditary There may be hereditary component
Not associated with HIV Increased incidence in HIV-infected population
Infectious in origin HSV-1, HSV-2, 80–95% of TEN and 50% SJS are precipitated by
progesterone therapy drugs (sulfonamides, NSAID, penicillin and
anticonvulsants, other causes are graft vs host
disease, mycoplasma pneumonia).
Epidermal necrosis of keratinocytes termed Much more widespread necrosis of epidermis
satellite necrosis and little vascular inflammation of dermis
Periascular infiltrate of CD4 and CD8 lympho- Remarkable absence of lymphocytes
cytes
Skin lesions show multiple target/iris lesions Target lesions are not well-defined and larger
All lesions typically present within 3 days of Lesion may appear 45 days of drug treatment
onset and a few days of repeat exposures
Nikolsky’s sign not positive Nikolsky’s sign positive
Lip involvement is almost universal Lip, buccal mucosae and palate may be involved.
Erythema multiforme shows variety of lesions These lesions spread over much surface of body
but only 10% of body surface is involved within short time. Large lesions more than 30%
define TEN
Prodormal symptoms are rare and if present are Prodrome occurs 7 to 14 days in advance of lesion
typically mild and non-specific (cough, rhinitis, (fever, malaise, headache, cough, rhitis, sore-
low-grade fever) throat, myalgia, arthralgia)
EM is recurrent phenomenon with highly Repeat attacks do not occur if the offending drug
variable frequency and severity of episodes is strictly avoided
Medical complication related to EM is rare The sloughing may involve oesophagus and
respiratory tree, conjunctival lesions may
proceed to blindness, and genital ulceration may
proceed to urinary retention and phimosis.
Sepsis from skin infections, cardiac compli-
cations, and renal failure may cause death.
Laboratory investigations—no significant Blood sedimentation rate is increased, moderate
abnormality leukocytosis, hyponatremia, anemia
Investigative focus is identification of infectious The effort to identify the drug
agent particularly HSV
Treatment is prevention HSV infections Indefinite avoidance of drug
78. What are typical and atypical target outer zone but may evolve to three zones of
lesions? color change.
Typical target lesions—skin lesions of ery- Atypical target lesions are dark red macules
thema multiforme are pathognomonic. which have a central blister, may or may not
They may accompany the oral condition, be raised and have a poorly delineated border
or there may be cutaneous manifestation or they may have two concentric zones and
without oral involvement. Skin lesions have a have area of palpable, rounded edematous
characteristic “bullseye” or “target” appea- lesions with poorly defined borders. They are
rance. Although the palms of the hands are a more common in SJS and TEN.
classic location, these lesions may occur any- The typical target lesions are acral while
where on the skin. A target lesion consists of atypical target lesions are usually truncal.
concentric zones of color change with evidence
of damage to the epidermis in central zone 79. What is centripetal and centrifugal
such as bulla formation or crust. Early target spread? Give examples of oral mucosal
lesions will have a central dusky zone and a red lesions with same spread?
The lesions of the disease which spread
towards centre or axis are called centripetal.
The lesions of the disease which spread away
from the centre or axis are called centrifugal.
The target lesions of erythema multiforme
form on extensor surfaces of acral extremities
and spread centripetally, rocky mountain
spotted fever has centripetal rash, staphylo-
coccal TSS has erythematous rash which
spreads centripetally.
Chickenpox rash begins on trunk and
spreads on face—centripetal spread while it
also has centrifugal spread to extremities.
Varicella rash has centripetal distribution, in
contrast, variola rash has centrifugal distri-
bution and common on trunk, face.
Varicella spreads centripetally from skin to
neurons centripetally to dorsal root ganglion
where it remains latent and upon reactivation
results in centrifugal spread which results in
shingles.
Lesions of ACLE also involve palms and
soles and may spread centripetally.
Cutaneous invasive squamous cell carci-
noma may spread centripetally rarely along the
trigeminal nerve axis into the cavernous sinus
and gasserian ganglion.
Rabies virus may spread centrifugally from
Typical target lesions CNS to salivary acinar cells.
80. What is angina bullosa hemorrhagica? Strawberry gingivitis: Particularly straw-

Angina bullosa hemorrhagica is a rare and berry-like gingivitis or hyperplastic gingival
benign disorder, usually localized in the subep- lesions are suggested to be a characteristic sign
ithelial layer of the oral, pharyngeal and eso- of granulomatosis with polyangitis. This sign
phageal mucosa. The lesions are characterized consists of reddish-purple exophytic gingival
by their sudden onset. They appear as a pain- swellings with petechial hemorrhages, thus
less, tense, dark-red and blood-filled blister in similar to strawberries. This lesion can remain
the mouth that rapidly expand and rupture localized in the oral cavity for unusually long
spontaneously in 24–48 hours. The bullae are periods of time before multi-organ involve-
present in the absence of any systemic disorder ment occurs.
and hematological disease.
81. What are strawberry like lesions in and

around oral cavity?
These are strawberry gingivitis, strawberry
tongue and strawberry nevus.
Strawberry tongue: It is seen in scarlet fever. 82. What are the types of denture stomatitis?
The tongue is initially coated with a white, • Type 1: Localized inflammation or pinpoint
furry tongue with red projecting papillae hyperemia.
(white strawberry tongue), by third or fifth day • Type 2: More diffuse erythema (redness)
the white coat slough off leaving a red swollen involving part or all of the mucosa which
tongue (red-strawberry tongue). is covered by the denture.
• Type 3: Inflammatory nodular/papillary
hyperplasia usually on the central hard
palate and the alveolar ridge.
83. Enumerate the conditions in which oral
mucosal and conjunctival lesions are
seen.
Benign mucous membrane, cicatricial pemphi-
goid, SJS, TEN, hereditary benign intra-
epithelial dyskeratosis even sometimes lesions
of discoid lupus erythematosus. Even lichen
planus is also reported in the literature.
84. What is linear gingival erythema?
Enumerate the conditions causing linear
gingival erythema.
This is unusual form of gingivitis appears with
a distinctive fiery linear band of erythema
Strawberry nevus (strawberry hemangioma):

It is also called congenital hemangioma
appears around time of birth and disappears
at childhood. These are raised, verrucous,
cutaneous vascular lesions with a reddish-
purple color.
that involves free gingival margin and extends form of gingivitis first reported in the United
2–3 mm apically. Sometimes it is seen as States, usually arises as a hypersensitive reac-
petechiae and diffuses gingival erythema and tion to a component of chewing gum, denti-
involves alveolar mucosa too. Formerly it was frices, or some of the dietary components. It
called HIV gingivitis. It is seen in HIV asso- commonly presents as a mild marginal
ciated periodontal disease and abnormal gingival enlargement, sometimes extending to
immune response. It is seen in association with involve the attached gingiva.
candidosis. The lesions may be generalized or
involve one or two teeth. No ulceration, pocket- Clinical Features
ing or loss of attachment is observed. Bleeding This disease is more prevalent in young
on probing is not present. The characteristic women. The initial symptom is soreness of the
feature is maintaining good oral hygiene and mouth, which is intensified by hot or spicy
gingival debridement does not resolve the food. It starts as mild marginal gingival
problems. enlargement and extends to attach gingiva, and
Similar clinical feature may be seen in in severe cases, extends to buccal and vesti-
neutropenia, the clinician should rule out by bular mucosa. Gingiva appears swollen,
doing routine blood investigations. erythematous, and friable with loss of stip-
Treatment should include debridement, pling. It may be granular sometimes. The
providone iodine irrigation, chlorhexidine involvement of other oral tissues like the
mouth rinses and antifungal medication. tongue and lips is common. They appear
atrophic, dry, and exhibit cracks or fissures.
85. What is plasma cell gingivitis?
The differentiating point from plaque induced
Plasma Cell Gingivitis gingivitis is that it involves the oral aspects of
Plasma cell gingivitis (atypical gingivitis, attached gingival tissue.
plasma cell gingivostomatitis). This distinct
Treatment and Prognosis • Pemphigus

Possible allergens should be identified by • Psoriasis
careful study of the patient’s history and • Bullous pemphigoid
eliminated. Topical and systemic steroids give • Epidermolysis bullosa
good results. • Contact stomatitits
86. Enumerate the conditions in which des- • Linear IgA disease
quamative gingivitis is seen. B. Endocrine disturbances
Desquamative gingivitis (DG) is a descriptive • Estrogen deficiency (following oopho-
term first introduced by Prinz in 1932, i.e. rectomy and in postmenopausal stages)
synonymous with the presence of erythema, • Testosterone imbalance
desquamation, erosion and blistering of • Hypothyrodism
attached and marginal gingiva. It is a clinical
term used to describe red painful, glazed, C. Aging
friable gingiva. Nikolsky’s sign often shows D. Immunological disorder
positive reactions with DG. It is more common • Crohn’s disease.
in middle aged to elderly female, affects labial/ • Chronic ulcerative stomatitis
buccal gingival frequently spares the marginal
gingiva. It can involve whole thickness of E. Idiopathic
attached gingiva. It does not respond to con- F. Chronic infections
ventional periodontal therapy or traditional • Tuberculosis
oral hygiene measures. Nisengard and Levine • Chronic candidiasis
suggested following criteria standard for • Histoplasmosis
clinical appearance of desquamative gingivitis: Overall mucous membrane pemphigoid, oral
1. Gingival erythema not resulting from lichen planus are most common causes
plaque accounting for 80% of cases while pemphigus
2. Gingival desquamation is second most cause. Desquamative gingivitis
3. Other intraoral and sometimes extraoral is the main oral feature of mucous membrane
lesions pemphigoid and may be sole presenting
4. Complaint of sore mouth particularly after feature.
eating spicy foods. • Pemphigus
A. Dermatological disorders • Benign mucous membrane pemphigoid
• Cicatricial pemphigoid • Erosive lichen planus
• Lichen planus • Desquamative gingivitis is not a diagnosis.
Presentation in pemphigus and cicatricial pemphigoid

Characteristics peeling of tissues showing desquamation
87. What are reactive lesions appearing in reacting to, such as bacterial, viral, or fungal
the oral cavity? Enumerate various infections or chemical or physical injury.
reactive lesions.
Some examples of reactive soft tissue enlarge-
Reactive soft tissue enlargements are caused by ments:
injury, such as infections, physical trauma,
• Mucocele (salivary extravasation pheno-
chemical trauma, or allergic reactions. Reactive
menon)
soft tissue enlargements usually have a rapid
• Necrotizing sialometaplasia
onset (short duration) and may increase and
decrease (fluctuate) in size and usually even- • Periodontal abscess
tually regress. Reactive enlargements are often, • Radicular (periapical) abscess
but not always, tender or painful and usually • Fibrous hyperplasia
have a more rapid growth rate (measured in • Inflammatory papillary hyperplasia
hours to weeks) than tumors. Sometimes Varix and acquired malformations, pyo-
patients with reactive enlargements will be genic granuloma, peripheral giant cell granu-
able to report the source of injury. Sometimes loma, scarlet fever.
reactive lesions are associated with tender Reactive lesions of salivary gland origin—
lymph nodes and systemic manifestations, mucous extravasation phenomenon, mucous
such as fever and malaise. Once it is decided retention cyst (obstructive sialoadenitis),
that a soft tissue enlargement is reactive, the maxillary sinus retention cyst, necrotizing
next step is to determine what the lesion is sialometaplasia, adenomatoid hyperplasia.
Reactive osseous and chondromatous 89. Enumerate the various inflammatory

metaplasia. Occasionally, cartilage or bone reactive hyperplasias and name there
may be discovered within soft tissue specimens etiological factors.
removed from the oral cavity. • Irritational fibroma
• Chronic inflammatory gingival enlarge-
88. What are inflammatory hyperplasias? ments
What are the characteristics of infla-
• Pyogenic granuloma
matory and fibrous hyperplasias?
• Hormonal tumor—puberty gingivitis,
This is an increase in the size of an organ or pregnancy tumor
tissue due to an increase in the number of its
• Fibroepithelial polyp/mucoepithelial
constituent cells, as a local response of tissue
polyp
to injury. It can be considered as an over-
• Epulis fissuratum
exuberant reparative response.
• Parulis
• No malignant potential
• Peripheral giant cell granuloma
• Periphery oral mucosa—trauma
• Pulp polyp
• Recurrences—failure to eliminate source of • Gingival polyp
chronic irritation
• Epulis granulomatosum
• Bone erosion—rare aggressive, malignancy.
Causative factors—trauma (chronic)—cal-
• Local excision—microscopic examination
culus, ill-fitting dentures, overhanging dental
(fibrous, granulation).
restorations, biting injury, fractured teeth.
Circulating hormones.
90. Discuss the differential diagnosis of most commonly occurring inflammatory reactive
hyperplasia.
The commonly occurring inflammatory reactive hyperplasia are fibroma, pyogenic granuloma
and peripheral giant cell granuloma.
Fibroma Pyogenic granuloma Peripheral giant cell
granuloma
Age of occurrence 4th to 6th decade Children, young adults 31–41 years
Intraoral common Buccal mucosa Gingiva/maxilla Gingiva/mandible
site
Bleeding Does not bleed Bleeds May/may not
Overlying surface Smooth, pale surface, Ulcerates, red, rapid May ulcerate, red to pale
pink, slow growth growth Not rapid growth
Clinical photographs
of lesion
91. Why pyogenic granuloma is called pyo- necrotic. The fact that this necrotic white
genic in spite of no frank pus formation? material clinically resembles pus prompted
Clinically the asymptomatic reddish papule, early clinicians to refer to the lesion pyogenic
nodule or polyp usually shows at least part granuloma. However, there is no pus in the
of its surface to be rough. Ulcerated and lesion.
92. Describe differences between gingival polyp and pulp polyp.

Gingi val polyp Pulp polyp
Originates from gingiva Originates from pulp
Runs towards centre Runs outwards from the centre
Broad base Narrow stalk
Proximal surface Occlusal surface
Can be separated from the tooth Attached to the tooth
Bleeds easily on probing May not bleed easily
Excision/local debridement Endodontic/extraction
93. Why peripheral giant cell granulomas

(PGCG) occur anterior to molar regions?
The etiology and nature of PGCG still remains
undecided. In the past, several hypotheses
had been proposed to explain the nature of
multinucleated giant cells including the
explanation that they were osteoclasts left
from physiological resorption of teeth or
reaction to injury to periosteum. There is strong
evidence that these cells are osteoclasts as they
have been shown to possess receptors for
calcitonin and were able to excavate bone in
vitro. Giant cells are present mainly in the
anterior to molar regions which are required
for resorption of deciduous tooth, hence
peripheral giant cell granulomas occur anterior
to molar region.
94. In which conditions central giant cell

lesions are seen?
Central giant cell lesions can be seen in hyper-
parathyroidism (“brown tumors”), cherubism,
Noonan syndrome and neurofibromatosis
type 1. In the last two, this association may be
coincidental.
95. What is parulis?

It is also called gum boil yellowish-white
gingival swelling caused by submucosal pus.
The cause is periodontitits or tooth abscess,
causing sinus tract. Usually, on buccal gingival
of children and young adults. The mandibulo-
alveolar mucosa and palate may also be
involved. Slight digital pressure on the peri- fibrinous base or slough surrounded by a small
phery of a parulis may force a drop of pus zone of erythema.
from the sinus opening, and this is almost
Second and most predominant type is a T-cell
pathognomonic. The lesion usually regresses
mediated immune reaction: Initially, the
spontaneously after the chronic odontogenic
offending drug is topically absorbed through
infection has been eliminated. If size is
intact skin or mucosa. During absorption, the
considerable and there is a substantial amount
drug contacts the Langerhans’ cells, which
of fibrosis, however, the lesion regresses
exist in the middle zone of the prickle cell layer
somewhat and then persists as FH (fibrous
in both skin and mucosa. The Langerhans’ cell,
hyperplasias).
which seems to be a type of histiocyte, proces-
96. What is bleb? Name the conditions ses the drug as an antigen. It will present the
exhibiting gingival bleb. drug on its cell membrane to T-lymphocytes,
creating antigen-sensitized T-lymphocytes.
Bleb is pooling of fluid below tissues. Gingival
When the drug is topically absorbed a second
blebs are seen in benign mucous membrane
time, the sensitized T-lymphocytes will react
pemphigoid, cicatrical pemphigoid. Blue to
by secreting an array of lymphokines that
purple colored blebs are seen in lingual varieces.
produce inflammation and tissue injury
characteristic of contact reaction “allergies.”
97. Enumerate the necrotizing conditions of
This may affect skin (contact dermatitis) or oral
oral cavity.
mucosa (contact stomatitis). Such reactions
Acute necrotizing ulcerative gingivitis, noma, will mostly be areas of boggy erythema corres-
necrotizing sialometaplasia, toxic epidermal ponding to the drug contact and the pattern
necrolysis (TEN). Diffuse gangrenous dispersal by tongue, lip, and swallowing
stomatitis (severe debilitating conditions like movements. If the reaction is more severe,
diabetes, uremia, leukemia, etc). However, actual vesicles or ulcers may form. The prime
erythema multiforme, pemphigus in severe offending agents have been cosmetics,
extent and lesions caused by electrical burns including lipsticks and lip balm, and dental
can be necrotizing in nature. Necrotizing preparations, such as toothpaste and some of
ulcerative periodontitis (NUP) and necrotizing its ingredients. In particular, mint and
ulcerative stomatitis (NUS) in HIV patients. cinnamon flavourings have been implicated in
Necrotic ulcers may occur in debilitating oral contact stomatitis. Cosmetic and skin care
systemic diseases such as leukemia, sickle cell preparations have been such prominent
anemia, and uremia. offenders that complete lines of hypoallergenic
products have been developed. Included in this
98. What are the types of contact drug
group is hypoallergenic surgeon gloves, which
reactions?
were developed because the powdered starch
These are of three types. in many gloves induced a typical contact
First type is a direct drug toxicity: Whereby dermatitis. One supposed cause of contact
the pH or an active chemical site produces a stomatitis that has been grossly overstated for
physical injury to the tissue. “Aspirin burn” years is that related to denture acrylic. There
caused by the acidic pH of aspirin and the is little if any direct evidence to support a true
chemical burn of capsicum in sharp peppers “denture contact stomatitis.” Most so-called
are examples of direct drug toxicity. Such denture reactions represent other diseases,
reactions are direct physical injuries, not actual such as candidiasis, pemphigoid, lichen
immune-based reactions. The lesions are planus, or mere chronic injury from an ill-
usually a localized, white painful area with a fitting denture.
Third type of contact drug reaction is a B-cell Orit is a procedure of applying pressure to
mediated immune reaction whereby anti- a suspected vascular lesion to visualize
bodies are produced: In a fashion similar to the evacuation of coloration and may facilitate the
mechanism noted for T-cell-mediated immune differentiation of small vascular lesion from a
reaction, Langerhans’ cells may present pigmented lesion. It will evacuate the blood
processed antigen to B lymphocytes, which in from small vessels allowing evaluation of other
turn manufacture specific antibody to the colors. It can be done intraorally also.
absorbed drug. On a subsequent absorption, Erythema due to vasodilatation blanches
antibodies attack the antigen at the epithelial when the vessels are compressed, while
or subepithelial level to produce inflammation purpura, on the other hand, does not blanch
and tissue injury. In plasma cell gingivitis, e.g. because the blood is present in tissue spaces not
the plasma cells are prominent because they in vessel. Telangiectasis will also blanch.
produce specific antibody in the area of antigen Diascopy is used to determine whether a
(the contact drug) absorption. Plasma cell lesion is vascular, non-vascular (nevus), or
gingivitis was common in the late 1960s and hemorrhagic (petechia or purpura). Hemor-
early 1970s but is rare today. It is believed that rhagic lesions and non-vascular lesions do not
the peak of incidence was related to formula blanch; inflammatory and vascular lesions do.
changes and ingredients in several dental Diascopy can also help identify sarcoid skin
preparations, which have since been lesions, which, when tested, turn an apple jelly
eliminated by the manufacturers. color. This is tested in lupus vulgaris.
99. Where is oral exfoliative cytology indi- It is detected to differentiate from localised
cated? area of vasoconstriction from a hypopig-
Oral exfoliative cytology is recommended as mented and depigmented skin patch, i.e.
an adjunct to open biopsy, for prebiopsy vitiligo. In the former the diascopy will blanch
assessment, for the examination of broad the lesion and in later the patch is still
surface lesions, and for the evaluation of detectable.
patients after definitive treatment.
100. In which conditions exfoliative cytology
is not useful?
Exfoliative cytology is unsuitable for the
following lesions: Homogeneous leukoplakias.
Smooth surfaced exophytic lesions, sub-
mucosal lesions, unulcerated pigmented
lesions, verruca vulgaris, papilloma, condy-
loma acuminata, etc.
101. What is diascopy? State in which condi-

tions it is positive.
Diascopy (vitropression) is a procedure in
which a diascope (more commonly a micro-
scope slide (rather than thin glass plate) or
magnifying glass, even a wafer of clear acrylic)
is pressed against a lesion with gentle pressure
down on to tissue or gently rocked from one
side to other to see whether it blanches.
103. Why the prednisone should be taken in

the morning and when the slow taper is
indicated?
The adrenals normally secret most of their
daily equivalent of 5 to 7 mg of prednisone in
the morning, all the prednisone should be
taken early in the morning to stimulate the
physiologic process, thus minimizing the
pituitary-adrenal axis and side-effects.
Slow steroid taper is not necessary if treat-
ment lasts for less than 2 weeks because adrenal
suppression is minimal.
104. Mechanism of action of corticosteroids

in suppressing inflammation.
The anti-inflammatory actions of cortico-
steroids include:
1. A reduction in the exudation of the leuko-
cytes and plasma constituents
2. Maintenance of cellular membrane integrity
with prevention of cellular swelling
3. Inhibition of lysozyme release from granu-
locytes and inhibition of phagocytosis
4. Stabilization of the membranes of the intra-
In treating spider angiomas and cherry cellular lysosomes containing hydrolytic
angiomas by laser it arrests the flow in central enzymes
arteriole by releasing the pressure it refills 5. Decreased scar formation by inhibiting
superficial branches making amenable for laser proliferation of fibroblasts and
treatment. 6. Possible effect on antibody formation when
administered in large doses.
102. Enumerate the diascopy results of
various varicosities and hemorrhagic Corticosteroids have also been shown
lesions. to suppress T-cell formation (Wood & Goaz,
5th ed.).
Lesion Blanching with diascopy
Petechiae Negative 105. Which is the steroid of choice for mucosal
Purpura Negative lesions? What are different steroid
Ecchymosis Negative regimens?
Hematoma Negative Prednisone, an anti-inflammatory glucocorti-
Lingual varicosities Positive coid, is the first drug of choice. This drug affects
Venous varix Positive mostly the cellular phase of inflammation and
(Venous lake) in particularly lymphocytes. Dexamethasone
Hemangioma Positive is more potent and affects the exudative phase
of inflammation, ultimately it remains an
Lymphangioma Positive
excellent drug for reducing surgical inflam-
Telangiectasis Positive
mation (mostly edema fluid).
Systemic corticosteroids are the most pre- individual, and the every other day use conti-
dictable medications used to control auto- nues to allow the adrenal cortex to regain activity.
immune diseases and certain immune-based This regimen is the preferred regimen
inflammatory diseases. Most of these diseases because it facilitates a long-term remission and
are incurable; the goal of therapy is a long-term has reduced side-effects. It is very effective but
and if possible permanent drug-induced requires close attention by the clinician and
remission. absolute compliance by the patient.
Systemic Corticosteroid Regimen I Systemic Corticosteroid Regimen II

It is indicated for most oral lesions associated It is usually applied to resistant pemphigus
with pemphigus vulgaris, erosive lichen cases and selected cases of systemic lupus
planus, and severe non-ocular pemphigoid erythematosus or sarcoidosis. This regimen is
also indicated in pemphigus vulgaris, erosive
1. Prednisone, 100 to 120 mg per day by mouth
lichen planus, and severe non-ocular pemphi-
(1.5 mg/kg per day) for 2 weeks.
goid. It is the preferred regimen in the Stevens-
2. A tapering schedule is instituted till 20 mg Johnson form of erythema multiforme.
per day is reached. It may be achieved by
1. This regimen begins with prednisone, 100
reducing prednisone by 20 mg per day each
to 120 mg per day by mouth (1.5 mg/kg
week.
per day), for a period of 2 weeks, at which
3. This dose of 20 mg per day continued for time the drug is abruptly discontinued.
1 month. 2. The rationale for this approach is to gain
4. Then 10 mg per day for 3 months. rapid suppression of disease activity and
5. The dose is then reduced to 10 mg every then discontinue the drug before side-
other day for another 3 months. effects develop or significant adrenal
6. Followed by 5 mg every other day for suppression occurs. This approach is effec-
6 months. tive and much more straightforward than
7. After 6 months of a 5 mg dose of predni- systemic corticosteroid regimen I. Its draw-
sone every other day, the drug may be back is that exacerbations are more frequent,
discontinued with a high possibility of an and the disease process is less controlled.
extended remission in a drug-free state. Systemic Corticosteroid Regimen IIIA
The rationale for this approach is to gain a This approach is suited to those cases with
rapid suppression of disease activity with a disease intensity and organ involvement that
high loading dose and to taper this dose rapidly lower doses of prednisone cannot control.
enough to avoid most of the more serious side- 1. This regimen begins with prednisone, 100
effects of high-dose prednisone. The 20 mg/day to 120 mg per day by mouth for 2 weeks.
dose is significant because at that dose or 2. A tapering schedule reduces prednisone by
below, side-effects are significantly reduced. 20 mg per day each week until the lowest
The tapered dose is extended in length with possible prednisone level is reached
each decrease in dose to prevent an exacer- without exacerbating the disease. Many
bation at the time of dose reduction or after individuals remain on 20 mg per day or
drug discontinuation. The every other day even higher doses for long periods because
dose is designed to permit the hypophyseal- lesser dosages are associated with disease
adrenal cortical axis to regain its function. exacerbations.
The 5 mg, every other day, dose is called a These patients require lifelong dosage
“maintenance dose” because 5 mg of pre- adjustments and follow-up. They also develop
dnisone equals the daily 20 mg of cortisol the many of the late complications of ongoing
adrenal cortex produces in an unstressed corticosteroid therapy.
Systemic Corticosteroid Regimen IIIB mucosa and as an adjunct in treatment of

The approach is reserved for refractory cases orofacial angioneuratic edema.
and for patients in whom corticosteroid Erythema multiforme systemic adminis-
complications pose a greater risk (diabetes, a tration and oral rinse of antihistamines mixed
history of tuberculosis, peptic ulcer disease, with kaopectate in 50:50 are recommended.
osteoporosis (in women), and cataracts). It Radiation mucositis oral rinse is recom-
is recommended as a regimen for ocular mended. These oral rinses are used to control
pemphigoid. pruritis in lichen planus. Chelitis glandularis
1. This regimen begins with prednisone, 100 systemic antihistamins may be used.
to 120 mg per day by mouth for 2 weeks. The recomanded preparation is dexame-
2. A tapering schedule reduces prednisone by thasone elixir 0.5 mg/5 ml (100 ml) rinse with
20 mg/day each week until a prednisone one teaspoonful for 3 min four times daily, and
level is reached at which the disease is expectorate until the lesions resolve and not to
exacerbated. This level and slightly higher swallow.
levels of prednisone may still be associated Systemic anaphylaxis occurring in dental
with disease activity. office.
3. Cyclophosphamide, 50 to 100 mg twice
daily by mouth; azathioprine, 50 to 100 mg 108. What is recommended antibiotics trial
twice daily by mouth; and methotrexate, for aphthous stomatitis?
25 to 50 mg per week, individually or in For aphthous ulcers that are numerous and
combinations, is then added to the pred- frequent enough to debilitate patients, a trial
nisone therapy. with antibiotics is useful before resorting to
The rationale for this approach is to affect systemic corticosteroids. The three most
the disease with double-drug therapy so that effective antibiotic regimens are:
the dosage and, therefore, the side-effects of 1. Erythromycin, 250 mg, by mouth four times
each can be reduced. daily
2. Tetracycline (achromycin, lederle), 250 mg,
106. What are steroid sparing agents (SSAs)? by mouth four times daily, and
Enumerate various SSAs.
3. A mixture often called “tetranydril elixir,”
These are drugs mainly immunosuppressive which consists of 250 mg tetracycline and
which are used along with long-term steroid 12.5 mg diphenhydramine hydrochloride
therapy to reduce the side-effects of steroids. (Benadryl, Warner Lambert) per 5 ml of
Hydroxychloroquine, azathioprine and myco-
kaopectate (Pharmacia and Upjohn).
phenolate mofetil are systemic steroid sparing
agents that are more commonly used, while The patient is instructed to use 1 tsp at a time
levamisole, cyclosporin A, methotrexate can and swish, hold the solution in their mouth as
also be used. long as possible, and swallow, three times
• Hydroxychloroquine (200–400 mg daily) daily.
• Azathioprine (5 to 150 mg daily) These regimens have been variably useful
• Mycophenolate mofetil (1 gm twice daily for in controlling the number, frequency, and
6 months) duration of lesions. Patients will have “break-
through” lesions, but they are a few and much
107. What are indications of antihistaminics more tolerable. Any of these regimens can be
in oral lesions? continued for extended periods (2 to 6 months)
Chronic ulcerative stomatitis, sometimes in before withdrawal to attempt continued
geographic tongue. Allergic lesions of oral control in a drug-free stage.
If these antibiotic regimens fail, systemic After administration in skin they enter skin
corticosteroids are the treatment of choice. and then variable quantity is distributed
109. What are the side-effects of topical corti- through the body, finally eliminated. The
costeroids? What is sufficient thera- concentration of topical agents decreases from
peutic effect? skin to the subsurface, whereas opposite is true
for systemic administration so if lesion is in
Candidiasis, epithelial atrophy, telangiecta-
epidermis the topical applications are favoured
sias. On skin it may produce skin-striae, hypo-
(as highest doses are delivered).
pigmentation, acne folliculitis. These effects
may occur after prolonged or intense dermato-
111. What is plasmapheresis? Enumerate the
logic use.
conditions in which it is indicated.
The therapeutic effect for oral ulcers (espe-
Plasmapheresis is a procedure in which blood
cially aphthous ulcers) 15 g of topical steroid
is separated into cells and plasma (liquid). The
over 2–4 weeks and with minimal compli-
plasma is removed and replaced with fresh
cations.
frozen plasma, a blood product called albumin
110. What are advantages of topical agents? and/or a plasma substitute. The procedure is
There is minimal risk for topical use and nearly often referred to as plasma exchange. The terms
every drug can be formulated to use this. The plasmapheresis (PP) and plasma exchange (PE)
drug preparations are safe (low serum levels are often used interchangeably, but when
for systemic side-effects). Ease of use, con- properly used, denote different procedures.
venience (as medication can be applied at Plasmapheresis refers to a procedure in which
home), ability to treat large lesions and to reach the plasma is separated from the blood either
those of critical sites. Better cosmetics result by centrifugation or membrane filtration. Once
than surgery. Rapid onset of action. separated the plasma can be manipulated in a
Limited drug-to-drug interaction. After the variety of ways. Plasma exchange refers to
application of small amounts of drug locally discarding the plasma totally and substituting
very high local concentration of drug can be a replacement fluid.
achieved, these may prove toxic if adminis- 1. Pemphigus
tered systematically. 2. Thrombotic thrombocytopenic purpura
Alternative method for patients who cannot 3. Myasthenia gravis
swallow pills or fear of needles. 4. Severe systemic lupus erythematosus.
2
Orofacial Pain and Disorders of
Temporomandibular Joints
1. Define pain. What is orofacial pain? Del is the unit to measure pain, dolorimetry
What is the unit of pain measurement? is a lab method to measure painfulness and
IASP defines pain as an unpleasant sensory dolorimeter is the device used to measure
and emotional experience associated with the pain. Human body can bear up to 45 Del of
actual or potential tissue damage, or described pain.
in terms of such damage. 2. What is chronic pain?
OR It is defined as pain that lasts longer than
It is the subject’s conscious perception of six months and often presents with different
modulated nociceptive impulses that generate circumstances, the more functional definition
an unpleasant sensory and emotional experience is pain that lasts longer than normal healing
associated with actual or potential tissue damage time. Chronic pain is often not a symptom but
or described in terms of such damage (Bell’s). a disease in its own right.
Orofacial pain can be attributed to condi-
tions of pain in and around the eyes, ears, nose, 3. What is field of orofacial pain?
including sinuses, teeth including paradontics, This is the discipline of dentistry which
mouth including lips, jaw bones, salivary glands, includes the assessment, diagnosis and
throat, cheeks, temporomandibular joints and treatment of patients with complex chronic
periauricular area (Huggar et al. 2006). orofacial pain and dysfunction disorders,
OR oromotor and jaw behaviour disorders and
Orofacial pain (OFP) symptom of broad chronic head and neck pain. As well as pursuit
spectrum of diseases that involve diseases of of knowledge of underlying pathophysiology
orofacial structures, musculoskeletal diseases, and mechanism of these disorders.
rheumatic diseases, diseases of peripheral or
central nervous system, psychological abnor- 4. What is chronic orofacial pain?
mality, referred from intracranial pathology or It is a term used to describe painful regional
cervical muscles. syndromes with a chronic unremitting pattern.
48
Orofacial Pain and Disorders of Temporomandibular Joints 49
Clinically migraine, TMJ dysfunction, atypical facial

It is subdivided into three classes: Musculo- pain, irreversible pulpitis.
skeletal (temporomandibular disorders), Protracted pain is one in which pain continues
neurovascular (migraine, facial migraine, from one day to the next, e.g. post-herpetic
cluster headache, hemicrania, paroxysmal neuralgia (it develops protracted pain syn-
hemicrania and SUNCT), and nauropathic drome), masticatory pain dysfunction syn-
(trigeminal neuralgia, painful post-traumatic drome.
neuropathies, burning mouth syndrome,
glossopharyngeal neuralgia). Localized pain is one in which patient is able
to define pain in exact anatomic location, e.g.
5. Classify facial pain.
periodontal pain is localized owing to
Facial pain can be classified broadly into three mechanoreceptors, lost/cracked tooth, syno-
groups: vitis/capsulitis produce localized pain, atypi-
1. Pain arising from diseases of orofacial cal odontalgia.
structures.
Diffuse pain is one in which the location is less
2. Pain arising from disorders of nerves and
well-defined and somewhat vague and anato-
central nervous system.
mically variable, e.g. myospasm, i.e. myogenic
3. Pain arising in distant organs and referred
pain in TMJ diffuse distribution on facial area,
to facial region.
fibromyalgia, pain originating in mucosa may
6. What are different behaviours of pain? be associated with widespread mucosa,
Intermittent pain is one in which suffering systemic disease, and food impaction pain may
distinctly comes and goes, leaving pain free be diffuse.
intervals of noticeable duration, e.g. focal Radiating pain is one in which rapidly
reversible pulpitis, TMJ dysfunction syn- changing pain is there or when the pain is
drome, trigeminal neuralgia. experienced from one part of body towards
Continuous pain is one in which pain-free another. It is the pain that is felt from the
intervals do not occur, e.g. non-arthritic inflam- source and all along the route of nerve, e.g.
matory pain in TMJ, post-traumatic neuro- suppurative and tender gingival lesions can
pathy, neuritis. cause pain radiating to ear, throat and floor of
mouth, glossopharyngeal neuralgia pain
Recurrent pain is one in which episodes of
radiates to ear, entrapment of inferior alveolar
pain, whether continuous or intermittent, are
nerve can cause pain which radiates from TMJ
separated by an extended period of freedom
to mandible, chest pain may radiate to lower
from discomfort only to be followed by another
jaw, causes pulpitis type of pain in one or
similar episode of pain, e.g. trigeminal
several mandibular teeth and extends as far as
neuralgia, headache or facial pain attributed to
mental nerve outflow.
TMJ disorders.
Spreading pain is one in which more gradually
Momentary pain is one in which duration can
pain is seen, e.g. acute orofacial pain due to
be expressed in seconds, e.g. ankylosis of TMJ,
gingival/periodontal conditions may spread
developmental disorders of TMJ pain is
to remote areas of head/face. Neuropathic
momentary associated with stretching of liga-
trigeminal orofacial pain usually has a narrow
ment, cracked tooth syndrome, dentinal hyper-
well-defined field (single tooth) and then
sensitivity caused by abrasions, fractures.
spreads wider to involve more teeth. TMJ pain
Longer lasting pain is one in which duration sometimes may occur in temples and may
is expressed in minutes, hours and day, e.g. spread downneck/shoulders.
Lancinating pain is one in which a momentary 9. What is splintting pain?

cutting exacerbation is seen, e.g. trigeminal This is a protective function. It involves muscle
neuralgia, glossopharyngeal neuralgia, tightening and occurs when any part of body
secondary expansion caused by contaminated is injured and requires rest. In orofacial region
amalgam can produce lancinating pain. splintting of masticatory muscle may be in
Enlarging pain is one in which pain progres- response to increased tension, stress, clenching,
sively involves adjacent anatomic areas. bruxism, recent dental restoration, occlusal
interferences, local anesthesia, and TNJ pain.
Migrating pain is one if the pain changes from Management includes removal of cause, moist
one location to another, e.g. atypical facial pain, heat, rest, short course of muscle relaxants.
vascular type of pain.
10. What is neuropathic pain?
Referred pain is a spontaneous heterotrophic Neuropathic pains are those which are
pain that is felt in an area innervated by a generated within the nervous system itself and
different nerve from the one that mediates the are due to abnormalities in components of
primary pain. It never crosses midline unless nervous system and not the peripheral or deep
it originates in the midline. Referred pain is structures in which the pain is felt. Neuropathic
generally referred upwards, e.g. acute orofacial pains are associated with burning, hyper-
pain can refer itself, i.e. acute pulpitis in decayed algesia, dysasthesia and sometimes anesthesia,
upper molar can refer pain to a non-decayed e.g. neuralgic pain, neuritis, stomatodynia,
lower tooth, pain from lower molar is referred phantom tooth pain, etc.
to ear, referred dental pain is frequently felt as
headache, it may be felt in orbital or frontal 11. What is formication? Enumerate the
area, in maxillary sinus area, in auricular/ conditions causing formication in
preauricular parts or throughout face. Pain due orofacial region. What is the significance
to angina is referred to as mandible. The of it?
superior part of masseter can refer the pain to Formication (from Latin word Formica, which
TMJ and maxillary teeth while deep layer refer means to ant), a neurosis that produces the
to mandible sternocledomastoid muscle can sensation of snakes or insects crawling on or
refer to TMJ. In oral submucous fibrosis pain under the skin. It is also called parasitosis.
in ear due to stenosis of eustachian tube. Orofacial complications of methamphetamine
7. What is sharp stabbing pain? abuse may show formication in orofacial area.
The other entities sometimes may show post-
Short duration which is seen in fractured tooth
herpetic, post-traumatic and post-surgical
or restoration, hypersensitivity of dentine,
neuralgias. Anesthesia dolorosa may show
exposed dental pulp (acute pulpitis due to
formication. It may be seen in regenerative
caries), neuralgias (glossopharyngeal, trige-
phase of tissue injury. It can be seen with use
minal), salivary gland duct obstruction.
of (more likely withdrawal from) substances
8. What is projected pain? Name the condi- such as cocaine, amphetamines and even
tion causing projected pain in orofacial alcohol.
region. Tinel’s sign of formication is seen in variety
It is the pain which is felt in the peripheral of somatic conditions such as delirium, high
distribution of the same nerve that mediates the fever, diabetic neuropathy, herpes zoster,
primary nociceptive input, e.g. the radicular peripheral nerve regeneration and neuro-
pain of posterior root compression. Paroxysmal pathy.
neuralgia, peripheral neuritis, herpes zoster The significance is the sensation causes the
and post-herpetic neuralgia. patient to attempt to remove the perceived
parasites, usually by picking at the skin with 16. Enumerate the conditions causing
fingernails, resulting in widespread traumatic paresthesia and anesthesia.
injury. The factitial damage can alter dramati- 1. Injury to regional nerves:
cally the facial appearance in short period of i. Anesthesia needles
time, these lesions are called speed bumps, ii. Jaw bone fractures
methsores or crank bugs.
iii. Surgical procedures
12. Enumerate the conditions of facial pain 2. Malignancies
that may be a symptom of neurological 3. Medications—hypnotics, tranquilizers,
disorder. sedatives
Orofacial pain associated with paresthesia, 4. Neuritis
anesthesia or weakness indicate that it is 5. Diabetes
associated with neurological disorders. Many 6. Pernicious anemia (megaloblastic)
of the neurological disorders which cause
7. Multiple sclerosis
headache may also cause facial pain. (These are
8. Acute infections of jaw bones
cluster headache, temporal arteritis and
occasionally migraine.) 9. Psychoses
10. Trigeminal neuralgia
13. Give indications of opiate analgesics in
orofacial region. 17. Enumerate the causes of glossopyrosis.
Opiate analgesics alone or in combination are The preferred site for the pain is the anterior
routinely used for chronic, intractable pain. portion of the tongue. Sometimes the anterior
After implant surgery these are indicated portion of the hard palate and the labial mucosa
with ibuprofen/acetaminophen. In oral of the lip may be involved.
cancer patients for control of pain, opoid • Low concentrations of vitamin B complex
analgesics should be avoided in atypical (notably B12), folic acid and iron that can be
odontalgia. identified by blood tests.
• Oral candidiasis (oral thrush) where small
14. Which are the adjuvant analgesics in white plaques (specks) are present on the
orofacial pain? mucosa.
These are anticonvulsants (carbamezapine, • Some patients report the onset of BMS after
gabapentin, and pregablin), antidepressants a significant ‘life event’ (e.g. death/separa-
(clonazepam, doxepin), anxiolytics (amitry- tion of spouse or other major emotional
ptaline, nortryptaline) and muscle relaxants shock).
(tizanidine). • The majority of BMS patients, however, are
idiopathic (unknown cause).
15. What is anesthesia dolorosa?
The denervated area continues to hurt even 18. What is burning mouth syndrome?
though it is anesthetic/report by a patient that Enumerate different types of it.
a painful area which is numb/pain in the area Burning mouth syndrome (BMS) is characteri-
which is anesthetic. It is a chronic intractable zed by burning and painful sensations in oral
pain syndrome that may persist indefinitely. cavity with clinically normal mucosa with no
This arises after damage to the nerve or known organic cause. The sensation is more
ganglion. Neurosurgery in the area may also common on tongue (tip or one side), inner
be the cause. Or even neurolytic alcohol surface of lips. Gingiva is more resistant. The
and glycerol blocks treatment by tricyclic diagnosis is by application of topical anesthetic
antidepressants. to painful site. Treatment by analgesics for
palliative treatment, remove the cause, anti- 21. What is styloid process? What are the
inflammatory agents and medical consultation, different points considered during
if necessary. examination of styloid process?
The name styloid process was derived from the
Lamey and Lewis classified into three types: Greek word “Stylos” meaning a pillar. It is a
Type 1: Involves symptom-free walking, with bony cylindrical needle-shaped projection
sensations developing in the morning and which originates from the postero-inferior side
progressively increasing to severe by evening. of petrous bone, immediately in front of the
stylomastoid foramen and goes obliquely
Type 2: Involves continuous symptoms
down and forward. The points during
throughout the day.
examination are length, angulation, and
Type 3: Includes intermittent symptom-free morphology.
periods throughout the day.
1. Length of the styloid process
19. What are the points considered for
diagnosis of burning mouth syndrome? • Short, i.e. less than 2 cm, long 2–4 cm and
elongated more than 4 cm.
2. Angulation of the styloid process
• Narrow is less than 65 degree, normal
65–75 degree and wide is more than
75 degree. It ranges from 55° to 90.5° in
the transversal plane and from 76° to 110°
in the sagittal plane.
3. Morphology of styloid process
• Absence, normal appearance and other
morphological findings.
22. What are different types of styloid

process?
Normal styloid process: Cylindrical bone
arising from temporal bone in front of the
stylomastoid foramina, which is not elongated
20. What are different taste disturbances? and less than 30 mm in length.
Enumerate the causes of taste distur-
bances.
Ageusia (absence of taste), hypogeusia
(blunted taste), cacogeusia (unpleasant taste),
dysgeusia (altered taste sensations).
The diseases known to cause Bell’s palsy,
zinc deficiency, diabetes mellitus with perio-
ral neuropathy, cancer/oral head and neck
irradiation, oral candidiasis, gingivitis, peri-
odontitis, hypothyroidism, multiple sclerosis,
parkinsonism, pernicious anemia (vitamin B12
related), renal failure, Sjögren’s syndrome, Type 1: Uninterrupted styloid process, styloid
Zn-deficiency, upper respiratory disturbances, process longer than 30 mm without any
influenza. interruptions.
Type 2: Pseudoarticulation, it is characterized

by styloid process apparently being joined
by the stylohyoid ligament by a single pseudo-
articulation giving the appearance of an
articulated elongated styloid process.
According to the Calcifications
a. Calcified outline, it is also called external
calcification or boundary calcification.
Image of the styloid process is continuous
with no signs of calcifications.
Type 3: Segmented styloid process, it consists

of interrupted segments of the mineralized b. Partially calcified, image of the styloid
ligament sometimes creating the appearance process with the presence of radiopaque
of multiple pseudoarticulations. calcified segments.
of the stylohyoid ligament complex. It is an

important cause of paroxysmal dull pain in the
throat and ear.
Symptoms are sore throat dysphagia otalgia
the sensation of foreign body in the throat.
Facial pain radiating to ear or along the
mandible and head and neck.
24. What is Eagle’s syndrome?
Eagle’s syndrome is the condition in which the
elongated styloid process can elicit painful
symptoms when it is forced into adjacent
c. Nodular, styloid process image with soft tissues of the neck during normal head
nodular are radiopaque calcifications. movements. The updated term is diffuse
intraosseous skeletal hypertrophy (DISH)
syndrome. This complex symptom is now
recognized as only one part of a total body
syndrome known as diffuse intraosseous
skeletal hypertrophy, or DISH syndrome.
DISH syndrome is suspected to be a reactive
immune-based disease similar to myositis
ossificans but targeting only ligaments.
25. Which are the other syndromes consi-
dered in differential diagnosis of Eagle’s
syndrome?
Trotter’s syndrome (Morgagni’s sinus syn-
d. Completely calcified, image of the styloid drome), Costen’s syndrome, myofacial pain
process is radiopaque, calcified and totally syndrome, stylohyoid complex syndrome.
homogeneous. Trotter’s syndrome consists of three sym-
ptoms in patients suffering from naso-
pharyngeal carcinoma. These are neuralgiform
pain in lower jaw, deafness and blockage in
ear associated with palatine asymmetry and
trismus (due to pterygoid muscles).
Costen’s syndrome has auricular, articular
and cranial symptoms. Pain in joint, hearing is
poor, dizziness, and headache.
Myofacial pain syndrome—it manifests
muscular spasm, restricted mobility.
26. What are the types of Eagle’s syndrome?
Eagle described two types: The classic and the
23. What is stylagia? What are the symptoms styloid carotid artery syndrome.
associated with the elongation of styloid The classic type is characterized by the
process? symptoms like dysphagia, foreign body
Autonomous entity related to abnormal length sensation in the neck and oropharyngeal,
of the styloid process or to the mineralization cervical and craniofacial pain. The pain is often
exacerbated by rotation of the head to the elongated hyoid bone, can cause the same
contralateral side, swallowing, extending the symptom complex. Symptoms can include
tongue, and yawning and may radiate to lateral neck pain especially with chewing,
distant areas. The pain is referred to the ear, swallowing, and head movement, and pain in
neck, tongue, teeth, temporomandibular joint the area of the submandibular space and deep
(TMJ) area and even the chest and upper limbs. to the angle of the mandible. We believe that
Risk factors for the development of this the symptoms are related to the tension of the
syndrome are an elongated or more anteriorly stylohoid complex that irritates surrounding
angulated styloid process as well as ossified structures and causes pain with movement of
stylohyoid or stylomandibular ligaments. the complex. Surgery to interrupt this complex
The styloid-carotid artery syndrome is at any point is likely to improve the symptoms.
characterized by ipsilateral headache, orbital
pain and transient neurological symptoms in
form of transitory ischemic attacks caused by
a transient compression of the internal carotid
artery and sympathetic chain. It was also
suggested to distinguish three forms:
• The classical form, caused by trauma
• The styloid syndrome is the most common
form, defines the condition in which the Orthopantomograph demonstrating a large
patient’s symptoms appear earlier in life radiolucent area running below, laterally and parallel
to the mandible on the right side
owing to a non-traumatic developmental
anomaly in the ossification of the stylohyoid
ligament or to an elongated stylohyoid
process, and
• The pseudostyloid syndrome, on the other
hand, defines a tendinosis at the junction of
the stylohyoid ligament and the lesser cornu
of the hyoid in older individuals with no
history of trauma and no evidence of styloid
process elongation or stylohyoid ligament
ossification on radiologic examination.
27. What is stylohyoid complex? What is
stylohyoid complex syndrome?
The styloid process, the stylohyoid ligament
and the lesser horn of the hyoid bone form the
stylohyoid chain or stylohyoid complex. This
complex traverses the area from the lateral
skull base to the anterolateral neck, forming a
band that crosses the upper lateral neck. The
term ‘stylohyoid complex syndrome’ has been
proposed to classify all lateral neck and/or
facial pain conditions resulting from an
elongated styloid process, ossified stylohyoid
ligament, or elongated hyoid bone. Three Three-dimensional computed tomography
different pathologies, elongated styloid confirming a complete and very thick hypertrophic
process, calcified stylohoid ligament, and an ossified stylohyoid chain on the right side
be produced or aggravated by emotional

disturbances. In general, psychosomatic
disorders are harmful effects resulting from
psychic influences on the organic control of
tissues.
Thorakkal Shamim recently produced
classification on primary symptom. This
includes pain related disorders, disorders
related to altered oral sensation, disorders
induced by neurotic habits, autoimmune
Stylohyoid complex calcification on right side
significantly disorders, and miscellaneous disorders.
Altered perception of dentofacial form and
28. What are conservative and surgical treat- function were added to provide the revised
ment modalities of Eagle syndrome? classification.
The conservative treatment involves injections 1. Pain related disorder
of long-lasting anesthetics and/or local a. Myofacial pain dysfunction syndrome
corticosteroid into the tonsillar fossa as (MPDS)
well as administration of non-steroidal anti- b. Atypical facial pain (AFP) and atypical
inflammatory drugs. Other means are adminis- odantalgia (AO)
tration of anti-epileptics and anti-histaminics, c. Phantom tooth pain (PTP)
vasodilators, neuroleptics, anti-depressants d. Munchausen’s syndrome (MS)
and tranquilizers as supportive therapy.
e. Self-mutilation and oral artefactual
Injections of corticosteroids diluted in local
disease (OAD)
anesthetics close to the styloid process is
2. Disorders related to altered taste sensations
another alternate. Such injections have been
described for diagnostic as well as palliative a. Burning mouth syndrome (BMS)
purposes, via mostly an intraoral approach b. Idiopathic xerostomia
transpharyngeally, into the region of anterior c. Disturbances of taste
pillar and deeply into the anterior tonsillar 3. Miscellaneous
fossa. Even injection of long-acting local a. Recurrent aphthous stomatitis (RAS)
anesthetics are also used. b. Lichen planus
Manual fracture of the ossified styloid c. Psoriasis
process under local anesthesia is another d. Geographic tongue
approach that has, however, unsatisfactory e. Chronic periodontal disease
results. Also, the fracture should be regarded f. Acute necrotizing ulcerative gingivitis
critically because of its vicinity to the internal (ANUG)
carotid artery. Surgical removal of styloid
g. Erythema multiforme and herpes labialis
process is a method of choice.
h. Bruxism
29. What are psychosomatic diseases? i. Body dysmorphic disorder (BDD), also
Enumerate the various psychosomatic known as dysmorphophobia, is an under
diseases affecting oral cavity. recognized yet relatively common and
The term psychosomatic means something severe mental disorder. These people are
pertaining to mind–body relationship or concerned about facial profile, teeth,
having bodily symptoms of psychic, emotional chin, smiling, talking, and laughing.
or mental origin. Psychosomatic diseases j. Anorexia nervosa (AN) and bulimia
are actual physical diseases which may nervosa (BN)
k. Delusional halitosis (DH). It is a 33. What are the doses of carbamazepine?

psychosomatic condition in which some How are they started? What care has to
individuals believe that they have an be taken?
offensive mouth odour which neither the Carbamazepine is the primary drug used in the
dentist nor any other clinician can medical management of pain of trigeminal
perceive. There is no local or systemic neuralgia. A starting dose of 200 mg everyday
disease. is recommended; this can be increased by up
30. What is pre-trigeminal neuralgia? to 200 mg everyday as tolerated against side
effects, to a maximum of 800 mg per day. The
This is early form of trigeminal neuralgia,
dosage must be regulated for best therapeutic
characterized by a dull continuous pain
effect, and a baseline complete blood count is
(days to years) in one of jaws. It has been noted
recommended because of its dose-related effect
in 18% of trigeminal neuralgia patients.
of bone marrow suppression. To keep the
It may be mistaken for dental pathology
tegretol dose low and reduce side-effects if
(toothache/sinusitis pain) by throbbing pain
they occur, gabapentin, 300 mg three times
caused by thermal stimuli. The pain may be
daily, or divalproex sodium 50 mg everyday,
aching type with several hours duration.
and/or amitriptyline, 50 mg by mouth at
The pain is spontaneous but with no trigger
bedtime, may be added to the tegretol.
zones. The duration of PTN pain may be
in minutes or hours or in some cases constant 34. Why routine blood investigations are
in comparison to the pain in seconds/minutes advised during carbamazepine therapy?
as in classic TN. It is responsive to car- The carbamazepine is given 100 to 200 mg
bamezapine. twice daily. Usual maintenance day is
31. What is atypical neuralgia? 600–1200 mg/day, in divided doses until the
symptoms subside. The common side-effects
Post-traumatic trigeminal neuralgia combines
are drowsiness, dizziness, nausea, anorexia.
characteristics of both painful neuritis and
Rarely complications like aplastic anemia,
paroxysmal neuralgias. The disorder has
leucopenia and agranulocytosis may occur.
persistent, unremitting, variable bright,
Periodic complete cell blood count, liver and
burning pain that suggests painful neuritis
kidney function tests are necessary in these
and it may be accompanied by other
patients. Complete blood count every two
sensory, motor and/or autonomic effects. The
weeks during first two months and quarterly
basic background neuritic pain may be
thereafter is recommended. The complete
interrupted by paroxysms of neuralgic
blood count has to be done because of its dose-
pains. This is called atypical trigeminal
related bone marrow suppression.
neuralgia.
35. What is oromandibular dystonia?
32. What is para-trigeminal neuralgia?
It produces involuntary, excessive contractions
It is also called reader’s syndrome. It is of tongue, lip and jaw muscles. The proposed
characterized by frontotemporal pain and pathogenesis is related to defective inhibitory
occulosympathetic paresis. Tic like pain control of basal ganglion of the forebrain,
sensation in the first and second division of thalamus and brainstem. Treatment by
trigeminal neuralgia. The pain may be injection of botulinum toxin and neurosurgical
described as intense or throbbing, there may interventions.
also be drooping of eyelid and contraction of
pupil (miosis). Some experience dysgeusia 36. What is orofacial dyskinesia?
possibly due to involvement of chorda tympani These are abnormal, involuntary movements
nerve. of tongue, lips and jaws. This may be a
contributing factor for TMJ degenerative tooth, but the two disorders can be dis-
changes, mucosal lesions, damage to teeth tinguished by determining whether placing
and prosthesis. Complete loss of teeth is food in the mouth without chewing or whether
considered to be one cause of oral dyskinesia. gently touching the soft tissue around the
Lack of replacement and ill-fitting dentures trigger zone will precipitate pain. TN pain will
may initiate it. Clinically, characterized by be triggered by touching the soft tissue,
observation of involuntary mouth movements whereas pressure on the tooth is required
and their effect on jaw muscles, TMJ, oral to cause pain from a cracked tooth (Burkitt’s
mucosa and teeth. Emphasis on prevention as 12th ed.).
no treatment is safe.
39. What are the characteristics of hyperten-
Tardive dyskinesia is associated with sion headaches and tension headache?
antipsychotic medications. Tardive dyskinesia
Headache in the occipital area may be due to
has been reported to cause facial pain. It may
severe hypertension. The nature is pounding
be persistent even after drug therapy is
like. This is often accompanied by blurred
stopped. The management is by changing
vision, ringing in ears, tingling in hands/feet,
medications with discussion with physician
shortness of breath and fatigue.
and clonazepam, baclofen.
The pain of tension type of headache is
37. What are trigger points? bilateral, dull, aching and sometimes band like.
Myofascial trigger point Increases with age and is more common in
A hyper-irritable spot, usually within a taut females. The patient may report an increased
band of skeletal muscle or in the muscle fascia, tenderness of pericranial muscles and its
that is painful on compression and that can give attaching fascia. It gets relieved by rest and
rise to characteristic referred pain, tenderness anxiolytic medicines and rest.
(secondary hyperalgesia), motor dysfunction 40. Why TMJ is called synovial joint?
and autonomic phenomena. The internal surfaces of superior and inferior
From the trigger points masticatory joint cavities are surrounded by specialized
impulses pass into CNS and return in the form endothelial cells that form a synovial lining.
of painful sensations on some other structures. This lining along with a specialized synovial
Such places where the patients feel pain flinge located at the anterior border of the
sensation are called zones of impact (zone of retrodiscal tissues produces synovial fluid
referral, referral zone). (serous in nature) which fills both joint cavities
and the TMJ is referred to as synovial joint. The
38. What are trigger zones? synovial fluid serves by providing metabolic
Pain in TN is precipitated by light touch on a requirements to the articular disc which
“trigger zone” present on the skin or mucosa is avascular and as a lubricant during function.
within the distribution of the involved nerve This also has bacteriocidal property.
branch. Common sites for trigger zones include
the nasolabial fold and the corner of the lip. 41. What are functions of inferior and
Shaving, showering, eating, speaking, or even superior lateral pterygoids?
exposure to wind can trigger a painful episode, The superior and inferior lateral pterygoid
and patients often protect the trigger zone with muscles are present anterior to condyle disc
their hand or an article of clothing. Intraoral complex. The inferior pterygoid muscle inserts
trigger zones can confuse the diagnosis by on neck of condyle, whereas superior lateral
suggesting a dental disorder, and TN patients pterygoid muscle inserts on neck of condyle
often first consult a dentist for evaluation. The and the articular disc. Superior lateral
stabbing pain can mimic the pain of a cracked pterygoid is considerably smaller.
The inferior lateral pterygoid muscle is increased by clenching the teeth nor by bitting
active with depressing muscles, i.e. mouth against separator. Pain occurs due to inflamed
opening. capsule is stretched by translator movement of
Bilateral inferior pterygoid muscle contrac- the condyle and therefore is accentuated by
tion simultaneously results in mandibular protrusion, contralateral excursion and on
protrusion. Unilateral contraction creates a wide opening. Macrotrauma and injury in
mediotrusive movement of that condyle and open mouth position. It may also develop to
causes a lateral movement of mandible to adjacent tissue breakdown and inflammation.
opposite side. It may occur due to habits that entail excessive
Superior lateral pterygoid muscle is shown mandibular movements and from abusive joint
to active with elevator muscles, i.e. mouth hypermobility.
closing. 45. What is retrodiscitis?
The superior lateral pterygoid muscle is a Retrodiscitis is inflammation of retrodiscal
stabilizing muscle for condyle disc complex tissue. It is characterized by dull aching pain
specially during unilateral chewing. It helps often increased by clenching (as the retrodiscal
slight anterior and medial force on disc. It tissues are highly vascularised and innervative
helps in power stroke (the movement that and are not in a position to tolerate the loading
involves closure of mandible against resistance forces) and such pain is decreased by biting
such as in chewing or clenching the teeth against a separator on the same side. The pain
together) and when the teeth are held together. is increased by forced ipsilateral excursive
42. What are temporomandibular disorders? movements of mandible. Trauma is major
etiologic factor, macrotrauma in open mouth,
Temporomandibular disorders are the functio-
blow to chin causing the forceful movement of
nal disturbances of masticatory system. This is
condyle on retrodiscal tissues.
a collective term used for a number of clinical
problems that involve the masticatory muscle, Acute malocclusion may be caused as
temporomandibular joint and/or associated swelling may occur and force the condyle
structures. slightly forward down the posterior slope of
the articular eminence. Intraorally seen as
43. What is synovitis? disengagement of ipsilateral posterior teeth
Inflammation of synovial lining or the synovial and heavy contacts of contralateral canines.
tissues that line the recess areas of the joint The inferior lateral pterygoid muscle pain
become inflamed. The pain is localized and may produce same symptoms but can be
enhanced with joint movement. It may cause differentiated by absence of pain in resisted
swelling due to effusion within joint cavity and protrusion of mandible in retrodiscitis.
alteration of synovial fluid. It is caused by
46. What are different joint sounds?
irritation within joint, localized trauma,
abusive use, toxemias, specific infections or an These are also called TMJ joint noises. Articular
allergic response. It may occur as a mani- disc displacements are more common cause of
festation of arthritis. joint noises. Clicking, popping, snapping and
crepitus are different types of joint noises.
44. What is capsulitis? Clicking single, brief event, e.g. articular disc
Inflammation of capsular lining or capsular displacements. Pop is usually loud click that
ligament becomes inflamed. Tenderness is audible click and may be very annoying to
on extra-auricular palpation. Occasionally the patients. It is also described as loud noise
fluctuant swelling as well. The pain is localized or thud. It usually occurs during maximal
and even in static joint position. The joint mouth opening, it is seen in joint hyper-
movements increase the pain. The pain is not mobility. Pop is also noted during maximum
opening in adherence when patient tries to considered when determining normal range of
relief stiff which has occurred. Popping is movement. A restricted mandibular opening
usually reversible and indicates an internal is considered to be any distance less than
derangement, it may suggest osteophyte or 40 mm.
tumor. Snapping sound is noted in disc
49. Enumerate the causes of restricted
displacement with reduction. Crepitus
movements of mandible.
(crepitations) is long-grating sound, e.g.
degenerative diseases. This is multiple, rough, These are extracapsular or intracapsular
gravel like sound and is complicated. sources. Extracapsular causes are related to
muscle disorder. The intracapsular are due to
Subluxation of TMJ mouth opens to fullest
disc–condyle function and surrounding
extent, a momentary pause occurs, followed by
ligaments and are related to disc derangement
sudden jump or leap to maximally open
disorder.
position. This jump is accompanied by a thud,
sound which needs to be differentiated from The extracapsular muscle restrictions are
click. due to elevator muscle (masseter/medial
pterygoid) spasm and pain. These muscles
47. What is end feel test? restrict the translation and thus limit opening.
End feel test is done when mouth opening There is no effect on lateral and protrusive
is restricted. The end feel describes the movements. Soft end feel is present and they
characteristics of the restriction that limits the present deflection.
full range of joint movement. A normal range The intracapsular restrictions are due to disc
of mouth opening is considered 53 to 58 mm. derangement disorder. The movement is
A restricted mouth opening is considered to be restricted due to structural resistance. The
any distance less than 40 mm. muscle also restricts the translation. They
The end feel can be evaluated by placing the present deflection.
fingers between the patient’s upper and lower
50. What is deflection?
teeth and applying gentle and steady force in
an attempt to passively increase the interincisal The opening pathway is shifted to one side and
distance. becomes greater with opening. At maximum
opening the midline is deflected to its greatest
Soft end feel is said if the opening can be
distance or it can be defined as any shift of
achieved and has to be done slowly. The pain
midline to one side that becomes greater with
which is present is intensified. This suggests
opening and does not disappear at maximum
muscle-induced restriction.
opening. It is due to restricted movement in one
Hard end feel is said to be if no opening is
joint.
achieved. This suggests intracapsular sources
(disc dislocations), acute non-reducing disc
displacements obstructing translation, uni-
lateral ankylosis.
Hard end feel may be suggestive of surgical
intervention while soft end feel suggest no
indication of surgical intervention.
48. What is restricted mouth opening?
The normal range of mouth opening when
measured interincisally is between 53 and
58 mm. The patients having extreme deep bites
vertical overlap of the anterior teeth must be
Deflection on ipsilateral side is seen on 52. How the examination for joint sounds is
capsular fibrosis, degenerative joint disease, done?
periarticular and capsular inflammation and 1. Palpation: Place the fingers over lateral
fibrous ankylosis. surfaces of joints and ask the patient to open
Deflection on contralateral side is seen and close. These can be perceived by
due to immobilization of TMJ due to invasive fingertips. Examination of joint sounds by
malignant tumors. placing in the ear is not advised, as
additional sounds may noted by the tissue
51. What is deviation?
The opening pathway is altered but returns to
normal midline relationship at maximal
opening or it can be defined as any shift of jaw
midline during opening that disappears with
continued opening (a return to midline). It is
the result of condylar movement necessary to
get past the disc during translation. Once the
condyle has overcome this interference the
straight midline path is resumed. This is
seen in disc displacement with reduction,
structural incompatibility and muscle
disorders (muscle engrams), subluxations. of ear canal cartilage is forced against the
The deviation seen in disc displacement posterior border of condyle and this force
with reduction (abnormalities in discal displaces condyle and produce additional
movement), the speed of opening alters the sounds.
location of deviation while the one seen in 2. Auscultation: This is done by stethoscope.
structural incompatibility speed of opening This may detect more sounds.
and closing does not alter the interincisal Note character of sound, degree of inter-
distance and location of deviation. incisal opening with sound, whether it
Deviation caused by muscle disorders are occurs during opening and closing.
commonly large, inconsistent, sweeping 53. What is disc displacement with reduc-
movements not associated with joint sounds. tion?
Ipsilateral deviation is seen in unilateral The disk is displaced from its position between
hypoplasia of mandibular condyle and the condyle and eminence to an anterior and
unilateral bony ankylosis. Contalateral medial or lateral position (more common is
deviation is seen in unilateral hyperplasia of anterior or anteromedial) but is reduced in full
condyle. mouth opening usually resulting in a noise.
Click occurs on both vertical opening and 54. What is disc displacement without
closing. The opening click is at least 5 mm reduction?
greater than on closing and this click is Disc displacement (medially, laterally and
eliminated on protrusive opening. It may cause anteriorly) does not assume the normal
a popping sound also. Pain may be present position. It is also called closed lock. In this case
when chewing hard foods. This condition the disc has been permanently displaced and
can be seen in chronic clicking condition in its shape has been deformed so that it prevents
patients who tend to clench and grind the the condyle of the mandible from translating
teeth at night and in patients with missing to a full open position. It can be seen with
posterior teeth with subsequent overclosure and without limited opening. It is diagnosed
of bite. It does not require treatment if the mainly by absence of joint sounds and
patient can open reasonably wide without deflection. If the disc displacement is associa-
discomfort, if pain occurs mild analgesics can ted with limited opening, then maximum
be used. unassisted opening will be less than 35 mm and
may increase passively by less than 4 mm and of the lateral pole of the condyle, structural
contralateral movement less than 7 mm. Pain irregularities of the articular eminence, loose
and change in patients perception of the bite intra-articular bodies than discs and dys-
generally results. functional movements, patterns or incordina-
If it is associated without limited opening tion. Single click during opening represents
maximum unassisted opening is more than the early stages of internal derangements.
35 mm and passively increases by more than Click can also be seen during early stage of
5 mm and contralateral movement is more than osteoarthritis. Retrodiscitis produced by
7 mm. The treatment involves analgesics and intrinsic trauma may produce clicking. Clicks
splints may help. can also occur during adherence (i.e. tem-
porary sticking of articular surfaces), shows
55. What is click? What are different types single click while breaking the adherences and
of clicks? State in which conditions click can be differentiated from disc displacements
is seen. by the fact that they occur only once following
The joint sound if it is a single, brief event of a period of static loading.
short duration is called click. Articular disc Reciprocal click is one in which click is noted
displacements (ADD) are thought to be most during opening and closing of jaws, this is seen
common cause of clicking. Clicking can be seen in disc displacement with reduction. In this a
in individuals who have normal disc position sound is heard during mandibular opening
on MRI, condylar hypermobility, enlargement when condyle is moving across the posterior
border of the disc to its normal intermediate at different interincisal opening, this is
zone and closing click occurs near the closed differentiating point.
or intercuspal position. Structural incompati- Reproducible clicks are the sounds which
bility of articular surface of joints adherence are present consistently on clinical examination
can occur and reciprocal clicks can be seen, here and not only as patient complaints. Repro-
the clicks while opening can occur where the ducible opening click (if they appear on two
mandibular opening is disrupted and while or three openings from maximum inter-
closing, it occurs at the same interincisal cuspation) while reproducible closing clicks if
opening while disc displacements show clicks they appear on two or three closing.
56. Give the schematic representation of TMJ sounds.
57. What is arthritis? What are the different osteoarthritis, osteoarthrosis, polyarthritides.
conditions affecting the temporomandi- Osteoarthritis is more common.
bular joints? 58. What are differentiating points between
Inflammation of the articular surfaces of rheumatoid arthritis and osteoarthritis?
the temporomandibular joints is referred as Soft tissue swelling rather than bony enlargements
arthritis. The different arthritic conditions are is a characteristic difference between OA and RA.
Table 2.1: Difference between osteoarthritis and rheumatoid arthritis
Osteoarthritis Rheumatoid arthritis
Age of onset It is <40 years Any age after 20 years
Prevalence Much more common Less common (1/10)
Cartilage breakdown It is deterioration of cartilage and It is related to body’s own immune
becomes thinner and overgrowth system, causes inflammation of
of bone spurs, due to age connective tissue in joints (synovial
(wear and tear) membranes) that leads to destruction of
articular cartilage.
Pain It gets worse at the end of day
or after exercising
Symmetry Symmetry not necessarily If one joint is involved, the other side is
present in osteoarthritis also affected.
Duration of morning <15 minutes (it becomes worse >40 minutes
stiffness after sitting down)
Joint involvement – One or two joints – Diffuse involvement
– Irregular involvement at distal – Symmetric involvement
interphalangeal joint
Contd.
Table 2.1: Difference between osteoarthritis and rheumatoid arthritis (Contd.)

Osteoarthritis Rheumatoid arthritis
Types of joint Weight bearing joints Small joints
involvement (knees, hips) (hands, wrists, elbows)
Rate of development Can take many years to develop It can come in months
Inflammation Mild/absent Severe
Anemia Rarely More common
Tenderness None/mild Moderate/severe
ESR Not raised Raised
ANA –ve +ve
Rheumatic factor Absent Present
Radiographic appearance Bony lumps and other deformities Bone looks thin and may show erosions
Treatment modalities NSAIDs (acetaminophen, aspirin, glucocorticoids (prednisone) and
ibuprofen, Cox-2 inhibitors) dietary immunosuppression agents in addition
supplements to prevent to NSAIDs dietary supplements fruits,
glucosamine/chondratin vegetables and fish
59. What is crepitus? State in which all lateral surface of condyle. These may break
conditions crepitus is seen. off and lie within the joint space and called
Crepitus is long grating sound (grinding/ as joint mice (deterioration component).
gritty feeling). It is irreversible. It is a multiple
rough gravel like sound. It is seen in arthritides
(diseases which involve destructive bony
changes), it indicates bone to bone contact. The
more common is in degenerative diseases
(osteoarthritis) and suggest lack of synovial
fluid to adequately lubricate joints. It is seen
in later stage of internal derangement.
60. Enumerate the various degenerative
changes involving condyle.
Normal condyle
The degenerative changes are joint deteriora-

tion and bone proliferation.
1. Osteophyte formation: New bone form- 2. Flattening of condyle (deterioration com-
ation at periphery of articular surface ponent and even sometimes flattening of
(proliferative component). They are seen on articular eminence): These are suggestive
anterior superior surface of condyle and of remodelling in absence of other features.
3. Irregularity on condylar surface: (Deteriora-

tion component—irregularity and erosion)
5. Ely’s cyst formation: Ely’s cysts are not true
cyst. These are areas of degeneration that
contain fibrous tissue, granulation tissue
4. Erosion of condylar head: Small to large

bites or scoops out of the articulating surfaces
of the joint resulting in loss of continuity of
cortices and eventually bone volume (deteriora-
tion component—severe arthritis erosion).
and osteoid. Radiographically small, round, 3. Decrease in pain and joint sounds are
radiolucent areas with irregular margins present. Osteoarthritis is supposed to be
surrounded by increased areas of bone density caused by mechanical overloading of joint.
deep to articular surfaces (proliferative If the cause of osteoarthritis is unknown,
component). it is called primary osteoarthritis. If the
6. Sclerosis of head: New bone formation in prescise cause can be identified it is called
subchondral region (proliferative component). secondary osteoarthritis. Disc dislocation
without reduction can cause osteoarthritis.
62. What is condylysis?
It is condylar resorption. It can be defined as
progressive loss of condylar shape with
decrease in mass. It primarily affects the
adolescent girls. It involves sudden lysis of
condyle that creates a rapid change in the bite
of individual resulting in open bite even that
is noticed by an individual. The occurrence of
progressive overjet is suggestive of condylysis.
As a result, most patients exhibit a decrease in
posterior face height, retrognathism and
progressive anterior open bite with clockwise
rotation of the mandible.
63. Define internal derangement of TMJ and
describe its various stages.
Internal derangement of TMJ is defined as an
abnormal positional relationship of the disc
relative to the mandibular condyle and the
61. What are stages of osteoarthritis? What articular eminence.
are primary and secondary osteoarthritis? OR
It is a degenerative disease of joint. Long-term Internal derangement of the temporo-
studies have shown the disc displacements and mandibular joint (TMJ) is defined as a
osteoarthritis can pass through three stages: disruption within the internal aspects of the
1. The first stage of clicking/catching TMJ in which there is a displacement of the disc
2. Mandibular movement restrictions and from its normal functional relationship with
pain the mandibular condyle and the articular
Stage Clinical Imaging

I. Early Painless clicking; no limitation of Mild disc displacement (on pening)
opening. The disc is reduced to with early reduction; normal disk
maximal opening which refers to osseous contours are normal
sliding back and corresponds to
audible click.
II. Early/Intermediate Occasional painful clicking, Mild to moderate disk displacement
intermittent locking. with late reduction, mild disc defor-
mity. The osseous contour remains
normal.
Contd.
Stage Clinical Imaging

III. Intermediate Joint tenderness, limited mouth Displaced, non-reducing disk moderate
opening, frequent pain, painful thickening of disc. Early stage it may
chewing. Disc is subjected to reduce and in later stage may not. The
deformity, as condyle pushes disc osseous contour remains normal.
downward and forward.
IV. Intermediate/late Chronic pain, limited opening Markedly thickened disc, severe dis-
placement without reduction, degenera-
tive osseous change and abnormal
contours in condyle and articular
eminence.
V. Late Variable joint pain, joint crepitus, Grossly deformed disc, non-reduction
pain with mandibular opening of disk with perforation of disk attach-
ment or disk degenerative osseous
changes. Deterioration and abrasion of
articular cartilage and disc surfaces,
occurrence of thickening and remodel-
ling of underlying bone.
Osteoarthrosis may be a final common pathway for several joint conditions.
portion of the temporal bone. These are the dis- various facial expressions. Avoiding
turbances in the arrangements of components extreme jaw movements, taking medica-
within joint itself primarily disc. It is most tions, applying moist heat or cold packs,
common disorder of TMJ. These derangements eating soft foods are other ways that may
are clicking joint type or locking joint type. keep the disorder from worsen.
Wilkes (1989) established 5 stages based on 3. Splints: They are plastic mouthpieces
clinical and imaging criteria. that fit over the upper and lower teeth.
They prevent the upper and lower teeth
64. What are the different treatment
from coming together, lessen the effects
modalities for internal derangements?
of clenching or grinding the teeth. Splints
The internal derangements are treated with are effective in reducing the intensity of
non-surgical methods and when these pain for patients with pain in jaw and
methods are unsuccessful they are managed by masticatory muscles by compensating
surgical methods. for or correcting perceived bite defects
1. Non-invasive methods: Non-surgical of the sufferer.
methods such as modification of the 4. Pharmacotherapy: The pharmacologic
diet, occlusal splints, physical therapy, agents which are commonly prescribed
pharmacotherapy, t r a n s c u t a n e o u s non-steroidal anti-inflammatory drugs
electrical nerve stimulation (TENS) and (NSAIDs) to reduce inflammation.
stress reduction technique. Muscle relaxants also prescribed for
2. Physical therapy: It is used to keep the treatment of muscle pain and spasm. To
synovial joint lubricated, and to maintain increase their benefit, muscle relaxants
the jaw motion. One of the exercises for the combination with NSAIDs are used.
jaw is to open the mouth to a comfortable 5. Arthroscopy: Lysis of adhesions and
fully-open position and then apply a joint lavage are the most commonly
slight additional pressure to open the performed TMJ arthroscopic surgical
mouth fully. Another exercise includes procedures to relieve painful hypo-
stretching the jaw muscles by doing mobility. The objective is to eliminate
restrictions on the disc and lateral by TMJ implants, is implanted to replace

capsule, to wash out micro-debris the temporal component of the joint.
resulting from the breakdown of the 9. Intra-articular: Injection of corticosteroid
articular surfaces, to irrigate the joint by intra-articular injection of corticosteroids
enzymes and prostaglandins and to alone or after arthrocentesis provides
stimulate the normal lubricating action long-term palliative effects on subjective
of the synovial membrane. In addition, symptoms and clinical signs of TMJ pain.
the presence of fibrous adhesions in the Recently, sodium hyaluronate (SH) has
superior joint space limits normal been proposed as an alternative thera-
translatory function of the disc condyle peutic agent which is high viscous, high
complex. molecular substance plays an important
6. Arthrocentesis: It is the simplest and role in joint lubrication and protection of
minimal invasive form of surgery in the the cartilage.
TMJ, aim to release the articular disc and 10. Low level: Laser therapy clinical studies
to remove adhesion between the disc of LLLT used on patients with disc
surface and the mandibular fossa by derangement disorders using either
means of hydraulic pressure from AlGaAs 830 nm diode laser in conti-
irrigation of the upper chamber of the nuous wave mode or He-Ne laser 632 nm
TMJ. This is very effective procedure in combined with a diode laser 904 nm in
patients with persistent or chronic closed pulsed mode have shown clinical
lock and anchorage in the upper articular benefits in terms of reduction in pain and
space. Lavage of superior joint space clicking. The application of laser beams
with saline exerts its effects through its diminishes pain while simultaneously
ability to eliminate joint effusion to reducing muscle contraction. The main
reduce the symptoms. It is considered as effects of laser light used in LLLT on
an intervening treatment modality tissue include: Analgesic, biostimulating,
between non-surgical treatment and anti-inflammatory, etc. Advantages
arthroscopic surgery. Being the least include aseptic, non-invasive, painless,
invasive and simplest form of surgical non-pharmaceutical and reversible
interventions into the TMJ, this procedure therapy, if used properly has no side-
carries a very low-risk and relatively easy effects. It has no post-operative discom-
to proceed in dental chair office under fort. Disadvantage has been the high-cost
local anesthesia alone or in combination compared to the conventional therapies
with conscious sedation. and the fast development in the field
7. Dissectomy and disc replacement: 11. Tissue engineering of the TMJ: The disc
Dissectomy used to regain the mandi- shows biomechanical properties that
bular motion and to reduce orofacial may be matched more easily in tissue-
pain, and may be followed by disc engineered constructs in contrast to other
replacement. musculoskeletal soft tissues.
8. Joint reconstruction: Several techniques Currently low level laser therapy and
have been proposed for re-construction tissue engineering show long-term
of portions of the joint or the entire joint promise for meeting this demand.
itself. A hemiarthroplasty may be used 65. What is anchored disc phenomenon?
to replace the superior articulating joint It is characterized by sudden, severe and
surface. During re-construction, joint persistent limited mouth opening that is
adhesions are lysed and a vitallium alloy characterized by more than disc displacement
fossa—eminence prosthesis, manufactured without reduction ( 10–30 mm). Since the disc
is not anatomically displaced the highly

innervated retrodiscal tissue is not compressed
and pain is experienced during forced mouth
opening. It is acute disc displacement without
reduction.
66. What is coronoid impedance?
It is a hypomobility disorder. During the
mandibular movement the coronoid process
will pass between lateral surface of maxilla
and zygomatic arch anterioinferiorly if its
pathway is impeded it will not slide smoothly
and restriction of movements will occur. This
is called coronoid impedence. Clinically limita-
tions especially during protrusion generally
painless. If it is unilateral the mandible will
deflect to affected side. The causes are:
a. Elongation of coronoid process (result of
chronic temporalis activity)
b. Tissure fibrosis (may be because of
trauma during surgery or prior infection)
c. Fractured zygomatic arch displaced
medially.
Treatment is remove the cause and gentle
passive stretching with ultrasound.
67. How the coronoid hyperplasia diagno-
sed? What is the radiographic sign?
Radiographically the coronoid process extends
1 cm above the zygomatic arch and restricting
the mouth opening. The appearance is called
as drumstick appearance on OPG or PA waters
view.
68. What are the features of condylar
hyperplasia?
Developmental anomaly, growth self-limiting
and stops with completion of skeletal growth.
• Mandibular asymmetry and chin deviates PA view showing right condyle elevated
to unaffected side.
• The movements may be restricted. 69. What is anterior positioning appliance?
• A depression may be noted at inferior An interocclusal device that encourages the
border of mandible where affected side mandible to assume a position more anterior
meets unaffected side. than intercuspal position (ICP). It is indicated
• Ramus vertical height is increased. to treat disc displacements, disc dislocations
• Radiographically normal cortical thickness with reduction. Patients with single or recipro-
and trabecular pattern may be seen (this cal click. Intermittent or chronic locking of
distinguishes from condylar tumor) joints. Retrodiscitis, an inflammatory disorder,
may be managed as anterior positioning may

be comfortable. The goal of treatment is to
change the position temporarily so as to
enhance the adaptation of retrodiscal tissues.
70. What is palpation? Describe various
types of palpation methods used for
orofacial structures.
Palpation is a procedure where examiner feels
or presses the structures examined. It gives Bi-digital palpation: With the help of two
more details about texture, dimension, consis- fingers of one hand (thumb and index finger),
tency, temperature and functional events.
Extraoral palpation: The structure is palpated
extraorally, e.g. parotid gland palpation, skin
over surface of swelling.
Intraoral palpation: Structure is palpated
intraorally, e.g. lateral pterygoid examination.
Unilateral palpation: Structure of one side is
palpated at a time, e.g. submandibular lymph
node, palpation of lateral pterygoid intraorally.
Bilateral palpation: Same structures on both
sides are palpated. Temporalis muscle, TMJ
palpation (extra-auricular/intra-auricular),
carotid artery not to be bilaterally palpated to
avoid carotid sinus stimulation and brady-
cardial reflex.
Bilateral palpation of TMJ and temporalis

Bimanual palpation: One structure is palpated
by fingers of both hands, e.g. duct of submandi-
bular gland and styloid process, body of
masseter muscle with one finger intraorally
and other extraorally corresponding the same Bi-digital palpation of upper labial mucosa,
location. sternocleidomastoid, buccal mucosa
e.g. sternocleidomastoid muscle, tongue no pain, then only superior pterygoids are
musculature, nodules of lips and buccal affected and not elevator muscles and side-
mucosa and helix of ear. The edentulous ways turning of mandible against resistance.
alveolar ridge, unilateral or bilateral when a Palpation of sternocleidomastoid muscle
clinician encounters pathosis, he or she should trapezius against resistance.
investigate the contralateral region of the body
to determine whether the condition is bilateral. 72. What are the indications of hot and cold
As a rule, if similar masses are present bilate- in orofacial region?
rally and in the same locations, they are most Application of moist heat or cold can be helpful
likely normal anatomic structures. in chronic centrally mediated myalgia moist
The carotid bulb in the bifurcation of the heat pack for 15–20 minutes while cold
artery. The mastoid process, the lateral pro- compresses for 5–7 minutes whichever will
cesses of the cervical vertebrae, and the wings work, will be repeated.
of the hyoid bone are such bilaterally occurring Moist heat/ice can be used if the patient
anatomic structures that are frequently mis- finds useful in disc dislocations with reduc-
taken for pathologic masses. Bilateral palpa- tions. Myospasm of muscles of mastication can
tion coupled with a knowledge of anatomy is be treated by vapocoolant spray, ice.
obligatory if these normal structures are to be Moist heat can be used to reduce pain and
differentiated from pathologic masses. inflammation after TMJ disclocation.
71. What are the different ways of palpating Coolant therapy is effective and simple in
muscles in orofacial region? reducing pain and the cold does relaxation of
muscles that are in spasm, and thus relieves the
Flat muscle palpation: When muscle can be
pain. Ice should be applied directly to the face
palpated over bone, e.g. masseter, temporalis.
on affected area and moved in a circular motion
Pincer palpation: When the belly of muscles without pressure to tissues until patient feels
can be held between two fingers, e.g. sterno- numb and even moist heat (moist towel or
cleidomastoid and even for examination of hot bottle) should be applied to the muscle
trigger zones. that increases circulation to the area by
Functional Method vasodilation.
Inferior lateral pterygoid: Patient asked to Moist heat during pain episodes in TMD’s
open the mouth against resistance if it pains heat is contraindicated in infectious swelling
then it is the source, as the contraction of this as it may aggravate the swelling and probably
muscle produces protrusion and/or opening will cause rupture.
of mouth. This muscle is stretched when the 73. What are superior and superficial loca-
teeth are clenched so even while clenching pain tions?
will also suggest pain in inferior lateral Superior location is the structure which is
pterygoid. superior in location related to any structure,
Superior lateral pterygoid: Contraction of this while superficial location is the one when a
during clenching, produces pain if tongue structure is closer to skin surface. For example,
blade is placed during maximal intercuspation the lingual nerve, submandibular duct and
still the pain increases, this is differentiating the hypoglossal nerve are superficial to the
point from inferior lateral pterygyoid where hyoglossus. The submandibular gland has
pain decreases on keeping tongue blade. It also large superficial lobe, the Stensen’s duct
stretches during clenching, if the pain occurs extends superficial to parotid gland. The deep
during this, it is due to superior head of lateral lobe of submandibular gland is superior to
pterygoid, at the same time if opening elicits superficial lobe.
75. What are the types of intracapsular

disorders of TMJ?
There are two types of intracapsular disorders
of TMJ.
1. Derangements of condyle disc complex,
(e.g. disc displacements with and without
reduction, disc displacement with reduc-
tion, disc dislocation without reduction).
2. Structural incompatibility of articular
surfaces.
76. What are TMJ subluxations and TMJ
dislocations?
Subluxation of joint is the articular surfaces
Deep lobe of submandibular node is superficial maintain a partial contact and condyle is able
(close to skin) to mylohyoid and superior lobe to return back to the glenoid fossa voluntarily.
Dislocation of TMJ occurs when condylar
head travels anteriorly to articular eminence
on maximal incisal opening and becomes
locked in front of eminence such that the
patient is unable to close the mouth.
These can be chronic/recurrent dislocations.
These are the one which occurs on periodic
basis. Prolonged/permanent dislocation. The
dislocation which is remaining for prolonged
time and patient ultimately get habituated
to it.
77. State Laskin’s criteria for MPDS.
There are four cardinal signs for MPDS. They
are as follows:
Positive Findings
Sublingual gland is superior to submandibular gland
1. Unilateral pain in the pre-auricular region
and submandibular gland is superficial to sublingual
gland 2. Muscle tenderness in the pre-auricular
region
74. What is closed lock? 3. Clicking or popping noises in the TMJ
An intracapsular biomechanical disorder 4. Restriction and deviation of the jaw to the
involving the condyle disc complex. In closed affected side during normal opening
mouth position the disc is in an anterior motion (Garg et al., MPDS an overview)
position to the condylar head and the disc does Negative Criteria
not reduce with opening the mouth. Medial 1. No radiographic evidence
and lateral displacements of the disc may also 2. No tenderness in TMJ via external auditory
be present. This disorder is associated with meatus.
persistent limited mandibular opening that
does not resolve with the clinician or the patient 78. What is jump sign?
performing a specific manipulative maneuver. In patient with myofascial pain dysfunction
This is also referred to as “closed lock”. syndrome, when a myofascial trigger point is
detected and palpated the patient gives a superior joint space under local anesthesia.
typical behavioural reaction, acknowledging One needle 100–300 ml of Ringer’s lactate
the tenderness felt in the area of pain reference, solution is injected into superior joint space, the
known as the ‘jump sign’ or it is involuntary second needle acts as an outflow portal, which
withdrawl of stimulated muscle, when taut allows lavage of joint cavity. Steroids or
bands are palpated on trigger points. It is sodium hyaluronate may be injected at the end
characteristic of fibromyalgia of cervical spine. of lavage to alleviate intracapsular inflam-
mation. Soft diet and analgesics may be
79. What is functional dislocation of disc?
prescribed.
The posterior border of disc becomes thin and
the attachment of superior lateral pterygoid 82. Describe various uses of botox in oral
muscle pulls the disc forward through discal facial disease.
space. The disc is trapped in forward position. Uses of botox in oral medicine:
The translation of condyle is inhibited because 1. In diagnosis: Diagnostic applications of
anterior and medial position of disc. The botox—it can be used to verify the correct
individual feels joint being locked in a limited diagnosis, e.g. to differentiate between
closed position, because the articular surfaces pulpal and muscular pain. The muscular
have actually been separated this condition pain will be relieved.
is called functional dislocation of disc. There 2. In TMJ disease:
will be no joint sounds the point to help • MPDS—botulinum toxin has been advo-
differentiate from functional dislocation. cated for the treatment of MPDS.
80. What is loading of TMJ surfaces? • Recurrent subluxations and dislocation—
treatment of recurrent subluxations and
TMJ loading (compression) is done for the
dislocations of temporomandibular joint.
diagnosis of intracapsular disorder and
myofascial pain. The operator is standing • Temporomandibular disorders—TMJ
behind the patient with placing fore fingers disorders in the muscles which inflict
under both sides of the mandible (it exerts soreness and discomfort.
bilateral upward pressure), at the same time 3. In parafunctional habits:
thumbs are placed in the mentolabial area of • Treatment of bruxism by bilateral intra
chin with slight downward pressure. This masseteric injection.
maneuver forces condyle into superior and • Snoring and sleep apnea—injection of
anterior position. botox into masticatory muscles will
The pain in the TMJ region suggests intra- enable the patients jaw more slightly
capsular disorder (retrodiscitis/capsulitis) forward during sleep, this opens the
airway sufficiently to reduce snoring.
While pain which radiates to other than TMJ
structures in orofacial area suggests myofascial 4. Cosmetics purpose:
pain. • Used in anti-ageing treatment to reduce
wrinkling of facial skin.
81. What is TMJ arthrocentesis? What are its • It weakens masseter muscle giving less
indications? angle at the angle of mandible.
It consists of TMJ lavage, placement of • Prominent gums—display of excessive
medications into joint, and examination under gingival tissue in maxilla upon smiling
anesthesia. Intravenous sedation may or may (gummy smile). Oral hygiene and esthetic
not be used. It is indicated in painful limited issue.
mouth opening, the conditions that involve • Asymmetrical smiles—these result due
inflammation in the joint. The technique to facial assymetries (acquired/familial)
involves injection of two 18-gauge needle into injection of botox into overactive muscles
produce gentle relaxation of muscles 83. What are the limitations, complications
resulting in a symmetrical smile. and contraindications of botox?
5. Muscle relaxation and dysfunction: There are a number of complications associated
• Oromandibular dystonia—injection of with botox therapy.
botox in masseter, medial/lateral ptery- Limitations: The therapeutic levels inhibit
goid has been reported to resolve muscle masticatory functions temporarily and
dysfunction. masticatory force will eventually return to
• Hemifacial spasm and mandibular previous levels once effect of drug has
spasm—involuntary, irregular or chronic subsided.
contractions of muscles innervated by Complications: Mild pain with injection, local
facial nerve on ipsilateral side of face. edema, erythema, hematoma, transient
• Blepharospasm—botox is injected super- numbness, weakness of muscle at sit of
ficially to the orbicularis oculi in four injection, post-injection bruising, local spread
locations in periphery of each eye. causing unwanted paralysis of nearby muscles.
• Palatal and stapedius myoclonus— • Mild nausea, transient headache, produc-
tinnitus is caused, relieved by botox tion of neutralising (IgG) antibodies against
injection in soft palate and local applica- botox, facial nerve palsy, dysphagia, flu-
tion respectively. like symptoms, development of tolerance
6. In neurological disorders and pain: and non-targeted muscle weakness.
• Treatment of oral incontinence in facial • The complications are transient and gene-
paralysis rally resolves within some days. Overdose
• Facial nerve paresis can be treated by antitoxin.
• In trigeminal neuralgia and injected in Contraindications: It is contraindicated in
trigger zones myasthenia gravis, Eaton-Lambert syndrome,
• Post-herpetic neuralgia motor neuron disease, concurrent uses of
• In refractory cases of migraine and aminoglycosides and sensitivity to toxin and
headache pregnant women and nursing women.
• Neck pain and torticollis
7. In salivary gland diseases: 84. What are complementary and alternative
• Salivary fistula—injection of botox in medicine in persistent orofacial pain?
proximity of parotid gland results in the Complementary and alternative medicine
blockage of parotid secretions which is (CAM) are group of unconventional medical
followed by glandular atrophy allowing systems, practices and products not presently
salivary fistula to eventually heal. considered part of the conventional biomedical
• Ranula—resolution of ranula by injection care provided by medical doctors and other
of botox. conventionally trained health professionals.
• Sialorrhea and drooling—intraglandular These measures are:
botulinum toxin injections can be used 1. Mind–body interventions: These increase
to improve sialorrhea in patients with the mind’s capacity to enhance bodily func-
Parkinson’s disease, parkinsonian syn- tions and reduce symptoms, e.g. biofeed-
dromes, motor neuron disease, and back, relaxation, meditation, hypnosis,
cerebral palsy. yoga and spiritual approaches (prayers).
• Frey syndrome 2. Manipulative and body-based therapies:
8. Miscellaneous These are physical modalities such as
• Dental implants and surgery massage therapy, chiropractic adjustments
• Rhinitis and osteopathic manipulations.
3. Biologically based therapies: Foods, disorders like degenerative disease and

vitamins, minerals, herbal products, etc. rheumatoid arthritis. Dexamethasone
4. Energy therapies: (1) The practitioners commonly used and more frequently in
intend to manipulate biofields theorized to acute phases.
exist within and around the patient. (2) Use b. These can be used in relieving pain and
of unconventional use of electromagnetic restricted movements.
fields for therapeutic purposes. c. These can be used to prevent fibrosis
5. Alternative medical systems: Homeopathy after reduction of TMJ dislocations.
and naturopathy. d. Chemical arthroplasty in arthrosis of
85. What is functional diagnosis? Give TMJ (hydrocortisone/triamcilone).
example of it. 3. Systemic use of corticosteroids is not
A functional diagnosis is one that is more indicated for TMDs the exception is acute
comprehensive and centred around biome- generalized muscle and joint inflammation
chanics and disease, relating the two into a with polyarthrides.
more conceptual definition. To diagnose the 4. Severe myositis and TMJ dysfunction.
organ must be in function, e.g. diagnosis of 5. Dental surgeons are often advised to use
disc displacements, TMJ subluxation. corticosteroids during and after third
molar removal and other dentoalveolar
86. Enumerate the muscles of mastication. surgery to reduce post-surgical edema. The
The muscles of mastication are the paired most commonly used forms of cortico-
masseter, paired medial and paired lateral steroids in dentoalveolar surgery include
pterygoid, and paired temporalis muscles. The dexamethasone (oral), dexamethasone
paired buccinators are considered as accessory sodium phosphate and dexametha-
muscles of mastication. sone acetate, and methylprednisolone
87. Enumerate the uses of steroids in non- acetate and methyl prednisolone sodium
mucosal agents. succinate. Methylprednisolone is usually
administered via the intramuscular or
1. More recently for central giant cell lesion
intravenous route though the possibility
the intralesional corticosteroid use has
of topical (intra-alveolar) application has
shown some value, inducing complete
been described, with a reduction in
involution in many cases and partial invo-
morbidity and possible side-effects.
lution in others. The suggested treatment
is triamcinolone, 10 mg/ml, of which 1 ml 6. Topical and intralesional steroid injections
is injected for each 1 cm of jaw involve- in tonsillar fossa in Eagle’s syndrome
ment throughout the lesion, once a week 7. Intracanal corticosteroid in root canal
for 6 weeks. Each injection sequence is per- therapy.
formed with local anesthesia (bupivacaine) 8. Anaphylaxis.
added to the injection solution. 9. Temporal arteritis.
2. Intra-articular injections: 10. Post-herpetic neuralgia
a. In the superior compartment of tem- 11. Ramsay Hunt syndrome
poromandibular joint involving the 12. Bell’s palsy.
3
Benign Lesions of Oral Cavity
1. What is tumor? What is benign tumor? properties. Thus, benign tumor by definition
What are the differentiating points of does not grow in an unlimited aggressive
benign and malignant tumors? manner, does not invade the surrounding
It is an abnormal mass of tissues the growth of tissues and does not metastasize.
which exceeds and is uncoordinated with that 2. What are hamartoma, choriostoma and
of normal tissues, and persists in the same teratoma? Give an example of each.
excessive manner even after the cessation of 1. Hamartomas are non-neoplastic over-
stimuli which evoked the change. growth of mature/differentiated tissues
The term benign implies mild and non- indigenous to the specific part of the body
progressive. It is one which lacks the malignant in which they develop.
Features Benign Malignant

Periphery Smooth, well-defined, Ill-defined, absence of
encapsulated encapsulation
Cortication Often present Lack of cortication
Surrounding tissue Compressed Invaded
Size Usually small Often large
Growth rate and mode Slow and with expansion Rapid and infiltrative
Progression Slow progressive, remain stationary Progressive and always fatal if
and may regress and rarely fatal untreated.
if untreated.
Spread Direct extension Metastasis
Location Specific anatomic site Anywhere
Internal structure RO, RL, mixed RL
Effect on surrounding Resorb teeth root, displace the teeth Destroy supporting alveolar
structure in bodily fashion without causing bone so that the teeth may be
mobility floating.
77
A hamartoma is also defined as a dis- and contains gastrointestinal glandular

organized proliferation of mature tissues, structures.
composed of elements that are normally The rare finding of bone or cartilage in
found in the specific location in which it the tongue, and the occasional development
develops, often with one predominating of thyroid tissue in the posterior tongue.
element. The more commonly seen ectopic seba-
Hamartoma represents a dysmorphic ceous glands known as Fordyce granules
proliferation of tissue that is native to the and salivary gland tissue within lymph
area and does not have the capacity for nodes may also be considered choristomas.
continuous growth but merely parallel that Each has a limited proliferation.
of the host. The distinction between a Salivary gland choristoma central and
hamartoma and a benign neoplasm is often gingival, both have ectopic salivary gland
arbitrary; in fact, most benign tumors of tissue appearing as a raised tumor-like
infancy and childhood are actually develop- mass, must not have any connection with
mental hamartomas. The salient features of normal minor or major salivary glands.
hamartomas are that they cease growing Cartilaginous and/or osseous choristomas
at some points in their course and they do of oral soft tissue are rare lesions occurring
not infiltrate into surrounding tissues. most frequently on the tongue.
Therefore, in bone they may be treated for Cartilaginous choristoma: It is composed of
cure by enucleation procedures and in soft mature hyaline cartilage in fibrous tissue
tissue by local pericapsular excisions. that resembles perichondrium; usually multi-
Hamartomas are limited proliferations of lobulated; chondrocytes vary from small to
tissue with no known stimulus and no large, but lack atypia osseous choristoma:
truly invasive. For example, hemangioma, composed of dense mature bone; osteocytes
lymphangioma, odontome, pigmented are compact and unremarkable; no pro-
nevi, etc. minent osteoblastic rimming; occasionally
2. Choristoma that is defined as a histologi- bone and cartilage are present in the same
cally normal tissue proliferation or nodule lesion, lingual thyroid choristoma, lingual
of tissue, of a type not normally found in sebaceous choristoma, glial choristoma
the anatomic site. gastric/respiratory mucosal choristoma
It is also known as a tumor-like mass con- (solid, cystic).
sisting of normal cells in an abnormal 3. Teratoma is a congenital growth which
location. contains tissue or organ components from
A choristoma is defined as a histologi- all 3 embryologic germ layers or Weaver
cally normal tissue proliferation or nodule et al defines teratoma as a tumor consisting
of soft or hard tissue type not normally of multiple tissues that are not indigenous
found in the anatomic site of proliferation. to their site of origin.
Choristoma tends to resemble tumors, as In greek teratoma is monsterous tumor.
they present a relatively well-organized It is a tumor composed of multiple tissues
proliferation. Choristomas are similar to foreign to the normal organ from which
hamartomas except that they are dysmor- it arises. Teratomas are true neoplasms
phic proliferations of tissue that are not originating from pluripotent cells and are
native to the site. These are one of rarities composed of tissues from all three germinal
and has limited proliferation. layers, usually benign in nature. It is rare
For example, the rare heterotopic to find in head and neck regions.
gastrointestinal cyst, which may be found Epignathus is commonly used to describe
in the tongue or floor of the mouth of infants a congenital teratoma in the oropharyngeal
Benign Lesions of Oral Cavity 79
region. Teratomas of the oral cavity are neck, the jaws, and the floor of the mouth
divided anatomically depending on their on rare occasions.
location. They can be sublingual, genio- One tumor of particular interest is the
hyoid and lateral. Teratoma of tongue may benign cystic teratoma of the ovary.
exhibit skin, hair, bone, cartilage or mucous Because of its origin from three germ layers,
membrane on the surface. The dermoid it will form various components of skin
cyst is sometimes considered a variant (including hair and sebaceous glands),
of teratoma containing ectodermal and teeth, and bone. The degree of differentia-
mesenchymal derivative. tion and normal arrangement can be quite
Teratomas, which are often thought of as remarkable including bone with erupted
hamartomas or choristomas, are actually teeth and even a fibrous periodontal ligament.
true neoplasms with the capacity of
continual growth. They are neoplasias that 3. Enumerate the tumors that can cause
arise from multiple germ layers and thus large and disfiguring size.
produce tissues that are foreign to the part Ossifying fibroma is one of a few allowed by
in which they develop. They are distinct patients to reach the largest and most
from other neoplasias that may also show disfiguring size in all the benign tumors of
tissue diversity, such as pleomorphic the head and neck areas. The others are
adenomas of salivary glands, which are ameloblastomas, odontogenic myxomas,
derived from native tissue. The majority of neurofibromas, and pleomorphic adenomas.
teratomas occur within the ovary (usually The reason is probably because of its persis-
benign), or in the testes (predominantly tently steady but slow rate of growth and its
malignant). Teratomas are also seen in the painless character.
4. Give differentiating points of fibrous dysplasia and ossifying fibroma.
Fibrous dysplasia Ossifying fibroma

Age Ist and IInd decades IIIrd and IVth decades
Sex predilection Monostotic equal predilection More in women
Polyostotic female predilection
Common jaw site Maxilla Mandible
Types Monostotic/polyostotic Juvenile/psammomatoid form
Radiographically Opacity diffuse border blending Opacity circumscribed borders well-
defined
Growth pattern Self-limited stabilizes at puberty Continuous not hormone related
No. of bones involved One (monostotic) or more Only one
(polyostotic)
Syndrome associated McCune-Albright syndrome None
Malignant potential Less than 1% usually with Nil
polyostotic
Histologically Vascular matrix woven bone Cellular fibrous matrix bony islands
trabeculae and trabeculae
Treatment Recontour for cosmetics Excise
5. What are exostoses? alveolar bone most often in posterior region.

These are single or multiple localised bony These are benign growths may be related to
excrescences that arise from the cortical plates, stress placed on bone from function of teeth.
asymptomatic along the buccal aspects of They are less common than tori. They are
discovered most often in adults. Exostosis are 6. What are tori? What are the varieties of
seen less commonly in the lower jaw. Buccal palatal torus and torus mandibularis?
exostoses occur as a bilateral bony hard Localised nodular enlargements (exostoses) of
nodules along the facial aspect of maxillary and the cortical bone at midline of palate (torus
mandibular alveolar ridge. palatinus) and lingual aspects of mandible
(torus mandibularis).
Classification of Tori
Class 1: Tori are absent or minimal in size and
do not interfere with existing denture.
Class 2: Clinically several tori of moderate size,
often mild difficulties in denture construction
and use of surgery is not required.
Class 3: Tori are of large size, they compromise
function of dentures and require surgical
excision.
Palatal torus can be classified according to their
morphological appearance into:
a. Flat torus: Broad base, slightly convex
smooth surface. The extension is sym-
metrically on both sides of midpalatine
raphe.
b. Spindle torus: A midline ridge is present
along the palatal raphe and sometimes
median groove is present.
c. Nodular torus: It is seen as multiple
protuberances each with an individual base.
The protuberances may coalesce forming
grooves between them.
d. Lobular torus: It is a multilobulated mass
and arises from single base. They may be
sessile or pedunculated.
Mandibular torus presents as bony protube-

rance along the lingual aspect of mandible
above the mylohyoid line most commonly in
the region of premolars. They may present as
a. Single nodules
b. Multiple lobules paralleling the teeth
c. Rarely do they become large enough to
meet in midline.
7. What are the differences among buccal

exostosis, torus palatinus, and torus
mandibularis?
These entities are all very site specific. The
palatal torus is seen only in the midline of the
hard palate, whereas the torus mandibularis
occurs only on the lingual surface of the
mandible. Buccal exostosis is found only on the
facial surface of the alveolar bone, most
commonly the maxillary alveolar process.
8. What is reactive subpontine exostosis?
It is also called subpontic osseous prolifera-
tion or subpontic osseous hyperplasia. It is
an uncommon but interesting variant. This
develops from alveolar crestal bone beneath exophytic growth, hypertrophy, hyperplasia,
the pontic of posterior bridge. It may need to neoplasia, and the pooling of fluid are four
excise for oral hygiene purpose. mechanisms by which exophytic lesions may
be produced.
9. What is exophytic growth? What are the
mechanisms by which exophytic lesions 10. What are different shapes of exophytic
are produced? lesions?
Any pathologic growth that projects above the Papillomatous, verrucous, nodular, dome
normal contours of the oral surface is called shaped, polypoid, and bosselated.
included in this are squamous papilloma,

verruca vulgaris and condyloma accuminatum
and heck disease. Clinically, OPLs can appear
as a sessile/pedunculated, white (heavily
keratotic) or corol pink growths. Generally,
solitary (except condyloma accuminatum seen
in clusters) and asymptomatic. They are small
1. Papillomatous, e.g. squamous papilloma, (less than 1 cm) can occur intraorally and on
2. Verrucous, e.g verrucous ca., verruca vermillion border. OPLs are mildly contagious.
vulgaris proliferative verrucous leuko- Treatment is surgical excision. Interferon-
plakia alpha intralesionally may be useful specially
in HIV patients. They have favourable
prognosis except for laryngeal papillomatosis.
Papilloma and giant cell fibroma are more
common papillary lesions. Diffuse papillary
3. Nodular, e.g. exostosis, tori, fibroma lesions represent oral markers of systemic
disorders.
4. Dome shaped, e.g. ranula, buccal space
infections Squamous papilloma: Most common
benign oral epithelial neoplasm. The common
sites are ventral tongue, frenal area, palate and
mucosal surface of lips. These may occur
spontaneously.
Verruca vulgaris: It is common skin wart
appear on vermillion border and less
commonly intraorally. The intraoral locations
5. Polypoid, e.g. pulp polyp, gingival polyp
are palate and keratinized gingival tissues. It
6. Bosselated, e.g. torus palatinus.
is associated with HPV (2, 4, 40).
Papillomatous or verrucous originate in
surface epithelium, e.g. verruca vulgaris, Condyloma accuminatum: It characteristi-
papillomas, squamous cell carcinoma, cally situated in anogenital area and presence
verrucous carcinoma and keratoacanthoma. in mouth indicated sexual transmission.
Those with smoothly contoured shaped Intraoral common sites are lips—commisures
originate in the deeper tissues and are beneath and gingival mucosa. It is associated with HPV
and separate from stratified squamous (6 and 11) and frequently seen in HIV positive
epithelium. For example, tori, fibroma, lipoma patients.
and malignant mesenchymal tumor.
12. What is the difference between intraoral
11. What are oral papillary lesions? growth and swelling?
Papillary lesions represent swellings with The growth projects above the surface of
finger like projections imparting cauliflower normal contour, while swelling is present in
appearance; these projections are rounded and between two surfaces. The growth is excised
blunt like fungiform papillae of tongue. Oral while swelling is aspirated before it goes for
papillary lesions (OPL) are growths of oral surgical excision, e.g. irritational fibroma may
mucosa which are verrucous (white with rough produce growth on buccal mucosa while minor
surface) and papillary (multiple finger like salivary gland tumor or mucocele may
projections) in nature. The entities which are produce swelling on the same location.
13. Describe various surface textures of oral soft tissue lesions.

Various surface textures of oral soft tissues are:
Types Example Diagram Clinical photograph

Verrucous Verrucous
leukoplakia
Papillomatous Squamous
papilloma
Fissured Fissured
tongue
Corrugated Hyperkeratosis
Crusted Paraneoplastic
syndrome
14. Enumerate oral psoriasiform lesions. 15. Which are the anatomical baselines used
Psoriasiform mucositis (microscopically in cephalometric and extraoral radio-
engorgement of capillaries in the connective graphy?
tissue and mixed inflammatory infiltrate). The anatomical baselines which are used in
Reports of oral psoriasis that are well- cephalometrics and extraoral radiography are:
documented show no consistent lesion 1. Anthropological
pattern. Patterns range from raised, white, 2. Orbital meatal
scaling lesions predominantly on the palate 3. Interpupillary
or buccal mucosa to well-demarcated,
flattened, erythematous lesions with a slightly
raised, white, annular or serpiginous border.
Benign migratory glossitis, reactive arthritis
(previously called Reiter’s syndrome),
erythema migraines.
16. Enlist what all types of fibromas can be hyperplasia or atrophy), actinic keratosis
seen in oral cavity? Name the syndromes (erosion and white brown crusting on
associated with fibroma. vermillion border of lip), freckle. Actinic
The true fibroma, irritational fibroma, giant cell cheilosis is characterized by atrophy of the
fibroma, desmoplastic fibroma, central vermilion border, which may develop dry,
cementifying/ossifying fibroma and central scaly changes. As the condition progresses,
odontogenic fibroma. The true fibroma ulcerated sites may appear which partially
(fibroma) is a connective tissue tumor which heal, only to recur at a later date. (The patient
is rare to find. Irritational fibroma (traumatic often mistakes these recurring ulcerated
fibroma) is common benign exophytic oral lesions for “fever blisters.”) The evolving
lesion that develops secondary to tissue injury, cancer slowly becomes a crusted, non-tender,
trauma, and local irritation. Giant cell fibroma indurated. Keratoacanthoma seen on upper lip
is a benign tumor of oral mucosa with on sun exposed lesions. Ephelides darken on
distinctive clinicopathological features. The sun exposure.
name is given as it shows large multinucleated 18. What are causes of gingival hyperplasias?
fibroblasts that tend to occur in close proximity
1. Local: Plaque, calculus, bacteria
to overlying epithelium and shows nodular
appearance clinically. 2. Systemic:
Desmoplastic fibroma is rare. It shows a. Hormonal imbalance: Estrogen, testo-
fibroblast and collagen fibres seen in mandible sterone
commonly and more than 30 years of age. b. Drugs: Phenytoin (dilantin), cyclosporin,
It shows painless enlargement of jaws nifedipine and other calcium channel
aggressive lesion. blockers
Central ossifying/cementifying fibroma has c. Leukemia (leukemic infiltrates and/or
cellular fibrous stroma and calcification. local factors)
It is seen in adults in 3rd/4th decades. Com- d. Genetic factors
monly in female and in mandible. Radio- e. Syndromes
graphically shows lucent/opaque appearance. 19. Enumerate the syndromes associated
Central odontogenic fibroma is uncommon, with gingival fibromatosis.
slow growing variety. It is non-aggressive,
1. Murray-Puretic-Drescher syndrome: Gingival
well-defined lesion. Radiographically showing
fibromatosis with multiple hyaline fibro-
unilocular, root resorption.
mas of the skin and scalp
Syndromes Associated with it 2. Laband syndrome: Gingival fibromatosis
1. Cowden’s syndrome (multiple hamartoma with formative defects of the ear, nose,
and neoplasia syndrome): Multiple fib- nails, bone and hepatosplenomegaly.
romas, multiple papules on lips and gin- 3. Rutherford syndrome: Gingival fibro-
givae producing cobblestone appearance. matosis and corneal opacities.
2. Tuberous sclerosis: Seizures, mental retar- 4. Cross syndrome: Gingival fibromatosis
dation with hamartomatous glial proli- with microphthalmia, skin hypopigmen-
feration, wart-like lesion on cheek in tation, mental retardation, and corneal
butterfly-like distributon. opacities.
17. Enumerate the lesions which are associa- In each of the above syndromes, the
ted with sun exposure. gingival fibromatosis is usually less severe
Actinic chelitis, basal cell carcinoma, solar than it is in hereditary gingival fibro-
keratosis (squamous epithelium may undergo matosis.
20. Enumerate the causes of swellings in Epidermoid

floor of mouth. Dermoid cyst: Asymptomatic mass usually
1. Inflammatory/trauma: Mucous retention in midline.
cyst (ranula)—elevated, fluctuant bluish
3. Neoplasms: Salivary gland tumor—solitary,
white mass in lateral floor mouth. Most are
asymptomatic, firm mass. Malignant
due to sialoliths.
tumors may cause pain, parasthesia.
Ploughing ranula: When the contents herniates
through mylohyoid muscle and presents as Mesenchymal neoplasms: Firm, asympto-
swelling in submandibular or cervical areas. matic rarely malignancies less likely to
2. Developmental: Lymphoepithelial cyst asym- recur lipoma.
ptomatic nodule less than 1 cm in diameter. 4. Infectious: Ludwig’s angina.
21. Enumerate the causes of swellings of palate.
Differential diagnoses of palatal swelling

Onset and course
Acute Palatal abscess (painful and non-vital tooth)
Chronic Torus palatinus, median palatal cyst, pleomorphic adenoma, hyperplastic
candidiasis
Shape
Globular Palatal abscess, torus palatinus, median palatal cyst, pleomorphic adenoma
Peppled Hyperplastic candidiasis
Consistency
Fluctuant/tense Palatal abscess, median palatal cyst
Rubbery/firm Torus palatinus, pleomorphic adenoma, hyperplastic candidiasis,
lymphoma
Associated pain
Yes Palatal abscess, hyperplastic candidiasis, infective or traumatic complica-
tions of: Torus palatinus, median palatal cyst, pleomorphic adenoma
(malignant variety may cause parasthesia)
No Uncomplicated: Torus palatinus, median palatal cyst, mucous extravasa-
tion phenomenon, (bluish) pleomorphic adenoma
Associated fever
Yes Palatal abscess (but may not be present)
No Hyperplastic candidiasis, uncomplicated: Torus palatinus, median palatal
cyst, pleomorphic adenoma
Patient attributes
Poor oral hygiene/caries Palatal abscess
Diabetes/HIV Palatal abscess
Denture wearer Hyperplastic candidias
Other regions/systems Neoplasm of maxilla or maxillary sinus: Palatal swelling with or without
ulceration tumor arising from CNS.
22. What is cutright lesion? 2. Cartilaginous rests are known to exist in the
It is also called reactive osseous and chondro- area of the nasopalatine duct.
matous metaplasia. Occasionally 3. Cartilaginous metaplasia secondary to
chronic denture trauma leads to formation
1. Cartilage or bone may be discovered within
of cartilage within flabby soft tissue removed
soft tissue specimens removed from the oral
from maxillary edentulous alveolar ridges
cavity.
of long-term denture wearers.
Clinically it shows an extremely tender and on the palate beneath a complete or partial
localized area of the alveolar ridge associated removable denture. It is more commonly
with local enlargement. These changes almost associated with a flipper-type partial
always arise in patients with extensive atrophy denture or a full denture. Approximately
of the mandibular alveolar ridge, leading to a 10% of the people who wear maxillary
knife edge-like crest and sometimes in maxilla. dentures have this condition, and most
Although most examples involve the posterior wear their dentures continuously.
mandible, similar areas may rarely be seen
overlying the maxillary alveolar ridge or
associated with anterior portions of the
mandible. It is also called cutright tumor. This
represents hyperplasia of existing embroyonic
cartilaginous rests due to inflammatory factors
induced by ill-fitting dentures.
Tender, elevated nodule along the thin crest of

mandibular alveolar ridge
They differ from soft tissue choristoma in

that they arise directly from the bone beneath
the lightly bound mandibular alveolar ridge.
These are treated by recontouring the thin
mandibular ridges and supplemented with 2. Epulis fissuratum (denture induced fib-
graft material. Implants may also reduce the rous hyperplasia, inflammatory fibrous
traumatic injury to the ridge and lessen the hyperplasias, denture injury tumor,
chance of recurrence. If the ridge modification denture epulis) is an IH lesion observed
is not made, the continued injury to the site at the borders of ill-fitting dentures. In most
occasionally results in recurrence of the lesion. instances the dental flanges overextend
secondary to alveolar bone resorption and
23. Name the oral mucosal lesions that are settling of the denture. The exophytic, often
caused by acrylic dentures. elongated lesion usually has at least one
1. The inflammatory hyperplasia (IH) cleft into which the denture flange fits,
lesion known as papillary hyperplasia: The with a proliferation of tissue on each side.
palatal hyperplasia (PHP and palatine Commonly seen in vestibular mucosa and
papillomatosis) occurs almost exclusively less likely in lingual sulcus.
and sits in a slightly cupped-out depres-

sion. The pedunculated nature can be
easily demonstrated by lifting with probe.
The edge of lesion is often serrated and
resemble like a leaf.
4. Denture stomatitis: The diffuse redness of
the palate seen under dentures has posed
a diagnostic problem for years. It is often
classified as a form of erythematous candi-
diasis. Causes are apparently multifactoral;
denture trauma, improper designing of
denture causing unusal pressure, allergy
to denture base, inadequate curing,
denture plaque and candidal infection are
the most important. Denture stomatitis
occurs under either complete or partial
dentures and is found more frequently in
women. The lesions are usually confined
to the palate and seldom if ever involve
the mandibular ridge. In approximately
50% of the patients, there is an associated
angular cheilitis with or without an
inflammatory papillary hyperplasia of the
palate.
3. Leaf like denture fibroma (fibroepithelial

polyp): This characteristic lesion is a
flattened pink mass attached to palate by
a narrow stalk, occurs on hard palate
beneath maxillary denture. This is a
flattened mass closely applied to palate
5. Denture papillomatosis (inflammatory

papillary hyperplasia): Some investigators
classify as a part of denture stomatitis. The
causes are ill-fitting dentures, poor dental
hygiene, wearing the dentures continuously
and possibly candida. Clinically, occurs
under hard palate beneath the denture
rarely on mandibular mucosa. The mucosa
is erythematous and has pebbly surface,
most cases are associated with denture
stomatitis.
6. Atrophic candidiasis: The most common 8. Focal hyperkeratosis (frictional hyper-

clinical presentation of atrophic candi- keratosis): Most commonly seen in
diasis is the red, velvet-like, tender palatal alveolar ridge associated with ill-fitting
mucosa under a denture. Here the high- lower denture.
frequency, low-intensity trauma of a 9. Ulcers and erythema: These are associated
denture surface compressing the palatal with denture flange.
mucosa during swallowing alters the 10. The lesions associated with suction disc:
barrier defense, allowing the normally On palate with upper denture and
innocuous candida organisms to become hyperplasia due to negative pressure a
pathogenic. heart shaped or round area of mucosal
heperplasia may appear on hard palate.
This type of hyperplasia occurs if a relief
chamber exists at centre of basal plate of
denture.
7. Angular cheilitis: Dentures with reduced

vertical dimensions. It is also called
perlèche, which often begins when a loss
of occlusal vertical dimension creates a
constant moisture and cracking at the
commissure and predisposes the tissue to
candida proliferation and invasion. In this
form, the commissures are tender, fissured,
and often crusted, and there may also be
some skin erythema.
cause local burns either due to heat

evolving during polymerization or to
monomer excess. The mucosa is red with
or without erosions.
13. Atrophy of maxillary alveolar ridge: This
may occur due to excessive occlusal trauma
because of poor fitting denture common in
women in anterior maxilla. The alveolus
becomes flabby and red and may co-exist
with epulis fissuratum.
24. What are Epstein’s pearls?

A similar palatal cyst of the newborn is
commonly found in the posterior midline of the
hard palate, where it arises from epithelial
remnants remaining in the stroma after fusion
of the palatal processes which meet medially
11. Cutright tumor (reactive osseous and to form the palate. As originally described, the
chondromatous metaplasia): It is a carti- cysts along the median raphe of the palate were
laginous choristoma with very mature and called Epstein’s pearls and the term Bohn’s
localized submucosal cartilage. nodules was used for cysts which originated
12. Acrylic resin: Burn autopolymerizing from palatal gland structures and were
acrylic resins which are used for the scattered more widely over the hard and
construction of temporary prosthesis may soft palates. Today these two terms are used
interchangeably for both palatal and gingival
cysts of newborns.
25. What is eruption hematoma?

It develops as a result of separation of dental
follicle around the crown of erupting tooth,
i.e. within the soft tissues overlying the
alveolar bone. It is seen in crown of deciduous
and permanent teeth (eruption cyst). The
presentation is soft, transclucent swelling
overlying gingival mucosa. Commonly seen in

children younger than 10 years of age, with
deciduous mandibular central incisors most
commonly affected, then first permanent
molars and then deciduous maxillary incisors.
The surface trauma may result in considerable
amount of blood which imparts a blue to
purple brown color. These lesions are called
eruption hematoma.
26. What are buccal bifurcation cyst and
paradental cysts?
Buccal bifurcation cyst is an uncommon, inflam-
matory, odontogenic cyst that characteristi-
cally develops on buccal aspect of mandibular
first permanent molar (commonly) and second
permanent molars. Common in pediatric
population, may be seen bilaterally. The
affected tooth is vital. It has been associated
with teeth that demonstrate buccal enamel
extensions into bifurcation area.
Paradental cyst attached with mandibular third

molar while radiograph showing radiolucency at
bifurcation area by straight arrow and preservation
of follicular space curved arrow
27. What are two-thirds tumor?

The adenomatoid odontogenic cyst (AOC) has
been sometimes referred as “two-thirds tumor”
because about two-thirds occur in the maxilla,
two-thirds occur in young women (pre-teen
and teenage years), two-thirds are associated
with an unerupted tooth, and two-thirds of
those teeth are canine teeth. The two-thirds
The term paradental cyst sometimes has
statistics vary slightly, but the rough distri-
been used synonymously for buccal bifurca-
bution is accurate.
tion cyst. These lesions occur distal or buccal
to the partially erupted mandibular third It is a cystic hamartoma arising from odonto-
molars with pericoronitis. It should be distin- genic epithelium. It will characteristically have
guished from inflamed dentigerous cyst. a lumen lined by epithelium from which
proliferations fill much and sometimes all of
the lumen space, then mimicking a solid tumor.
This cyst will present as an expansile lesion
usually in the anterior region of either jaw. The
cyst’s clinical emergency may be subtle and
discovered only as an incidental clinical or
radiographic finding, or it may be discovered
by rapid clinical expansion causing alarm and
pain. Some will reach in very large sizes (10 cm)
and distort facial contours.
28. What are the radiographic appearances
of calcifying odontogenic cysts?
These are discovered as an incidental radio-
graphic finding. Early in their development,
they will appear completely radiolucent.
As they mature, they develop calcifications
that produce a well-circumscribed, mixed Maxillary cross-sectional occlusal radio-

radiolucent-radiopaque appearance. graph with contrast reveals well-defined
ovoid radiopacity 2 cm in greatest diameter
Three General Patterns of Radiopacity are superimposed on the crowns of 1514 and roots
Seen. of 13–11.
• One is a salt-and-pepper pattern of flecks,
32. What is cervical ranula?
• The second is a fluffy cloud-like pattern
throughout, and the third is a crescent- A plunging ranula, also known as a cervical or
shaped pattern on one side of the radio- diving ranula, is a rare clinical entity. The name
lucency in a “new moon” like configuration. ranula derives from its similar appearance to
• The third is a crescentic-shaped pattern. the air sacs in a frog’s neck where the Latin
name rana means frog. A ranula is an
29. In which conditions residual cyst occur? extravasated mucocele derived from the
Residual cyst may occur after endodontic sublingual gland which lacks a proper capsule.
therapy which has failed either to eliminate Rupture of the main ducts or acini of the
inflammatory focus or had undiagnosed sublingual gland occurs due to obstruction
accessory canal. Less frequently it may occur which can lead to the formation of a ranula. The
with successful seal where residual infection extravasated mucus triggers a localized
in periapical area is remaining. inflammatory response and becomes envelo-
ped in fibrous granulation tissue. In general,
30. Enumerate the cysts occurring in the
ranulas continue to enlarge because the
midline region of the oral cavity.
sublingual gland is a constitutive secretor of
Glandular odontogenic cyst, globullomaxillary mucus. Ranulas can be limited to the intraoral
cyst, nasolabial cyst, median mandibular cyst, region or they can expand and herniate
nasopalatine cyst. through or around the mylohyoid muscle
31. What is cystography? which serves as an anatomical barrier between
the sublingual and submandibular regions.
Cystography is a procedure of injecting a
When a ranula extends through or around the
radiopaque dye into the cystic cavity to
mylohyoid muscle, it is termed a plunging
visualize the boundaries of lesion. The injection
ranula and often presents with swelling in the
of radiopaque contrast medium (‘conray 420’).
submandibular or cervical areas.
Histologically Three Variants

Conventional or vascular type (95%):
Osteolytic lesion with blood-filled cavities and
sinusoidal spaces, separated by fibrous
connective tissue septa with osteoid trabeculae.
Variable amount of hemosiderin and giant cells
can be found.
Solid type (5%): This form is non-cystic variant
with osteoclast-like giant cells. Osteoblastic
differentiation areas with osteoid and
calcifying fibromyxoid tissue complete the
picture.
Mixed type: A third form or mixed variant
demonstrates features of both the vascular and
solid types. It may be a transitory phase of the
lesion because sudden activation or rapid
enlargement of stable lesions has been
33. What are pseudocysts? Enumerate the reported.
pseudocysts occurring in oral and
35. What are different cystic lesions
paraoral structures.
associated with maxillary sinus?
Pseudocysts appear radiographically as cyst
like lesions but microscopically exhibit no a. Antral pseudocyst (benign mucosal cyst of
epithelial lining. maxillary sinus): Detected on routine radio-
logical examination (localised dull pain in
Aneurysmal bone cyst (more common in antral region radiographically spherical,
mandible): Traumatic (simple) bone cyst intra- ovoid, dome-shaped radiopacity with
bony cavity related to trauma. Static bone cyst smooth uniform outline). Most cases showed
(Stafne’s bone defect) developmental entity a possible source from an adjacent infection.
mainly due to entrapment of salivary gland
b. Sinus mucoceles: These are due to accumu-
tissue.
lations of mucin that are encased by
Focal osteoporotic bone marrow defect epithelium. It occurs after trauma (surgical
(hematopoietic bone marrow defect): An angle of ciliated cyst, traumatic ciliated cyst) and
mandible and tuberosity area, where hemo- surgery (postoperative maxillary cyst). It
poiesis is seen. may occur from an obstruction of the sinus
Maxillary sinus retention cyst: Lining of ostium blocking normal drainage.
maxillary sinus. c. Retention cysts: No evidence clinically and
Mucocele, ranula and plunging ranula. are located around the ostium or within
antral polyps and discovered during
34. What are the types of aneurysmal bone histological examination of antral polyp.
cyst (ABC)? These are called intrinsic cyst of maxillary
ABCs exist in two clinicopathological forms— sinus.
as a primary or as a secondary lesion arising
from another osseous condition. It includes Extrinsic Cysts
fibrous dysplasia, cementifying fibroma, Develop outside sinus but encroach upon it.
giant cell granuloma and certain unspecified • A thin sclerotic border usually delineates
lesions. the cyst from the rest of the sinus.
• May occupy the entire sinus and may be 38. What is ameloblastoma in situ and mural
difficult to diagnose. ameloblastoma?
• The differentiation is on that the normal Ameloblastoma in situ is an ameloblastoma
antrum has an undulating outline where- developing in the lining or into the lumen of a
as a cyst will be more rounded. dentigerous cyst, because dentigerous cyst
• Odontogenic-radicular, kerato, dentigerous epithelium retains some primordial odonto-
and neurogenic meningocele—neurogenic genic cells capable of ameloblastoma expres-
cystic condition, i.e. surgical ciliated cyst sion as discussed in the preceding section.
which follows surgical procedure and The ameloblastoma in situ may initially
sometimes after many years remains as an encompass a focal area of the cyst lining (mural
implantation cyst. ameloblastoma).
Intrinsic Cysts 39. What is peripheral ameloblastoma?
These are not true cysts as they are not This ameloblastoma is not a true neoplasm and
epithelial lined. lacks the biologic potential of the central amelo-
a. Mucous retention cyst: Due to obstruction of blastoma. It is a hamartomatous proliferation
duct of minor seromucinous gland of odontogenic epithelium arising from rests
b. Serous retention cyst: Inflammatory in origin. of Serres or perhaps from the basal cells of the
Consists of loculated fluid in the mucoperi- oral mucosa. Usually not attaining a size larger
osteum and thus has no epithelial lining than 3 cm, it will present as a firm single or
c. Mucocele due to gradually expanding polyploid mass arising exophytically from the
collection of fluid within the sinus initiated gingiva. It does not invade bone, and, as a true
by the obstruction of the ostium. Rare in peripheral ameloblastoma, it is not associated
maxillary sinus. Mucous retention cyst and with a radiolucent area. Some central amelobla-
serous retention cyst generally also referred stomas have been misdiagnosed as peripheral
to as mucocele. types when they eroded through the alveolar
bone and presented with a soft tissue mass.
36. Classify diseases of maxillary sinus.
Peripheral ameloblastomas are managed by
1. Developmental diseases: Agenesis, aplasia, local soft tissue excision with 2 to 3 mm
hypoplasia, supernumerary maxillary sinus margins. Recurrence is not seen.
2. Inflammatory diseases: Mucositis, maxi-
40. What is desmoplastic ameloblastoma?
llary sinusitis, empyema, antral polyps
3. Cysts of maxillary sinus: Odontogenic, The desmoplastic ameloblastoma is a rare but
non-odontogenic, intrinsic and extrinsic histopathologically and radiographically
unique ameloblastoma. It is otherwise identical
4. Traumatic diseases: Oroantral fistula,
to the more common central ameloblastoma
root/foreign body in antrum, pneumocele
and is treated in the same fashion. Its unique
5. Tumors involving maxillary sinus: Benign
radiographic appearance is that of a mixed
and malignant
radiolucent-radiopaque lesion unlike the
6. Other diseases: Fibro-osseous diseases, strictly radiolucent quality of other amelobla-
granulomatous diseases, antroliths. stomas. Therefore, it is usually a surprise diag-
37. What is unicystic ameloblastoma? nosis from a differential list composed mostly
The term unicystic ameloblastoma is an of fibro-osseous diseases and odontogenic
important example of this problem. It has been cysts and tumors that are characteristically
used to describe an ameloblastoma developing radiolucent-radiopaque. These include ossifying
within the lining, lumen, or wall of a cyst as fibromas, fibrous dysplasia, osteoblastomas,
well as an invasive ameloblastoma that has a osteosarcomas, calcifying epithelial odonto-
single cystic space rather than multicystic spaces. genic tumors, and calcifying odontogenic cysts.
41. What is extreme ameloblastoma? 43. What is malignant ameloblastoma?

Occasionally, the oral and maxillofacial Malignant ameloblastoma is defined as an
surgeon may be confronted with an extreme ameloblastoma with typical benign histologic
ameloblastoma of excessive size. These features that is deemed malignant because of
patients are usually from third world rural its biologic behaviour, namely metastasis. The
areas and brought to medical centres for histologic features may not correlate with the
treatment. Although these ameloblastomas are clinical behaviour. The clinical behaviour and
benign, they are nonetheless life threatening. not the histology that justifies a diagnosis of
Many have eventuated in death due to airway malignant ameloblastoma (metastasizing
obstruction, starvation from restriction ameloblastoma). Metastatic ameloblastoma
of feeding, and complications of hypo- are mostly seen in lungs.
proteinemia produced partially by the
44. What is ameloblastic carcinoma?
restriction of feeding and partially by protein
loss into the cystic spaces of the tumor, which Ameloblastic carcinoma is a rare amelo-
then leaks it out through the mouth. blastoma and primary odontogenic mali-
gnancy exhibiting the histologic criteria of a
42. What is odontoameloblastoma? malignant neoplasm, such as increased and
The odontoameloblastoma is an extremely rare abnormal mitosis and hyperchromatic, large,
odontogenic neoplasm of which only a handful pleomorphic nuclei. It is a lesion which histo-
have ever been reported. It essentially re- logically shows the features of both ameloblas-
presents an invasive ameloblastoma occurring toma and squamous cell carcinoma. This may
simultaneously with an odontoma in what arise de novo or in pre-existing benign odonto-
may be thought of as a “collision tumor”. genic tumor or cyst.
Neither seems to arise from the other. The
45. What is carcinoma ex-ameloblastoma?
unfortunate term ameloblastic odontoma is
often used to describe this lesion as well, but It is a carcinoma arising from an ameloblas-
its name believes the invasiveness characterized toma. It is also called carcinoma in ameloblas-
by an ameloblastoma. It instead suggests the toma and ameloblastic carcinoma secondary
biologic behaviour of an odontoma, which is type. This entity arises when an ameloblastoma
entirely misleading; therefore, it should not be undergoes dedifferentiation, that is, when a
used. less differentiated proliferative clone arises
within an ameloblastoma. This aggressive
The odontoameloblastoma, like most
clone overgrows the ameloblastoma and
ameloblastomas, presents as a painless jaw
becomes the dominant component.
expansion. The radiograph usually shows a
multilocular, mixed radiolucent-radiopaque 46. What is de novo ameloblastic carcinoma?
lesion, although it can also be unilocular. The If the carcinoma lacks component of conventio-
odontoma component will most likely be of a nal ameloblastoma its direct categorization as
complex type because most occur in the molar an ameloblastic carcinoma is less warranted.
ramus region, but its mineral density will be These lesions diagnosed on subjective inter-
greater than that of bone. It will approach the pretation are called de novo ameloblastic
mineral density of dentin. This tumor is rare carcinoma.
because of the remote likelihood of two coinci-
ding odontogenic developmental disturbances: 47. What is atypical ameloblastoma?
One an aberrant attempt at tooth formation, Atypical ameloblastoma is used to denote
the other a neoplastic genetic alteration of odonto- lesions with fatal outcome for various reasons
genic epithelium. There is no evidence that these either metastasis, histological atypia or relent-
two components are part of the same process. less local spread. It shows basilar hyperplasia
and increased mitotic index. Some authors 51. What are the various characteristics of
called it proliferative ameloblastoma. keratocystic odontogenic tumor? Why
the anteroposterior expansion is seen?
48. What is the differentiating point of AOT
from dentigerous cyst in pericoronal It may be asymptomatic, may be small,
location? unilocular/large multilocular an odontogenic
keratocyst may present in a variety of sizes and
The AOT also shows complete radiolucency in
situations. Some are small and unilocular,
pericoronal location in early stages and is
others large and unilocular. The larger cysts
difficult to distinguish from dentigerous cyst
will cause expansion and may cause tooth
while evidence of more or less calcifications is
mobility. Some will rupture and leak keratin
suggestive of AOT.
into the surrounding tissue, provoking an
49. What are the reasons for calling odon- intense inflammatory response that causes
togenic keratocyst into keratocystic pain and swelling. The cysts will not affect
odontogenic tumor? nerve sensation, although they will frequently
Keratocystic odontogenic tumor (KOT) is displace the inferior alveolar neurovascular
defined as “a benign uni or multicystic, bundle to the inferior border.
intraosseous tumor of odontogenic origin, Their resorption of bone will include cortex
with a characteristic lining of parakeratinized and inferior border, but at a slower rate than
stratified squamous epithelium and potential the intermedullary trabecular bone, which is
for aggressive, infiltrative behaviour. less dense. Therefore, they extend further
1. Clinically shows aggressive growth. anteroposteriorly than buccolingually.
2. A tendency to recur after surgical excision. This principle of further extension through
3. The mitotic activity is increased in cystic bone that is less dense also explains the finding
epithelium and tumor like characteristics of of greater buccal expansion than palatal
lining epithelium. expansion in the maxilla. The cysts also
4. Potential for budding in the basal layer, frequently resorb the roots of adjacent teeth in
unlike cysts which generally grow by a smooth and regular pattern.
osmotic pressure the epithelium has got 52. Which tumor is associated with pain?
innate potential consistent with benign Osteoid osteoma (it is bone-forming tumor
tumor. characterized by small size, limited growth
5. Presence of daughter cysts in cystic wall. potential and disproportionate pain) and
6. Association of nevoid basal cell carcinoma osteoblastoma. The osteoblastoma is larger
syndrome. than 2 cm while the osteoid osteoma is smaller
7. Chromosomal abnormalities and genetic than 2 cm. The pain in osteoid osteoma
alterations such as mutation of PTCH responds to aspirin and other NSAIDs while
gene. in osteoblastoma does not.
Although the gross and radiological 53. Enumerate the bony lesions can cross
appearance is like cystic in nature. midline.
50. Enumerate the syndromes associated Keratocystic odontogenic tumor, central giant
with keratocystic odontogenic tumor. cell granuloma, large ameloblastomas,
Basal cell nevus syndrome (nevoid basal cell calcifying odontogenic cyst, osteitis deformans
carcinoma syndrome or Gorlin-Goltz syn- cause midline. Osteosarcoma, glandular
drome)—multiple nevoid basal cell carcinomas odontogenic cyst (sialo-odontogenic cyst),
on skin, skeletal abnormalities, CNS abnor- odontogenic myxomas cross midline especi-
malities, eye lesions and multiple KOTs. ally in mandible, lymphomas, gigantiform
cementoma starting as multilobular masses, made by moving to adjacent areas to obtain the
primary intraosseous carcinoma. aspirates. Aspiration of every swelling in oral
Fibrous dysplasia does not cross midline. cavity should be done. Aspiration should be
done with 16 to 20 gauge needle. Some viscous
54. What are the intraoral sites of neuro-
fluids may not be aspirated.
fibromatosis?
The tongue, alveolar mucosa and gingival. Aspiration of pus indicates inflammatory
lesions.
55. What is axillary freckle sign?
Radiolucent lesions in bone may represent
One of the most characteristic locations for an idiopathic bone cavities, infections, cysts, and
NF-1-related café-au-lait macule is the axilla, cystic or solid tumors. Aspiration of most
which is specifically examined in suspicious radiolucent lesions is done before biopsy to
cases (called the “axillary freckle sign” or assess for potential bleeding that may occur
“crowe sign”). Café-au-lait macules almost during the biopsy. Aspiration should be
always develop years before neurofibromas. accomplished with a 20-gauge or larger needle.
They can be distinguished from a freckle The lesion should also be aspirated in three
(ephelis) by their larger size and their occur- areas by directing the needle tip to three loca-
rence on areas not exposed to the sun. These tions within the lesion from a single entrance
develop in 90% of NF-1 related patients, point. This maneuver is recommended because
especially in middle of childhood. many lesions are compartmentalized into solid
56. In which condition bag of worm feeling and fluid spaces. A 10 ml syringe containing
is seen? 1 ml of saline is used. The clinician should
A neurofibroma may present as an asympto- observe the first component of the aspirate. If
matic mass within the subcutaneous or sub- bubbles of air or a serosanguineous fluid
mucosal tissues. The mass will be diffused. The precede blood, an idiopathic bone cavity is
edges will gradually blend into normal tissue likely. Aspirated blood does not confirm an
and there will be no clear distinction. The mass arteriovenous hemangioma. Lesions of lower
will infiltrate into and incorporate normal vascular pressure such as cavernous heman-
tissues such as muscle, glands, and lymph giomas, central giant cell tumors (including
nodes. Its palpable quality will be that of a what was formerly called “aneurysmal bone
lobulated surface is called bag of worms cysts”), and idiopathic bone cavities will return
feeling. blood upon aspiration. If blood is returned, it
is useful to disconnect the syringe barrel from
57. What are fine needle aspiration biopsy the needle. Low-pressure vascular lesions,
(FNAB) and fine needle aspiration cyto- which will not represent a significant clinical
logy (FNAC)? Name the different bleeding concern, will yield blood flow from
aspirates. the needle hub but stop within 1 minute. High-
FNAC are diagnostic procedures used to pressure vascular malformations will result in
investigate superficial lumps or masses. In spurting blood from the needle hub.
these techniques a thin hollow needle is
• Space abscess: Usually aspiration produces
inserted into the mass for sampling of the cells
yellowish pus.
that after being stained are examined under
microscope. There could be cytological • Subcutaneous emphysemas and laryngo-
examination of aspirate ( FNAC) or histological celes are masses that are filled with air and
examination (FNAB). Aspiration is withdrawal can be completely deflated by aspiration.
of fluid from body cavities. Aspirate is the • Cysts: When aspirated from cyst, cystic
material withdrawn. If nothing is been content must be withdrawn and then again
aspirated then several attempts should be aspirated to withdraw content from the
capsule of the straw-coloured fluid or blood- • Dentigerous cyst: Aspiration often yields
tinted fluid may indicate cyst. Odontogenic a straw-colored, thin liquid. Cholesterol
cysts both developmental and inflam- crystals may be seen in the aspirate when
matory share an identical cytomorphology. the syringe is slowly rotated in front of a
Aspirates contain abundant anucleated strong light.
squamous cells similar in appearance to • Nasopalatine duct cyst: It will usually
superficial and intermediate cells of strati- return straw-colored fluid, confirming its
fied squamous epithelium, and occasionally cystic nature.
keratocystic odontogenic tumor will show • Keratocystic odontogenic tumor: It may
evidence of mineralization within squamous reveal a thick, yellow, cheesy material
cells. (keratin).
• Non-infected cyst: Shows a thin, straw- • The papillary cystic adenoma and papil-
colored fluid. lary cystadenoma lymphomatosum: Are
• Noninfected radicular cyst: Produces often fluctuant and contain thin, straw-
alight, straw-colored fluid, usually con- colored liquid that can be aspirated.
taining an abundance of shiny granules • Lipoma: Aspirates of lipomas usually yield
(cholesterol crystals). an oily fluid that when smeared has an
• Mucocele, cysts of glands of blandin and glistening appearance.
nuhn, ranula and sometimes from the • An idiopathic bone cavity: Aspirates will
tumors of minor salivary glands: Show a often return blood. It does so not because it
clear, viscous, sticky fluid. Occasionally, a is a blood-filled lesion, but because a tight
low-grade mucoepidermoid tumor pro- needle fit through the cortex will cause an
duces enough mucus to clinically resemble excessive negative pressure in the marrow
a mucocele and yields mucus on aspiration. space, which disrupts capillaries and causes
• Benign retention cyst: An aspiration is a return of blood. To distinguish this pheno-
usually clear and has watery to viscous menon from the return of blood associated
consistency. with an arteriovenous malformation or a
cavernous hemangioma, 1 ml of saline
• Nodular oncocytic hyperplasia: More than
should be placed in the syringe before
one nodule in salivary gland. Aspiration
aspiration and the first part of the return
contains cohesive clusters of cells.
observed carefully. An idiopathic bone
• Acute inflammatory salivary gland lesion:
cavity will return a few air bubbles or a
Fibrin, cellular debris, neutrophills, lym-
small amount of straw-colored fluid into
phocytes and histocytes.
the syringe before blood appears. The
Ultrasound guided fine needle aspiration syringe should be disconnected from the
biopsy is useful in case of deep, mobile or needle after a syringe of blood is obtained,
non-palpable lesions. It is indicated for keeping the needle in place. If an idiopathic
distinct salivary gland masses and for bone cavity is present, the oozing of blood
evaluation of pathology of submandibular from the needle will cease, whereas more
space. prominent vascular lesions will show a
• Sialocele: Clear/non-transperant , stringy, continued brisk oozing or even a spurting.
sometimes blood tinged often brownish After aspiration, a cortical window is
fluid with a very low cellular content. removed and the bony walls are curetted.
• Traumatic bone cyst: Aspiration usually is • Warthin’s tumor: Will yield thin, watery
fruitless, but in some cases serosanguineous mucoid appearance and consists of a mixed
fluid, a small quantity of blood or a serum- population of lymphocytes, occasionally
like fluid may be obtained. plasma cells and oncocytes.
• Ex-pleomorphic adenoma: Usually cellular the bone is to be perforated rather than to

and contain dual population of malignant introduce the needle directly over the
cells/residual benign PA cells. The hemangioma. The bleeding that results
aspirates are usually dominated by from the former method usually is more
malignant cells because of low cohesiveness easily arrested. Since the mucosa over the
of malignant cells. point where the bone was penetrated is still
• Lymphangioma: Aspiration yields lymph intact and the channel through the mucosa
fluid that is high in lipid content. can be more effectively compressed.
• Hemangioma: Aspiration shows bluish • A-V shunt: If on insertion of the needle, the
blood with a fine-gauge needle, scant of plugger is almost forced out of the syringe
cellularity. The aspirates are characterized by the flow of blood, an arteriovenous shunt
by a highly bloody background in which is suspected, e.g. blood under pressure is
are dispersed single, plump, spindle- A-V shunt. The hemostasis is difficult to
shaped cells and clusters of spindle-shaped attain.
to ovoid cells. Most of the aspirates are scant • Thalassemia: Patients aspiration biopsy of
of cellularity. The aspirated tissue frag- the bone marrow reveals a specimen with
ments often show a three-dimensional very active, immature hematopoietic tissue.
arcade architecture with preserved lumen. FNAC is highly accurate procedure for
• Cavernous hemangioma: Aspiration of an differentiating benign and malignant
intrabony hemangioma readily yields a lesions. Diagnosis of aspirates from cystic
copious amount of blood and caution is lesions may be less specific than the solid
necessary. A recommended approach is to lesions due to paucity of specific lesional
introduce the needle through the mucosa cells in the former and also due to
some distance from the point where superimposed infection.
4
Infections and Autoimmune
Disorders of Oral Cavity
1. What are epidemic, pandemic and en- region to infect large numbers of people
demic diseases? Give an example of each. worldwide. The black death was one of the
The element dem in epidemic, endemic, and worst pandemics in human history, killing at
pandemic comes from the ancient Greek word least 75 million people on three continents,
demos, which meant people or district. the Franco-Prussian war triggered a small-
An epidemic (epi (among) + demos = epi- pox pandemic of 1870–1875 that claimed
demic) is a widespread occurrence of an 500,000 lives. The 1918 spanish influenza
infectious disease in a community at a parti- pandemic is estimated as being responsible for
cular time. Annual influenza epidemics follow the deaths of approximately 50 million people
a winter seasonal pattern in the United States or more. Dental caries and periodontal diseases
with typical activity peaking during late are pandemic. AIDS is also becoming endemic
December to early February. An intense flu to pandemic.
epidemic spreading across the nation has 2. What is focus of infection?
already taken a tragic toll in Michigan. It is referred to as circumscribed area of tissue,
Endemic (en (in) + demos = endemic) is an which is infected with exogenous pathogenic
adjective that refers to a disease or condition micro-organisms and usually located near the
regularly found among particular people or in mucous membrane or cutaneous surface.
a certain area. In many malaria-endemic
countries, malaria transmission does not 3. What is focal infection?
occur in all parts of the country. Polio remains It is a localized or generalized infection caused
endemic in three countries—Afghanistan, by dissemination of microorganisms or toxic
Nigeria, and Pakistan. Endemic dental products from focus of infection.
fluorosis in the North State of Minas Gerais,
Brazil, pertussis is endemic worldwide, even 4. What are oral foci of infection? What is
in areas with high vaccination rates. its significance?
A disease becomes pandemic (pan (all) + Following varieties may present as oral foci of
demos = pandemic) when it spreads beyond a infection:
101
1. Infected periapical lesions such as cysts, delayed hypersensitivity reaction. Often

granuloma and abscess this is the consequence of infection by
2. Teeth with infected root canals certain microorganisms, such as Myco-
3. Periodontal diseases with special references bacterium tuberculosis.
to teeth extractions and manipulations. 3. Immune granuloma.
Bacteremia has been found to be closely
6. What are the reasons of granulomatous
related to severity or degree of periodontal
inflammatory conditions involving oral
disease present after manipulation of gingival
and paraoral tissues?
or more commonly tooth extraction. Bacteremia
can be produced by simple gingival massage. Foreign body reaction is the most common
Transient bacteremia in patients who have source. These may be endogenous/exogenous.
undergone tooth extraction with periodontal The other infections such as tuberculosis,
disease. The holding of tooth in socket with leprosy, cat-scratch disease, tertiary syphilis,
forcep before extraction produces bacteremia. histoplasmosis, cryptococcosis, blastomycosis,
paracoccidioidomycosis, sarcoidosis, Crohn’s
Pumping action occurring during dental
disease, orofacial granulomatosis.
extraction may force microorganisms from
gingival crevice into capillaries. Extraction of 7. What is Miescher’s granulomatosis?
teeth and even minor trauma may produce It is the presentation of orofacial granulo-
bacteremia. matosis. The clinical presentation is often
These oral foci may either cause or aggravate variable. The orofacial granulomatosis when
many systemic diseases. These are: involving lips alone is called Miescher’s
1. Arthritis—mainly rheumatoid type and granulomatosis.
rheumatic fever.
8. What are the causes of sinuses around
2. Valvular heart disease particularly SBE
lower jaw?
3. GIT diseases
4. Ocular diseases Osteomyelitis, tuberculosis, and actinomycosis.
5. Skin diseases 9. What is woody tongue and bull neck?
6. Renal diseases. It is seen in Ludwig’s angina when there is a
5. What is granuloma? What are types of massive swelling of neck that often extends
granuloma? close to clavicles. Involvement of sublingual
Granulomas are aggregates of macrophages space results in elevation, posterior enlarge-
that accumulate for the purpose of phagocytosis. ment and protrusion of tongue which can com-
It is a distinct compact microscopic structure promise airway, this is called woody tongue.
composed of epitheloid-shaped macrophages Submandibular space spread causes enlarge-
typically surrounded by rim of lymphocytes. ment and tenderness of the neck above the level
Sometimes it may show central area of caseous of the hyoid bone that is called bull neck.
necrosis. 10. What are lepromas and what are oral
There are three types of granulomas: manifestations of leprosy?
1. Foreign body granulomas: Foreign body It is oral manifestation of leprosy. Lepromas
granulomas, which consist of immature are discrete focus of granulomatous inflam-
macrophages that accumulate because of mation and nodular lesion caused by leprosy
the presence of concentrated inert material on skin and mucous membranes. They
such as silica or talc. usually appear in lepromatous leprosy and
2. Epithelioid granulomas: It consists of activa- occur in 20–60% of cases. They may take the
ted or mature macrophages and typically form of multiple nodules (lepromas) that pro-
develop through the action of T-cells in a gress to necrosis and ulceration. The ulcers are
Infections and Autoimmune Disorders of Oral Cavity 103
slow to heal, and produce atrophic scarring or A pectin, gelatin, sodium carboxymethyl-
even tissue destruction. The usual location is cellulose, and plasticized hydrocarbon gel base
on the hard and soft palate, in the uvula, on the (orabase) may be used as a vehicle to test for
underside of the tongue, and on the lips and contact allergy within the oral cavity. The
gums. There may also be destruction of the suspected chemical is incorporated in the
anterior maxilla and loss of teeth. The diagnosis, vehicle and applied to the oral mucosa.
based on clinical suspicion and the lepromin test. Fenretinide mucoadhesive patches were
In tuberculoid leprosy involvement of all attached (q.d. 30 min for 10 consecutive days)
nerves supplying the oral and related to the right buccal mucosa (blank patches on
structures occurs, sensory and motor involve- left buccal mucosa) immediately posterior to
ment of trigeminal and facial nerves also the intraoral commissure of the upper and
occurs. In lepromatous leprosy facial and oral lower lips.
involvement with ulceration, scarring and Intraorally patch testing can be done by
typical lepromas occur resulting in numerous keeping the antigen in the maxillary denture
esthetic and functional deformities. Nerve base and holding it in the mouth.
involvement may become manifest if the 12. In which diseases amyloidosis is likely
disease progresses. There may be transition to occur?
and overlap of signs and symptoms between
It is likely to occur in chronic disease like
these two types.
rheumatoid arthritis, chronic osteomyelitis,
11. What is patch test? How is it done chronic renal failure and 10% myeloma
intraorally? patients.
Patch-testing is a diagnostic procedure that is 13. What is strawberry tongue and raspberry
most commonly used for identifying the tongue?
possible causes of contact dermatitis (type IV These manifestations are seen in scarlet fever.
hypersensitivity reaction). This can be done The tongue develops a white coat within which
type I hypersensitivity reactions and in DRESS reddened and swollen fungiform papillae
(drug reaction with eosinophilia and systemic stand out (“strawberry tongue”). As the
symptoms) syndrome (type IVb hypersensiti- disease progresses, the skin erythema fades
vity reaction). and the white coating on the tongue is lost,
The procedure involves mixing the allergen leaving a swollen, irregular, beefy tongue
to be tested with white petrolatum (i.e. the (“raspberry tongue”).
vehicle), and applied in close proximity with the
14. What is valley fever?
skin. The first reading is taken after 30 minutes
to look for type 1 hypersensitivity reaction, Coccidioidomycosis is endemic in United
while a second reading is taken after 48 hours States that is known as valley fever.
to investigate for type 4 delayed hypersensiti- 15. Name the lesion associated with HPV.
vity reaction. Between the 2 readings, the Oral papilloma (types 6 and 11) verruca
patient should be instructed not to wet, rub or vulgaris (types 2 and 57) and condyloma
scratch the testing area, avoid exercise and acuminatum (CA) (6 and 11) are benign, rough-
sweating. The readings are evaluated using the surfaced exophytic hyperplasias of epithelial
International Contact Dermatitis Research tissue (focal epithelial hyperplasia), dysplastic
Group (ICDRG) grading system: ‘–‘ stands for wart, verrucous carcinoma.
negative, ‘+’ stands for a weak (non-vesicular)
positive reaction, ‘++’ stands for a strong 16. What is Heck’s disease?
(vesicular) positive reaction and ‘+++’ stands It is also called focal epithelial hyperplasia.
for extreme (bullous) positive reaction. These are most common in children with
normal mucosal color, caused by HPV. They Eczema herpeticum (Kaposi’s varicelliform
are characterized by multiple slightly raised eruption): Diffuse chronic skin disease and
papules that can become papillary. pemphigus may have life-threatening HSV
infection.
18. Enumerate the diseases caused by
coxsackie virus.
Hand-foot-mouth disease, herpangina, lym-
phonodular pharyngitis. Acute febrile respira-
tory disease, Bornholm disease (epidemic
pleurodynia) coxsackie B (B is for body) virus
can cause life-threatening pericarditis and
myocarditis in infants.
19. Enumerate the diseases caused by
varicella-zoster virus.
Primary disease (varicella, chickenpox),
secondary disease (herpes zoster, shingles),
post-herpetic neuralgia (morbid sequelae
of HZI).
20. Enumerate the lesions associated with
Epstein-Barr virus.
Infectious mononucleosis, Burkitt’s lymphoma,
oral hairy leukoplakia, Kaposi’s sarcoma,
rarely viral sialadenitis.
21. Enumerate the sites of latency of various
viruses.
Coxsackie virus in connective tissue probably
in the endothelium of connective tissue, white
blood cells and monocytes.
Herpes virus after the primary infection
travels along the sensory nerve axons and
remains latent in the sensory ganglions such
17. What are various lesions caused by
as (trigeminal ganglion). Extraneuronal latency
herpes simplex virus (HSV)?
is epithelium and plays role in lip lesions.
Primary herpes labialis, acute herpetic gingivo-
Varicella-zoster virus remains latent in
stomatitis, recurrent herpes labialis, recurrent
dorsal root ganglia or ganglia of cranial nerves.
intraoral herpes simplex infection, herpetic
genitalis, meningoencephalitis, conjunctivitis, Cytomegalovirus establishes latency in cer-
disseminated herpes simplex infection of new- tain undifferentiated cells like bone marrow
born, herpetic whitlow (herpetic paronychia). derived cells of monocytes (CD 14+), CD34+,
CD33+ progenitors are predominant sites of
Herpes gladiatorum (scrumpox): Infection
latency.
in the wrestlers and other atheletes who have
close physical contact with others. 22. What is greenspan lesion?
Herpes barbae: Bearded region of face HSV Sir Waal Van Der (1996) suggested this term.
infection into minor injuries created by daily Greenspan lesion, as an alternative term, is
shaving. suggested for hairy leukoplakia. The term
‘hairy leukoplakia’ is a misnomer due to 24. What is Forchheimer’s sign?

several reasons. First of all, hairy leukoplakia Forchheimer‘s sign refers to an enanthem of
is a definable lesion. Furthermore, the lesion red macules or petechiae confined to the soft
is not premalignant in nature. Therefore, the palate in patients with rubella. It may extend
use of the term should be abandoned. As an on hard palate. Generally arises with the rash,
alternative, the term ‘greenspan lesion’ has becoming evident in about 6 hrs after the
been suggested. first symptom and does not last longer than
12–14 hours. However, in 20% of the patients
it appears during prodormal period or on the
first day of the exanthema. Similar situation
seen in infectious mononucleosis and has been
termed Forchheimer’s spots.
25. What is AIDS-related complex (ARC)?

This is a syndrome caused by the AIDS virus
and characterized primarily by chronically
swollen lymph nodes and persistent fever—
sometimes a precursor of AIDS. Fatigue, night
sweats, diarrhea are other symptoms.
26. What is malar rash? Enumerate the
conditions causing malar rash.
23. What are zosteriform lesions? Malar rash (butterfly rash) is a mask-shaped
Lesions distributed along a dermatome or erythematous eruption involving the malar
lesions take linear arrangement along nerve areas and the bridge of the nose. It is characteri-
route. These are also called dermatomal zed by a symmetrical, fixed, erythematous,
patterns. Common examples are herpes zoster maculopapular lesions with slight scales.
and sometimes lichen planus and psoriasis, It is transient (days to months). It is typical for
other examples are zosteriform lentiginous systemic lupus erythematosus (SLE) (96%),
nevus, zosteriform metastasis. other cases moderately sensitive (57%) may
(Zosteriform metastatic skin-coloured solid show findings.
papules, nodules, and papulovesicles scattered Other causes are:
and confluent with a few crusted plaques a. Other autoimmune diseases SLE, discoid
seen on the left side of the neck in a typical lupus erythematosus (DLE) and dermato-
zosteriform distribution involving the left myositis
C3 dermatome.) b. Infectious diseases (Lyme disease, erysipelas)
Pellagra is determined by laboratory levels

of vitamins (especially vitamin B3)
Bloom syndrome (an autosomal recessive
mutation in BLM gene) rash occurs in child-
hood and adolescence. It has to be confirmed
by genetic studies.
Other cutaneous diseases include rosacea,
drug-induced photosensitivities, sunburn, and
pemphigus erythematosus. The dermatitides
including atopic, allergic, contact and sebor-
rheic, parvovirus, photoallergic reaction and
polymorphous light eruption.
27. What is Gottron’s sign?
It is a characteristic finding in dermatomyositis
typified by scaly erythematous eruption seen
on the dorsa of hands, metacarpophalangeal
joints and proximal and interphalangeal joints.
28. What are the different lesions of systemic
lupus erythematosus (SLE)?
The presenting symptoms of SLE are moreover
nonspecific constitutional signs such as fever,
fatigue and weight loss. Lupus is known as
great mimic. Then involvement of variety of
organs like:
• Mucocutaneous disease (Malar rash, dis-
coid lesions, photosensitivity and oral
ulcerations): Skin affected in 85% and cut-
aneous lupus can occur without multisys-
tem involvement. Raynaud’s phenomenon.
• Renal disease: It ranges from asymptom-
c. Vitamin diseases (pellagra) atic proteinuria to rapidly progressive
d. Some chromosomal disorders (Bloom glomerulonephritis (lupus nephritis indi-
syndrome) cator of poor overall outcome).
e. Parvovirus. • Musculoskeletal: Arthralgia, nonerosive
It is seen in SLE, DLE and dermatomyositis. symmetric arthritis, myalgia and myositis.
The malar rash of SLE does not involve • Neuropsychiatric manifestations: It is due
nasolabial fold. It involves nasolabial fold in to cerebral vasculitis (memory impairment,
dermatomyositis, as it is caused by inflam- delirium or coma, seizures, psychosis).
mation of muscles and skin. • Cardiovascular disease: Vasculitis and
Infectious causes include Lyme disease and pericarditis classically. Atherosclerosis is
erysipelas caused by streptococci. Lyme also noted (valvular heart disease).
disease is diagnosed by patient’s history, • Hematological manifestations (anemia,
biopsy, ELISA and confirmed by western blot. leukopenia, etc): The disease course is
Erysipelas diagnosed by pain, special stains characterized by disease flares which may
and aerobic cultures. require immunosuppression.
29. Describe oral manifestations of systemic localized skin plaques, 5 to 20 mm in diameter,

lupus erythematosus. on the face. These plaques will have a
The predominant oral lesions are ulcerations, predilection for the hairline and sun exposed
erythematous lesions, and discoid lesions. areas. A butterfly malar rash develops in DLE,
The ulcerations are characteristically just as it does in SLE. The skin lesions as they
painless, occur frequently on palate and mature, they develop a broad atrophic white
oropharynx. area with a perimeter of red resembling the
pattern of a grass fire. These are called grass
Isolated erythematosus areas are also
fire lesions. The scar within this white area will
common especially on palate. Atrophy and
be devoid of hair follicles, leaving patchy bald
telangiectasias are also present.
areas in men’s beards or a patchy alopecia on
Discoid oral lesions are similar to those the scalp. In darker-skinned individuals, these
occurring on skin and appear as whitish striae lesions leave multiple depigmented regions.
frequently radiating from central erythematous
area giving the so-called brush border appea- 31. What is patriotic sign?
rance. Buccal mucosa, labial mucosa and It is seen in progressive systemic sclerosis (PSS)
gingival are common sites. and crest syndrome. Raynaud’s phenomenon
is a vasospastic response brought on by cold.
It is the initial clinical manifestation of all forms
of PSS in 50% of cases. It can be brought about
by immersing the individual’s hands in cold
water. Raynaud’s phenomenon occurs in three
stages: The first is pallor (white), which is due
to vasospasms that are painful and paresthetic;
the second is cyanosis (blue), which heralds
relaxation of the vasospasm and is caused by
pooling of venous blood; and the third is
hyperemia (red), in which the relaxation of the
vasospasm creates a reactive hyperemia that
actually represents a mild reperfusion injury.
Because the red, white, and blue are often seen
together, Raynaud’s phenomenon is known as
the “patriotic sign”.
32. What is Auspitz sign?
Sir Heinrich Auspitz described this termino-
logy. It is the appearance of punctate bleeding
spots when psoriasis scales are scraped off.
This happens because there is thinning of
the epidermal layer overlying the tips of the
dermal papillae and blood vessels within the
papillae are dilated and tortuous, which bleed
It is unclear if the presence of oral lesions is readily when the scale is removed. It is also
predictive of disease activity in SLE. called Auspitz’s symptom.
30. Which conditions show grass fire Demonstrated in three steps
lesions? • When the psoriatic plaque is scraped with
These are the skin lesions of discoid lupus glass slide the scales are accentuated and
erythematosus. The development of dusky red separate from plaque, as silvery flakes.
• A thin glazed membrane appears, which is Angioedema is known side effect of drugs
removable into further scraping. commonly used in day-to-day practice.
• Within a few seconds of mechanical re- Angioedema is generally self-limited most of
moval of the membrane, the pinpoint dro- the times but sometimes may result in
plets of blood appear on the erythematous respiratory tract obstruction, which can prove
surface. fatal . The angioedema associated with allergy
or drugs typically present without urticaria.
33. What is Koebner’s phenomenon?
In 1876 Sir Heinrich Koebner described this The pathophysiology of angioedema
entity. It is also called ‘isomorphic phenomenon’ consists of the increase in local vascular
in patients suffering from psoriasis, the permeability causing plasma extravasation
development of psoriatic lesions following and consequently swelling of subcutaneous
trauma of normal appearing skin is known as tissue. The major cells involved in the causation
‘Koebner’s reaction or phenomenon’. Also seen of angioedema are mast cells and in a lesser
in lichen planus and vitiligo. extent basophils, which on activation release
histamine from preformed granules—a
34. What is angioedema? principle mediator involved in angioedema.
It is a particular form of urticaria in which Oral lesions typically self-limiting and heal
massive, abrupt and short-lived swelling in 2–3 days.
occurs in the area especially, of low pressure,
i.e. mid face, around eyes, neck and mucous 35. What is acrosclerosis?
membranes. Herditary and acquired (trauma, Scleroderma limited to hands is called
infection and temperature changes, medicine acrosclerosis. It shows thinning of fingers with
induced, allergic, idiopathic). Raynaud’s phenomenon.
Angioedema of lower lip and skin/upper lip following drug administration

5
Potentially Malignant Disorders of
Oral Cavity and Oral Cancers
1. What is potentially malignant disorder? The potentially malignant disorder conveys:

Why this terminology has been implica- i. Not all the lesions and conditions described
ted? under this term turns into cancer.
WHO (2005) defined potentially malignant ii. There is a group of conditions showing
disorder as the risk of malignancy being morphological alterations among which,
present in a lesion or condition either at time some may have increased potential for
of initial diagnosis or at future date. Or, these malignant transformation.
can be defined as clinical presentations that iii. These disorders of oral mucosa are also
may have a potential to become a cancer indicators of risk of likely future malig-
conveying the process of multistep process of nancies elsewhere (normal appearing
cancer development, but unlikely on priori mucosa) in oral mucosa and not the only
grounds, that there is uniformity in the way site-specific predictators.
individual patients or tissue behave. These
disorders may arise from preceeding lesions or 2. Enumerate the potentially malignant
may arise from normal appearing mucosa. disorders affecting oral cavity.
Precancerous lesion and precancerous condi- Recognized potentially malignant disorders
tions were the terminologies used previously. are leukoplakia, erythroplakia, palatal lesions
Confusion prevailed between these two in reverse smokers, submucous fibrosis, acinic
terminologies and many opinioned that the cheilitis, keratosis and elastosis and lichen
prefix ‘pre’ quotes that all the precancerous planus; carcinoma in situ rare potentially
lesions will eventually become cancer, whereas malignant disorders include Fanconi’s anemia,
studies found this to be untrue. Hence, it was discoid lupus erythematosus, dyskeratosis
recommended in the WHO workshop of 2005 congenita and xeroderma pigmentosum,
to abandon the distinction between precan- epidermolysis bullosa, syphilis and sidero-
cerous lesions and conditions and to use penic dysphagia.
instead the term potentially malignant dis- Leukoplakia is most common potentially
orders incorporating both the terminologies. malignant disorders of oral mucosa.
109
3. Classify potentially malignant disorders For erythroplakia the malignant transfor-

of oral cavity. mation potential is very high at 14% to 50%.
1. High risk: Erythroplakia, leukoplakia, oral The prevalence is at 0.02–0.83%.
submucous fibrosis, erosive lichen planus. Actinic cheilitis malignant transformation
2. Lifestyle related: Smokeless tobacco potential ranges between 1.4% and 36%.
keratosis, reverse smoker’s palate, actinic Plalatal keratosis associated with reverse
cheilitis. smoking has a malignant transformation rate
3. Infection: Hyperplastic candidiasis, viral of 12.5%.
(HPV, HIV, EBV, HBV, HSV), tertiary 5. What are the various diagnostic aids in
syphilis. detection of potentially malignant
4. Immunodeficiency: Solid organ trans- disorders of oral cavity?
plantation, graft vs host disease, chronic 1. Clinical methods
cutaneous lupus erythematosus. a. Conventional oral examination (COE)
5. Inherited disorders: Xeroderma pigmento- b. Vital staining
sum, dyskeratosis congenita, epidermoly- 2. Optical methods
sis bullosa, Bloom syndrome, Fanconi’s a. Vizilite
anemia. b. Micro Lux DL
4. Enumerate the malignant transforma- c. VEL scope
tion potential of potentially malignant d. Fluorescence spectroscopy.
disorders. 3. Imaging methods
Oral submucous fibrosis—the malignant trans- a. Computed tomography (CT)
formation potential is 7% to 13%. Incidence b. Magnetic resonance imaging (MRI)
over 10-year period at approximately 8%. c. Positron emission tomography (PET)
Epithelial dysplasia in oral submucous fibrosis d. Thalium-201 (201Tl) scintigraphy
tissues appeared to be 7–26%. e. Photoactive imaging
Oral lichen planus—risk is low and the inci- f. Optical coherence tomography (OCT)
dence of malignant transformation is 0–2% per g. Narrow band imaging (NBI)
year. The prevalence is between 0.3% and 3%. h. Nano diagnostic methods
The forms that undergo malignant transfor- 4. Histopathological methods
mation are erosive and atrophic. a. Scalpel biopsy
Leukoplakia has an overall malignant b. Oral CDx brush test
transformation rate of 15.6–39.2%. Homo- c. Cytology
geneous leukoplakia has a low annual malig- d. Laser capture micro-dissection
nant transformation rate between 1% and 7%. 5. Molecular methods
Verrucous leukoplakia, annual malignant a. Immunohistochemistry
transformation rate between 4% and 16%. b. Flow cytometry
Speckled leukoplakia, annual malignant c. Polymerase chain reaction (PCR)
transformation rate between 18% and 47%. d. Blotting techniques
Proliferative verrucous leukoplakia’s (PVL) e. Spectral karyotyping
annual malignant transformation rate is f. AgNOR
between 63% and 100%. In Western countries g. Fluorescent in situ hybridization (FISH)
somewhat high figures have been mentioned. h. DNA microarray
Following factors may be considered while i. Comparative genomic hybridization
studying malignant transformation rate of oral 6. Salivary diagnostic methods
leukoplakia—length of observation period, a. Protein electrophoresis
type of study, and therapeutic approach. b. Sialo chemistry
Potentially Malignant Disorders of Oral Cavity and Oral Cancers 111
6. What are risk factors and risk indicators? among all cancers in men even though it is only
Risk factor: Something that increases the the sixth most common cancer in men and 12th
likelihood of a disease occurring. most common in women worldwide. Cancer
Risk indicator: A marker for the presence of of oral cavity accounts for 3% of all mali-
another disease or condition. Risk indicator gnancies annually worldwide.
term may be given to tumor markers like 9. What are common signs and symptoms
alpha-5 and beta-6, the proteins found in of malignancies in jaw bones?
leukoplakia which indicates high risk of Old age more common, male predominance,
occurring cancer and surviving found in oral pain, paresthesia, loose teeth, premature tooth
submucous fibrosis patient also indicates risk loss, and rapid growth of lesion (swelling/
of carcinogenesis. ulcer).
In other words, a risk factor is causative (i.e.
Radiographic appearances: Spike like
chewing tobacco is a risk factor for oral cancer),
resorption of teeth, ill-defined lesion, uni-
while a risk indicator suggests that another
formly widened periodontal membrane space.
condition will be present but is not causative
(i.e. low educational and socioeconomic status 10. Compare the features of carcinoma
and heart disease). People with less education appearing on upper/lower lip.
and lower socioeconomic status may engage Carcinomas of the upper lip and commissure
in unhealthier behaviour resulting in more grow more rapidly, ulcerate sooner, and
heart disease, but their educational or metastasize earlier than lower lip cancer.
socioeconomic status is not considered cause Prognosis of upper lip is worse while prognosis
of heart disease. of lower lip is favourable. Approximately
7. What does CD stands for? 90% lip cancers occur on lower lip, 7% on upper
lip and remainder on commissures. The most
Cluster designation (CD) is a system for
frequent cause for lower lip cancers is
classifying cell surface markers that are
ultraviolet radiation and for upper lip is basal
expressed by leukocytes. These markers are
cell carcinoma. They are treated as skin cancers
used to distinguish cell lineages, stages of
rather than oral cavity cancers. Salivary gland
development, and functional subsets. The
tumors may be more common in upper lip than
system is based on computer analysis of
in lower lip.
monoclonal antibodies against human
leukocyte antigens with antibodies having Lesions larger than 2 cm or involving the
similar specificity characteristics grouped upper lip or extending to the lateral com-
together and assigned a number (e.g. CD1, missure have a poorer prognosis. Mandibular
CD4, etc). involvement with the tumor also results in a
poor prognosis and a higher incidence of
8. How cancer word is derived? What is regional metastases.
mortality rate of cancer?
Cancer is latinized from Greek word karkinos, 11. What are the characteristics of verrucous
meaning crab, denoting how carcinoma carcinoma?
extends its claws like a crab into the adjacent Verrucous carcinoma is a separate and distinct
tissues. Cancer is the second most leading form of oral carcinoma. It suggests a super-
cause of mortality in economically developed ficially spreading but non-metastasizing, non-
countries (following heart diseases) and the invasive type of papillary and exophytic
third most leading cause of death in developing cancer, but this is true only of a true verrucous
countries (following heart diseases and carcinoma. The true verrucous carcinoma
diarrhoeal diseases). In the Indian subconti- will present as a rough textured, exophytic,
nent the prevalence of oral cancer is the highest white to red papillary lesion.
12. What are the other names and the whereas in the malignant ameloblastoma they
common sites of occurrence of verrucose appear cytologically benign. Their behaviour
carcinoma? is similar to that of an aggressive squamous cell
Ackerman’s tumor, Buschke-Löwenstein carcinoma, for which they are often mistaken
tumor, florid oral papillomatosis, epithelioma until the histopathology identifies the pre-
cuniculatum, carcinoma cuniculatum. The ameloblast cellular atypia.
common sites are buccal mucosa, mandibular 15. What are clinical presentations of oral
alveolar crest, gingival and tongue with glottis squamous cell carcinoma?
larynx is most frequent nonoral site. The clinical presentations include:
13. Enumerate the fibroblastic malignancies. a. Exophytic variety: It is mass forming
Fibromatoses, fibrosarcoma, malignant fibrous generally irregular, fungating, papillary
histiocytoma. and verruciform variety. It is often indura-
14. What is odontogenic carcinoma? ted. The color may vary from red to white
Residual odontogenic epithelium from several depending upon vascularity and keratin
sources (rests of Serres, rests of Malassez, and production respectively.
reduced enamel epithelium) is composed of b. Endophytic variety: This is invasive, bur-
cells that are sufficiently undifferentiated so rowing and ulcerated variety. The most
that a series of genetic alterations can produce common presentation is depressed, irregu-
specific oncogenes or cause the loss of tumor lar shaped, ulcerated, central area with
suppressor genes, resulting in a malignancy. surrounding rolled border with normal,
Today, we recognize four types of odontogenic red, white mucosa. Rolled edges may occur
carcinomas: Primary intraosseous carcinoma due to invasion of tumor downward and
ex-odontogenic cyst (the primary intraosseous laterally under the adjacent epithelium.
carcinoma ex-odontogenic cyst may present as c. Leukoplakic: It is white patch.
an uncomplicated dentigerous cyst; the d. Erythroplakic: It is red patch.
diagnosis can be established only when the e. Erythroleukoplakic: Combined with red
histopathologic studies are completed). and white patch.
Primary intraosseous carcinoma de novo:
16. What are different presentations of
The primary intraosseous carcinoma de novo
carcinoma of tongue?
presents as a more clinically aggressive and
radiographically destructive radiolucent lesion It is mostly asymptomatic (two-thirds). The
in which the border with adjacent bone is common presentations are an indurated,
irregular. It may also cause an irregular and painless masses or nonhealing ulcer, as a red
jagged type of root resorption, in contrast to lesion, as a white lesion and as a red and white
the smooth regular root resorption seen with lesion. The most common location is posterior
odontogenic cysts and benign tumors. lateral border then anterior lateral border,
ventral surface and rarely dorsal surface.
Malignant ameloblastoma: The malignant
It is the site of only congenital carcinoma
ameloblastoma will most commonly present as
reported.
a multilocular radiolucent jaw expansion
typical of a benign ameloblastoma, but with a 17. What are characteristics of tongue
concomitant metastatic focus, usually in the cancer?
lungs. Infiltrative and exophytic are the two most
Ameloblastic carcinoma: Ameloblastic common morphologic types of cancer.
carcinoma differs from the malignant amelo- Exophytic types have less tendency to infiltrate
blastoma in the following features. First, the deeply. Early in the disease they appear as an
pre-ameloblasts are cytologically atypical, area of focal thickening or clinical leukoplakia
or as a painless superficial ulceration. The low grade adenocarcinoma non-Hodgkin’s

infiltrative type may show minimal or no disease. Lymphoma is second most non-
surface ulceration until late in its development. epithelial malignancy involving salivary
Cervical metastases occur more frequently glands. Lymphoma is second most malignancy
from cancer of the tongue than any other site in AIDS patients after Kaposi’s sarcoma.
within the oral cavity. Forty percent of patients 21. Which is rare location for I/O squamous
have nodal metastases on admission. cell carcinoma?
Bilateral or contralateral metastases are In the hard palate the squamous cell carcinomas
uncommon, in contrast to tumors of the tongue are rare but adenocarcinoms are common in
base, but may be present when the tumor this area.
involves the midline of the tongue. Metastases
22. What are the morphological types of
usually occur first in upper deep jugular (sub-
squamous cell carcinoma in oral cavity?
digastric) lymph nodes and then spread
downward along the jugular chain. Tumors Three gross morphologic growth patterns of
arising from the anterior third of the tongue squamous cell carcinoma occur in the oral
tend to metastasize slightly less frequently than cavity: Exophytic, ulcerative, and infiltrative.
those arising from the middle third. Unlike in Malignancies often display more than one of
the lip, the size of the primary lesion in tongue these manifestations.
cancer is not necessarily correlated with the The exophytic form is least common, except
presence or likelihood of cervical metastases. on the lip. The term exophytic is used
to describe outwardly growing tumor. It tends
18. What are most common intraoral malig- to grow more superficially and metastasizes
nancies? What are their common intrao- later, less frequently than the other types. This
ral sites? form begins as an area of thickened epithelium,
Squamous cell carcinoma of tongue is most which heaps up and can protrude 1 cm or more
common intraoral malignancy, the most above the surrounding mucosa. Ulceration
common location is posterolateral surface of occurs early in its development. Exophytic
tongue (25–40%), floor of mouth is second carcinomas gradually become deeply infiltra-
most site (15–35%). The floor of mouth is almost tive in more advanced cases. On the lip this
as frequently as tongue in men, but is involved form of tumor may reach a size of 6 or 7 cm,
much less frequently in women. In descending with little local destruction of tissue.
order of frequency is soft palate, gingival, The ulcerative type is the most common
buccal mucosa, labial mucosa and hard form of squamous cell carcinoma in the oral
palate. cavity. These cancers burrow deep into mucosa
19. Enumerate the hematologic malignan- with breach in surface. It begins as a round or
cies. oval ulcer with a grey, shaggy base that bleeds
There are three main groups of hematologic readily. Ulcerative types manifest a greater
malignancies: Leukemia, lymphoma, and tendency for rapid infiltration and usually
plasma cell tumors. have a higher histologic grade than the
exophytic type. The ulcer eventually may heap
20. What are common oral cancers and oral up and become exophytic or remain lower than
squamous cell carcinomas? surrounding mucosa. The metastasis is more
Acinic cell carcinomas are second most frequent than exophytic cancers.
common intraoral malignancies. Mucoepi- Infiltrative malignancies are common in
dermoid carcinomas are most common the tongue and initially appear as a firm mass
malignancies of salivary gland (26%), i.e. on or plaque covered by mucosa. This type of
palate (50–65%) followed by polymorphous tumor extends deeply into underlying tissues,
with minimal elevation above surrounding arrest. The weight loss and anemia of chronic
mucosa. As the neoplasm progresses, ulcera- disease develop despite gastric feeding tubes,
tion and exophytic manifestations may be iron and vitamin supplements, and even
observed. metabolic steroids. It has been observed that
Verrucous carcinoma, which is a clearly individuals will lose weight despite the intake
defined but uncommon variant of squamous of over 5,000 calories per day and otherwise
cell carcinoma. The term verrucous indicates normal bowel absorption. This is possible
its fine finger like projections. It typically because diabolic nature of cancer, i.e. its
occurs in elderly patients with poor oral replication rate, enzymes, and growth factors
hygiene or ill-fitting dentures and most it secretes. The normal cells are prevented from
commonly affects the buccal mucosa of males utilizing and metabolizing nutrients efficiently
and females with a history of tobacco chewing because as the tumor load increases, the
or snuff dipping. The tumor has a warty, bulky, tumor secretes a greater amount of blocking
elevated, and fungating appearance. It may factors and several vascular down-regulating
grow considerably through lateral spread enzymes, known as antiangiogenic factors.
and occasionally may be multifocal; it does These antiangiogenic factors, which were first
not invade deeply into underlying tissue. discovered in cancer cells, prevent normal
Verrucous carcinomas have an indolent tissues from recruiting new capillaries and
biologic behavior and do not metastasize. instead promote the formation of new
Tumors must be sectioned serially so that capillaries into the cancer.
the entire specimen is examined for a more It is important to note that this “tumor load”
invasive squamous cell carcinoma. It has got effect often is thought of as a failing immune
excellent prognosis. system. Such a concept is incorrect. The white
23. What is secondary osteosarcoma? blood cell and immunoglobulin counts are
usually normal and in proper function. Even
Osteosarcoma occurring at the site of another
when individuals progress to pneumonia, it is
disease process is called secondary osteosar-
not caused by a tumor-related depression in
coma. Commonly seen above 50 years of
their immune cells, but rather a loss of their
age. The disease is seen along with Paget’s
protective reflexes and their physical barriers
disease, previous radiation treatment, fibrous
to infection or from medication-induced
dysplasia, endochondromatosis, giant cell
immune dysfunction.
tumor, bone infarcts, chronic osteomyelitis,
osteochondromas, and osteogenesis imper- Infection (Pneumonia)
fecta. As the tumor load increases and causes
24. What are the reasons of death in cancer systemic weakness, infections, specifically
patients? pneumonia, become more likely. Individuals
The following are the mechanisms of death in are often anemic, hypoproteinemic, and
order of their frequency. possibly malnourished by the secretory
products of the tumor load (discussed above)
Tumor load, infection (pneumonia), compli-
and/or by the tumor-related dysfunction of the
cations of treatment, progression of co-
oral cavity and the effort required to eat or to
morbidities, paraneoplastic syndromes.
be fed by someone else. This weakness and
Tumor Load subsequent sedentary existence promotes
It is the most common, the slowest, and the atelectasis, which progresses to pneumonia.
gentlest pathway to death from oral cancers. Many individuals are also prone to pneu-
Most patients lose weight, become weak, lapse monias via aspiration related either to the
into a coma, and die from a cardiorespiratory tumor itself, to surgery, or to radiotherapy. In
addition, narcotic analgesics required for pain ischemic cardiovascular disease. The physio-
control both reduce the cough reflex and logic impact of surgeries, chemotherapy, and
depress respiration, thus enhancing the radiotherapy often exacerbate these diseases,
likelihood for a pneumonia. making them more difficult to control and
increasing their rate of progression. It is not
Complications of Treatment uncommon to have gained some control or
A smaller percentage of patients die from direct even a potential cure of the oral cancer at 3 years
complications of treatment or from side-effects only to have the patient die of a myocardial
of therapy. Chemotherapy occasionally pro- infarction or a cerebral vascular accident.
duces a severe marrow suppression, reducing Paraneoplastic Syndromes
white blood cell counts to less than 500/mm3
As discussed in the tumor load section above,
and resulting in a fatal systemic infection.
cancers secrete a wide variety of enzymes,
Surgery has produced events such as the
growth factors, and blocking factors. When a
“carotid blow-out” or internal jugular vein
tumor secretes a growth factor or a hormone
exsanguination. It also poses the threat of upper
with a single physiologic response, it is often
airway obstruction, where patients die after the
termed a paraneoplastic syndrome. One
attachments of the tongue are removed or
example of this is commonly seen arising from
bulky flaps are placed in the airway. Even
small cell (oat cell) lung carcinomas, but can
when tracheotomies are accomplished,
also be seen rarely arising from some oral
obstruction can occur from dried secretions in
cancers. This is the tumor secretion of
the tracheotomy cannula or from displacement
a parathyroid hormone-related peptide
of the tracheotomy as a result of patient
(PTHrp). This PTHrp is sufficiently close in its
movement. More rarely, exsanguinations
amino acid sequence and its active site
result from the tracheotomy cannula eroding
conformation to native PTH that it has an
through the trachea and then through the
identical effect. Such patients become signifi-
brachiocephalic vein. This is usually associated
cantly hypercalcemic, often with accompany-
with long-term tracheotomies requiring
ing overt symptoms of confusion, constipation,
ventilator support. Radiotherapy rarely
and bone pain. Untreated, this leads to death.
produces life-threatening complications
Similarly, some oral cancers will trigger a
during its treatment. However, the delayed
syndrome of inappropriate antidiuretic
effects of radiotherapy can be a significant
hormone (SIADH) by secretion of a small
factor in the patient’s death. Progressive later
peptide chain nearly identical to antidiuretic
dysphagia from fibrosis in the pharyngeal
hormone (ADH). These patients will have an
musculature reduces nutritional intake and
independent cancer-related increase in ADH
promotes aspiration. Osteoradionecrosis,
above the regulated native ADH levels, causing
limited jaw opening, xerostomia, caries, and
them to retain free water, develop hyponatre-
secondary candidiasis commonly affect
mia, and undergo a characteristic decreased
anyone who has had therapeutic radiotherapy
serum osmolality (> 280 mOsm/kg) and an
over 6,000 cGy.
increased urine osmolality (< 150 mOsm/kg).
Another example that may be seen in advanced
Progression of Comorbidities cancers is a paraneoplastic pemphigus, in
Most of these patients are often older and has which the cancer secretes desmoplakin to
a significant alcohol and smoking history. which the immune system develops anti-
Many who present with an oral cancer also bodies. These antibodies attack the inter-
have hypertension, chronic bronchitis, cellular bridge area, as often occurs in auto-
emphysema, peripheral vascular disease, and immune pemphigus vulgaris, because of the
similarity of the desmosomal antigen in 27. Which the body sites are likely to get
pemphigus (desmoglein) to the cancer-related affected by malignancies of body meta-
antigen desmoplakin. The result is the stasis?
development of progressive, painful vesiculo- The most frequent organs involved, ranked
bullous lesions. in decreasing order are: Lung, bone, liver,
25. How the cancer embolus travels from gastrointestinal tract, brain, skin, and kidney.
oral cavity to lungs? Carcinomas metastasizing to the bone are most
frequently adenocarcinomas.
The mechanism of oral cavity primary site
metastasis to the lungs is via the venous 28. What is occult neck disease?
system. The route begins with: It is defined as cancer present in the lymph
1. The intravasation of cancer cells into a small nodes in the neck that cannot be palpated
vein; clinically. Prophylactic neck dissections are
2. This cancer embolus may then drain into important in the management of early stage of
the pterygoid plexus or another local vein; oral squamous cell carcinoma. This is necessary
3. It then drains into the larger veins, such as for tongue squamous cell carcinoma, while
the facial vein or retromandibular vein, and floor of mouth, bucccal mucosa, maxillary
into the internal jugular vein; gingiva, mandibular gingival and lips carry
4. it then flows through the brachiocephalic lower but significant risk of the same.
vein, which forms at the junction of each
29. What is oral field cancerization?
internal jugular vein and the respective
subclavian vein; Oral field cancerization (OFC) implies that oral
5. The cancer embolus next passes through the cancer does not arise as an isolated cellular
superior vena cava into the right atrium of phenomenon but rather as an anaplastic
the heart; tendency involving many cells at once and
results in the multifocal development of cancer
6. As the heart contracts, the cancer embolus
at various rates within the entire field in
is pumped past the tricuspid valve into the
response to a carcinogen especially tobacco. It
right ventricle;
explains the concept by which the secondary
7. From there, further cardiac contractions,
primary tumors (SPTs) develop. The mucosa
pump it through the pulmonary valve into
of head and neck had undergone a change due
the pulmonary artery.
to exposure of carcinogen, and therefore
The cancer embolus then passes further into more susceptible to development of many
the branches of the pulmonary artery system, foci of malignant cells. Oral verrucous
which progressively narrows, until it physi- carcinoma associated with leukoplakia or
cally wedges into a small arteriole or capillary. submucous fibrosis may be indication of
26. Which malignancies of body are likely “field cancerization”.
to get metastasize to jaw bones? 1. Large areas of arodigestive tissue are
Statistics vary somewhat among reports, but affected by long-term exposures to carcino-
the most common originating site is the female gens. In this preconditioned epithelium
breast (35%) followed by the lungs (28%) and multifocal carcinomas can develop as a
kidneys (15%). After these, several other areas result of independent mutations.
deposit metastatic foci in the jaws at nearly the 2. A single cell is transformed and gives rise
same relative incidence: Prostate (6%), thyroid to one large extended premalignant field by
(6%), stomach, and lower gastrointestinal clonal expansion and gradual replacement
tract (6%). of normal mucosa.
30. What is fixation and induration? Cancers located more posterior in the floor
Fixation occurs due to abnormally dividing of the mouth, in the oral tongue, the buccal
cells invading the deeper areas of muscles mucosa, or the alveolar ridge between the
and bone. Induration is mucosal firmness or mental foramen and the retromolar trigone
hardness caused by an increased in number of will usually first appear in the submandibular
epithelial cells secondary to an inflammatory triangle (level II, yellow).
infiltrate. Both are signs of carcinomas. The submandibular triangle lymph node,
Induration can be seen in granulomatous and which is located on the surface of the
inflammatory diseases. submandibular gland and just deep to the
Fixation and induration may be result of marginal mandibular branch of the facial
neoplastic infiltration of deeper tissues if the nerve, is often called the node of Stahr after the
ulcer is malignant. In these instances fixation German anatomist Hermann Stahr, who in
is not accompanied by tenderness. 1909 noted that cancer of the tongue would
settle in this node.
31. What is WHO scale for oral mucosites? Cancers that appear in the retromolar
Grade 0: No oral mucositis trigone, tonsillar fossa, and pharyngeal tongue
Grade 1: Erythema and soreness will often first appear in the jugulodigastric
Grade 2: Ulcers, able to eat solid foods lymph node located where the posterior
Grade 3: Ulcers, require liquid diet because of digastric crosses the internal jugular vein
mucositis (level III, orange). Squamous cell carcinomas
arising from the nasopharynx area metastasize
Grade 4: Ulcers, alimentation not possible
to the posterior digastric lymph nodes around
because of mucositis.
the spinal accessory nerve (level V, pink). Each
32. What is sentineal node? of these nodes is referred to as the sentinel node
Gould et al. (1960) described the term sentineal for its respective tumor location.
node. The first tumor in drainage pathway of 33. Enumerate the various chainside investi-
malignant tumor or it is first lymph node to gations.
receive drainage from tumor. Pulp vitality test, toluidine blue staining,
Metastasis of oral squamous cell carcinomas Lugol’s iodine brush biopsy, Velscope, intraoral
is mostly to the regional lymph nodes of the radiograph, aspiration biopsy, incisional
neck. Cancers that have metastasized from the biopsy.
anterior floor of the mouth, anterior alveolar
ridge between the mental foramen, and lower 34. Enumerate various NRT products.
lip will first appear in the submental triangle Inhaler, trans dermal patch, nicogel, nicotine
lymph nodes along one of the anterior digastric pastiles, magneto therapy, chantix, buccal
muscles (level I, green). spray, electrical cigars, Zyban, gum, nasal spray.
6
Diseases of Salivary Glands,
Pigmented Lesions of Oral Cavity
1. Enumerate the diseases associated with extravasation/retention in floor of mouth,

salivary gland ducts. the extension in neck is ploughing ranula.
1. Accessory salivary gland ducts: Extra ducts 7. Salivary fistula: Injury to the duct may lead
may be present which either join the main to extravasation of saliva in the gland tissue,
duct or may open separately in the oral if the main duct is involved it is called
cavity. The most common location is ‘major fistula’ and if collecting ducts are
superior and anterior to Stensen’s duct. involved it is called minor fistula.
2. Diverticuli: A diverticulum is pouch or sac 8. Stricture is narrowing of salivary gland
protruding from the wall of duct, in major duct: It may produce obstruction. It may
salivary gland duct may produce pooling result from faulty chewing habit or external
of saliva and recurrent sialadenitis. trauma. It may produce inflammation and
swelling of gland. Four types of strictures
3. Atresia of salivary ducts: Rare congenital
are seen: (1) Sialectasis, (2) Pseudosialectasis,
disorder absence of ducts or even occlusion
(3) Punctate sialectasis, (4) Sialodochitis.
of ducts that may produce retention cyst.
Sialectasis (sialodochitis) is “dilation of a
4. Sialodochitis: Inflammation of salivary salivary duct” (ptyalectasis) from [sial – +
gland duct. Greek ektasis, a stretching]: A condition
5. Salivary duct: Cysts are acquired. Cysts that resulting from duct obstruction of the
are believed to develop from marked cystic parotid or submandibular glands associa-
dilatation of a salivary gland/duct, and ted with pain and swelling. The term
ductal obstruction is thought to be a princi- pseudosialectasis has been introduced for
pal etiologic factor. Salivary duct cyst may the radiographic appearances of these
occur in major (parotid) or minor glands. lesions as in autoimmune disease, they
6. Mucocele: Retention or extravasation type represent duct disruption than ectasia.
retention of saliva due to obstruction and Punctate sialectasis refers to saccular
rupture of duct and spillage into mucosa dilation of small ducts within gland, while
respectively, ranula may be due to sialodochitis refers to dilation of large ducts.
118
Diseases of Salivary Glands, Pigmented Lesions of Oral Cavity 119
9. Darier’s disease: It also shows abnor- dust and Zn poisoning, Sjögren’s syn-
malities like duct dilatation with periodic drome, dehydration or renal failure, and
strictures in the main system. shock
10. Salivary duct stone: Sialolithiasis most c. Drugs: Antihistaminics, anticholinergic
commonly seen in submandibular duct. (atropine), tricyclic antidepressants, anti-
11. Ductal papillomas: Sialoadenoma papillo- parkinsonism, antihypertensive drugs,
ferum, inverted ductal papilloma, intra- monoamine oxidase inhibitor.
ductal papilloma. 3 . Enumerate obstructive diseases of
12. Salivary duct: Carcinoma, intraductal salivary glands.
carcinoma. Obstructive diseases are more common in
13. Iatrogenic perforation: Iatrogenic per- submandibular gland than parotid gland.
foration of salivary gland duct specially These are mucous retention cyst (obstructive
parotid gland due to its curvature during sialoadenitis), sialolithiasis, strictures and
sialography. stenosis.
2. What are the functional disorders of Stenosis may be of four types:
salivary glands? 1. Membranous stricture
Saliva is stimulated by parasympathetic 2. Large stricture
and sympathetic nervous system. The nature 3. Diffuse stenosis of main duct
is watery (serous) and thick (mucinous) 4. Diffuse generalized stenosis
respectively. 4a. Without localised strictures
Sialorrhea (Ptyalism) 4b. With multiple strictures.
It is increased salivation. The causes are: 4. Mention unilateral causes of salivary
1. Physiologic causes: Infancy, starvation, gland swellings.
during eruption of teeth, foreign body 1. Unilateral swelling with acute pain, swell-
(may be dentures) ing, fever (acute bacterial sialoadenitis)
2. Pathologic causes: 2. Unilateral swelling with recurrent swellings
a. Local causes: ANUG, erythema multi- pain (chronic sialoadenitis, lymphoma,
forme, metal poisoning, ulceration Sjögren’s syndrome, sialolithiasis)
b. Systemic diseases: Mental retardation, epi- 3. Unilateral painless slow growing mass
lepsy, racial paralysis, alcoholic neuritis, (neoplasm benign or malignant)
parkinsonism, morphine addiction 5. Mention bilateral causes of salivary
c. Drugs: Potassium iodide, pilocarpine, gland swellings.
mercurial salts. 1. Bilateral swelling with acute pain, fever
(viral sialoadenitis)
Xerostomia (asialorrhea, pasties, cotton-
2. Bilateral swelling with systemic symptoms
mouth)
and slow course (Sjögren’s syndrome,
It is decreased production of saliva. The causes are: lymphoma and mycobacterial disease).
1. Physiological: Menopause
6. What are the non-neoplastic enlarge-
2. Pathological causes:
ments of parotid gland region?
a. Local causes: Salivary gland diseases
Non-neoplastic enlargements of parotid gland
(aplasia, hypoplasia, irridation of
are as follows:
salivary glands, etc.)
b. Systemic causes: Fever, dehydration, lung Inflammation or Infection
infections, typhoid, uncontrolled diabetes, Bacterial
hyperthyroidism, vitamins A and B com- Viral (mumps)
plex deficiency, occupational exposure to HIV sialopathy
Acute suppurative sialoadenitis, sclerosing

polycystic adenosis
Chronic sialoadenitis, uveoparotid fever
Autoimmune Diseases
Chronic recurrent parotitis
Sjögren’s syndrome
Granulomatous diseases
Sarcoidosis, tuberculosis, actinomycosis
Wegener’s granulomatosis
Kimura’s disease
Miscellaneous
Sialosis
Sialadenosis (hormonal, thyroid, drug-
induced)
Polycystic disease
Pneumoparotid
Benign lymphoepithelia lesions (Mikulicz’s
disease)
Parotid cyst
Radiation sialadenitis
Obstructive Enlargement
Sialoliths Pleomorphic adenoma raising the ear lobule on right
Enlargements which are non-parotid origin and left side respectively
Preauricular lymph node swelling 8. What are differentiating points of mas-
Idiopathic masseter muscle hypertrophy seteric hypertrophy and parotid swell-
Sebaceous cyst ings?
Preauricular cyst or abscess. The bulk of parotid gland is anatomically
7. In which diseases the position of ear located adjacent to upper two-thirds of ear,
lobule affected? while masseter muscle bulk is positioned at
The swellings with tale of parotid elevates the lower level on lower half of mandibular ramus.
ear lobe and submasseteric space infections. The enlarged parotid will accentuate the
The swelling obscures the visualization of ear ovalness of the face, while masseteric hyper-
lobe. trophy highlights facial rectangularity. The
rectangularity due to masseteric hypertrophy
is marked when it is present unilaterally, it
alters the facial lines, generating discomfort
and negative cosmetic impacts by many
patients.
On palpation the masseteric swelling will
increase in size when patient clenches the teeth.
In some cases, the area of insertion of the
Submasseteric space infection hiding the visualiza- masseter on the mandibular ramus will
tion of ear lobe on left side and right side in child patient respond by forming a bone projection that may
be palpable or seen on an anteroposterior dysphagia or gagging. These present orally as

radiograph. Presumably, this is due to the a bulge arising from the tonsillar fossa area.
tension created by the masseter muscle during
11. Which are most common tumor of minor
these contractions, which produce a periosteal
and major salivary gland?
reaction and activity.
The pleomorphic adenoma is the most
9. What are common presentations of common tumor both in major and in minor
pleomorphic adenoma? salivary glands. Warthin tumors, basal
The two most common clinical presentations cell adenomas, oncocytomas, acinic cell
are a painless firm mass in the superficial lobe carcinomas, and sebaceous tumors have a
of the parotid gland and a painless firm mass strong predilection for the major glands, but
in the posterior palatal mucosa. the polymorphous low-grade adenocarcinoma
has a marked predilection for the minor glands.
While most intraoral salivary gland tumors
favour the palate, the canalicular adenoma
favours the upper lip. The three most common
sites of minor gland tumors are palate, lip and
buccal mucosa.
12. Which sites in oral mucosa where
salivary gland tumors are less likely to
occur?
Midline and anterior hard palate, gingiva, and
attached alveolar mucosa.
13. Name the tumor of non-salivary gland
origin and nonductal origin which occurs
in the substance of salivary gland.
Tumors occurring within salivary glands are
predominantly of epithelial origin. However,
nonepithelial neoplasms also may arise within
the gland that are not actually of salivary gland
or ductal origin. Most of these are found in the
parotid gland. Among the more common
benign tumors is the hemangioma, which is the
Pleomorphic adenoma involving right side of most frequently occurring tumor in the parotid
superficial lobe of parotid gland and intraorally soft gland in children. Lipomas and neurogenic
and hard palate respectively tumors also may be seen. Hodgkin’s and non-
10. What are the presentations of pleomorphic Hodgkin’s lymphomas and, most infrequently,
adenoma in parotid gland? soft tissue sarcomas may develop. Metastatic
tumors such as renal cell carcinoma and
Eighty percent of all pleomorphic adenomas
melanoma may also occur.
in the parotid gland develop in the superficial
lobe. It presents as a freely movable, firm mass. 14. Enumerate lesions occurring at the
Peculiarly and rarely, these can fluctuate in size junctions of soft and hard palate.
or be painful. When a pleomorphic adenoma Mass lesions at the junction of the hard and
arises from the deep lobe of the parotid gland, soft palate mucosa are usually minor salivary
it usually goes unrecognized for a number gland tumors (adenoid cystic carcinoma,
of years until its size creates symptoms of mucoepidermoid carcinoma, adenocarcinoma,
and polymorphous low-grade adenocarcinoma). Cavernous hemangiomas, small lymphan-

Although other conditions and tumors such as giomas, and a venous varix will give a
neural tumors, non-Hodgkin’s lymphoma, and similar appearance. Although rare, a vascular
palatal abscesses are possible, they may be leiomyoma appears blue and has a predilection
diagnosed with the same biopsy principles. for the lip.
Epstein pearls occur along median palatine 18. What is MEP and MRC?
raphe.
The word mucocele is a clinical term that
Petechiae in infectious mononucleosis are applies to mucous extravasation phenomenon,
almost pathognomonic but can be seen in HIV that is, MEP. This occurs when saliva spills into
and rubella. Oral petechiae and ecchymosis are the connective tissue and forms a mass, due to
seen in thrombocytopenia. Fellatio can result trauma to minor salivary gland ducts. These
in palatal petechiae at the junction.
Necrotising sialometaplasia early in stage as
dusky red swelling while afterwards as ulcer.
15. Enumerate the diseases occurring on the
posterior part of palate?
Herpangina, intraoral mixed tumor, malignant
salivary gland tumor, necrotising sialometa-
plasia.
16. What is superficial mucocele and deep
mucocele?
A separate type of minor salivary gland
mucocele, known as a superficial mucocele, is
formed after a duct rupture in the subepithelial
location. Preferred sites are the palate and
retromolar areas. The mucoceles will appear
as small (1 to 5 mm) yellow to grey vesicles.
Superficial lesions take on bluish to transparent
hue.
Deeper mucoceles, which often occur on the
ventral surface of the tongue or the floor of the
mouth unassociated with the sublingual gland,
are frequently grey or yellowish in colour.
These are common in children and young
adults. Deep lesions are of normal colour.
17. What entities are considered in the
differential diagnosis of mucocele?
Mucoceles of minor salivary gland origin are
bluish and the history of trauma may be vague,
other lesions that may appear blue must be
considered.
Low-grade mucoepidermoid carcinomas
are the most significant. They will also produce
mucin in vacuolated spaces within the tumor,
imparting the blue colour.
are common among children and adolescents. sialolith/mucous plugs) which cause dilation
The common sites are lower lip, buccal mucosa, of ductal structure. These are more common in
ventral tongue, floor of mouth and retromolar adults. The common sites are upper lip, buccal
region. MEP appear as soft, bluish lesions with mucosa and floor of mouth. MRC are soft
smooth surface. mobile masses similar to adjacent mucosal
A clinically similar lesion is the mucous colour.
retention cyst that is called MRC. This is also MRC is less common than MEP. Both are
called mucous cyst. These are true salivary duct generally asymptomatic. Treatment for both is
cysts and some may occur from retention of generally surgical excision.
saliva in ductal tissues (by plunging from 19. What is sialocele?
Sialoceles are mucoceles of major salivary
glands. These are tissue reaction to extravasa-
tion of saliva from a gland/duct complex and
has a nonsecretary, nonepithelial lining
consisting primarily of fibroblasts and
capillaries.
Sialoceles of the submandibular gland and
parotid gland are uncommon. When they do
occur, they are more often related to
penetrating injuries rather than to surgery. In
either situation, the ductal injury is found in
the main duct or in one of the large interlobar
ducts.
Sialoceles of the parotid gland are more
common than those of the submandibular
gland. In the parotid gland, the extravasation
of saliva forms a cutaneous collection, which
thins the overlying skin, frequently to the point
of rupture, or communicates to an area of
penetrating injury to form a salivary cutaneous
fistula. This can occur after parotidectomy.
Seroma is clinically similar to sialocele but
differs in that it has lower amylase content on
fluid analysis.
20. Enumerate conditions associated with
drooling.
Drooling is an abnormal unintentional spillage
of saliva from mouth onto the face on clothing.
Primarily affecting patients with neuro-
muscular impairment and mental retardation.
It is also called salivary incompetence.
Drooling is not only unesthetic but can also
affect speech, eating, lead to functional, social,
psychological and clinical consequences for
patients, family, and caregivers. It can cause
skin irritation about the face and has been
reported to contribute to dehydration. The 2. Palatine glands:

presence of significant drooling warrants • Purely mucous
a systematic approach to intervention. • Glandular region of hard and soft palate
Conditions associated with drooling are as and uvula
follows: • Opening of ducts on palatal mucosa
1. Physiological in healthy infants stops by 3. Glands of tongue:
about 18 months, abnormal if it continues • Anterior lingual glands: Mixed
beyond 4 years.
• Posterior lingual glands: Purely mucous
2. Infants (teething period, i.e. 4 days before
• von Ebner’s glands: Purely serous
a tooth emerges, day of emergence and
3 days after it)
3. Alzheimer’s disease
4. Stroke
5. Pseudobulbar palsy or bulbar palsy
6. Cerebral palsy
7. Parkinsonism
8. Down’s syndrome
9. Bell’s palsy
10. Ataxia telangiectasia
11. Amyotropic lateral sclerosis
12. Drug induced (clozapine, nitrazepam)
13. Oral or dental deformities
14. Gastroesophageal reflux disease
15. Nasal obstruction
16. Painful swallowing (dysphagia)
17. Esophageal obstructions 23. What is the difference between hyper-
18. Epilepsy salivation and ptyalism?
21. Enumerate the drugs causing salivary Hypersalivation refers to excessive production
gland pain. of saliva while ptyalism includes both hyper-
Antihypertensives, antithyroid agents, salivation and drooling.
chlorhexidine, cytotoxics, ganglion blocking 24. What are methods of saliva collection?
agents, iodides, phenothiazines and sulfona- Draining, suction, spitting, and absorbent
mides may cause pain in salivary glands. (sponge) method. The saliva can be collected
22. How many numbers of minor salivary under rest and in stimulated stage. Under
glands are present? What are their loca- stimulation collection includes intraoral
tions? duct cannulation and Lashley’s cups and
Minor salivary glands are 600–1000 in number their modification as well as Schneyer’s
and are of 1–5 mm in dimension. They have got device.
single duct which directly secretes into oral 25. Enumerate the conditions causing
cavity and produce half of saliva in oral cavity discoloration of saliva.
at rest. Discoloration of saliva and other body fluids
1. Labial and buccal glands: into red or orange color may be seen in patients
• Mixed but predominantly mucous treated with clofazimine, levodopa, rifampicin,
• Under epithelium of lips and cheeks and rifabutin therapy.
26. What is salivaomics? less viscous because of its higher protein levels
The term “salivaomics” was coined in 2008 to and because the course of Stensen’s duct is
reflect the rapid development of knowledge downward and low mineral content. There is
about the various “omics” constituents of no association in either gland with altered
saliva (“salivary proteome”, “transcriptome”, serum calcium levels or renal stones 70% of
“microRNA” (miRNA), “metabolome” and parotid calculi are radiolucent and are observed
“microbiome”). and filling defect on sialogram or can be
directly visualized on sialoendoscope.
27. What are the signs and symptoms of oral
dryness? 30. What is sialodochoplasty?
The symptoms are related to decrease fluid in It is a procedure by which the stones that are
the oral cavity and have an effect on mucosal accessible in the floor of the mouth are removed
hydration and oral functions. Dryness of all via a direct approach. The damaged duct is
mucosal surfaces including lips, throat. sutured to the mucosa of the floor of the mouth.
Difficulty in chewing, swallowing and speak- With this approach there is always concern
ing. Other associated complaints oral pain, oral about the course of the lingual nerve in the floor
burning sensation, chronic sore throat, pain in of the mouth.
swallowing. Mucosa may be sensitive to spicy 31. Define sialography.
or coarse food. Dry lip is most common sign of A radiographic procedure used to study
oral dryness. the salivary ducts and glands with the aids
28. Which tests are done to indicate oral of contrast media or radiographic study of
dryness? salivary glands and ducts after injection of
The tests are lipstick test and tongue blade sign. contrast material.
Saliva would normally wet mucosa and aid in 32. What are the indications of sialography?
cleansing teeth. In lipstick sign the presence of Calculi, strictures, sialectasia (dilatation),
lipstick or shed epithelial cells on labial fistulae and other pathology.
surfaces of maxillary anterior teeth is an
indication of reduced saliva while positive 33. What are the contraindications of
tongue blade sign indicates that the tongue sialography?
blade when gently pressed against mucosa will Allergy to compounds containing iodine:
adhere the tissue. This tongue blade sign is also • Periods of acute infection/inflammation,
called “mouth mirror sign”. when there is discharge of pus from the
duct opening.
29. Why the parotid calculi are radiolucent?
• When clinical examination or routine
The so-called stones that form in the parotid
radiographs have shown a calculus close to
duct system are rarely calcified and are actually
the duct opening, as injection of the contrast
mucous plugs that do not appear on radio-
medium may push the calculus back down
graphs. Stones that form in the submandibular
the main duct where it may be inaccessible.
duct system are almost always radiopaque
because they are composed of calcium carbo- 34. What are the complications of sialo-
nate and calcium phosphate. Stones are graphy?
believed to be more common in the submandi- Injection of contrast medium can put the
bular duct system because of the more viscous sialolith further back, extravasation of medium
glycoprotein consistency of the secretions and in substance of gland, edematous ductal
the upward course of the duct, which makes orifices and damage to orifice (specially
it more prone to stasis and retrograde bacterial by conventional sialography), granuloma
invasion. The parotid gland secretion is much formation, rupture of salivary gland duct or
perforation of duct which is more common in flat spot or plaque with oval or irregular shape,
parotid gland due to its curvature, overfilling brown or blue in colour. Common on hard
of duct, exacerbation of infection, adverse palate. No malignant transformation potential.
reaction to contrast material and overfilling
may result in misdiagnosis of sialectasis.
35. What are the types of intraoral nevus?
Nevi are developmental malformations
originating from defective melanoblasts of
neural crests. Usually, seen in skin and rarely
in oral mucosa. They may be congenital/
acquired. The following are the categories of
acquired nevi.
Intramucosal Nevus
It is common representing 55%. The cells are
in connective tissue and are separated from Blue nevus on palate
epithelium by a band of collagen. More in Junctional Nevus
females and in any age. Asymptomatic, flat,
It is less common of oral nevi (3–5%). Histologi-
plaque like with brown or brownish black
cally shows nests of nevus cells along the
color. Common location is palate and buccal
basal layer of epithelium and some drop into
mucosa rarely seen on gingival and lips. Little
connective tissue showing junctional activity.
potential for malignancy.
Clinically these are seen as black or brown, flat
or slightly raised spots. Common location on
palate, buccal mucosa and alveolar mucosa.
They never seem to convert to a compound
nevus. Transformation into a melanoma may
occur.
Intramucosal nevus on buccal mucosa
Blue Nevus
It is the second most frequent nevus of oral
mucosa. This accounts for 30–36% of oral nevi.
The melanocytes are elongated and slender
containing melanin pigment and arranged in Junctional nevus on retromolar area
pattern parallel to epithelium in middle and
lower parts of lamina propria. No junctional Compound Nevus
activity. There are two types: One is involving The nevus cells are present in epithelium and
oral mucosa and skin while other is specific for underlying connective tissue. They present
skin. Seen at any age, no sex predilection. characteristic of intramucosal and junctional
Clinically, asymptomatic slightly elevated or nevus. It represents about 6–9% of all oral nevi.
Clinically, asymptomatic, slightly elevated black discolouration in the oral cavity.

flat spot with red brown or black brown color. Frequently the heavy metals are deposited
The size may be up to 1 cm. Common intraoral as a line or band on inflamed marginal
sites are buccal mucosa, palate and gingival. gingiva.
It may transform into malignant melanoma. 6. Prodromal signs of infectious mononucleo-
sis may occur a few days before the patient
becomes ill as 6 to 20 petechiae in the soft
palate. The hematoma is a pool of effused
blood confined within the tissues. When it
is superficial, it appears as an elevated,
bluish swelling in the mucosa.
7. Addison’s disease, hemochromatosis,
argyria, caviar tongue, oral nevus, cyanosis,
chloasma gravidarum.
8. In rarities aniline intoxication, arsenic
poisoning, carotenemia, chloroquine therapy.
38. Enumerate melanocytic lesions.
Compound nevus on palate
Melanocytic lesions appear brown or black due
36. Enumerate the various pigments and the to the deposition of melanin.
color given by them in the oral cavity. Ephelis: It is a freckle. It is flat, brown or black
Hemoglobin, hemosiderin and melanin are the in colour, and occurs on sunexposed surfaces.
pigments associated with color in oral cavity. It is due to increased production of melanin by
Hemoglobin imparts red/blue color and melanocytes. An ephelis requires no treatment.
indicates lesions with vascular disease. Oral melanotic macule: It is a localized pig-
Hemosiderin appears brown, as a result of mented lesion associated with increased
extravasation of blood and defect in hemostatic melanin pigmentation of the stratified
mechanisms. squamous epithelium. It is asymptomatic, flat
Melanin imparts black pigmentation and and not thickened, and appears similar to an
indicates increased sun exposure, certain drugs ephelis (freckle) of skin. It is a harmless lesion,
and genetic factors. but its significance lies in distinguishing it from
nevus or early melanoma. A biopsy should be
37. Enumerate the oral mucosal lesions that performed if any doubt exists about the
may show blue counterpart. diagnosis. If an oral pigmented lesion is not
1. Petechiae and purpura—they are red but thickened, but is larger in diameter, has any
turn bluish macules. variation in colour, cannot be diagnosed as
2. Congenital hemangioma, cavernous he- tattoo based on radiographic findings, or has
mangioma, congenital A-V malformations, irregular borders it should be excised.
varicosities and lymphangioma. Lymphan- Melanocytic nevus: It is a benign proliferation
gioma is less blue than hemangioma. of nevus cells (melanocytes). Nevi of skin first
3. Peripheral giant cell granuloma, eruption appear in childhood and progress through a
cyst, eruption hematoma, superficial series of clinical and microscopic stages. Most
ranula. people have between 10 and 40 nevi on their
4. Oral nevus and mucocele. skin. Nevi of skin that have uniform colour and
5. Chronic poisoning with heavy metals (such borders and are not changing in size or surface
as mercury, lead, bismuth, and silver), i.e. texture, are not considered premalignant
heavy metal lines may result in a bluish– lesions and do not need to be removed unless
they are chronically irritated or having a hard palate, gingiva, and alveolar ridge. It is
cosmetic problem. Nevi of oral mucosa are not possible to distinguish an oral melanocytic
relatively rare. They occur most commonly on nevus from early melanoma. If oral nevus
the gingiva and hard palate. Nevi of oral and/or melanoma are included in the clinical
mucosa should be completely excised because differential diagnosis, then a biopsy is indi-
they cannot be differentiated from melanoma cated. Biopsy is also indicated for flat, non-
based on their clinical features. thickened pigmentations that are changing
Melanoma: It is a malignant neoplasm of or have atypical colour, borders, or size.
melanocytes. Melanoma of skin has increased Treatment for melanoma is complete surgical
significantly in incidence, while melanoma of excision. The thickness of the lesion and depth
oral mucosa is relatively rare. The most impor- of invasion are the most important prognostic
tant clinical features of cutaneous melanoma factors.
are asymmetry of the lesion, variation in colour 39. What is melanoplakia?
(brown, black, red, white, blue), and diameter These are racial pigmentation common oral
greater than 6 mm. Oral melanoma begins as mucosal discoloration usually and exclusively
an irregular, brown to black macule. Later the in non-caucasian population. This is incidental
lesion will develop thickening and sometimes finding, commonly present as symmetrical,
ulceration. The most common locations are the band like zone of brown–black discoloration
at the junction of attached gingival and alveolar and buccal mucosa. These are called amalgam
mucosa. Buccal mucosa, tongue, hard palate, tattoo.
and lips are also involved. Recognition and
monitoring is recommended. Melanoplakia
may be present at birth and persists for life.
40. What is ABCDE of melanoma?
The clinical evaluation system is developed.
a. Asymmetry because it has uncontrolled
growth pattern.
b. Border irregularity with notching.
c. Colour variation, it shows shades of brown
to black, white, red, and blue. These shades
vary depending on amount and depth of
melanin pigmentation.
d. Diameter greater than 6 mm (i.e. diameter
of a pencil eraser).
e. Evolving as lesions show changes with
respect to size, shape, color, surface or
symptoms over time.
41. What are presentations of oral melanoma
intraorally?
The oral melanoma may present as one of four
lesions: A pigmented macule (various shapes,
possibly linear); a pigmented nodule; a large,
pigmented exophytic lesion perhaps associated
with macular pigmentation; or an amelanotic
(nonpigmented) variety of any of these three
forms.
42. What are coast of California and coast of
Maine?
44. Enumerate endocrine abnormalities
These are patterns of café au lait spots. associated with oral pigmentation.
Coast of California: Café au lait macules of The abnormalities are Albright’s syndrome,
NF-I have smooth edges. These macules are Addison’s disease, acromegaly, Cushing’s
small. disease and hyperthyroidism.
Coast of Maine: Café au lait macules of Albright’s syndrome: Polyostotic fibrous
fibrous dysplasia syndromes (McCune dysplasia, abnormal pigmentation, precocious
Albright’s syndrome) are craggy and irregular. puberty.
These are larger.
Addison’s disease: Diffuse brownish or
43. What is focal argyrosis? black discoloration in any part of oral mucosa
It is an iatrogenic lesion that follows traumatic commonly buccal mucosa, lips, tongue,
soft tissue implantation of amalgam particles gingival. It is due to adrenocortical deficiency.
or a passive transfer by chronic friction of Acromegaly: Hyperpigmentation is similar
mucosa against amalgam restoration. The to Addison’s disease and seen in 40% patients.
lesions are macular and grey seen in gingival It is usually due to pituitary tumor.
Cushing’s disease: It is from excessive

ACTH production from pituitary tumor.
Hyperthyroidism: It is due to increased
MSH production. Pigmentation is same as
Addison’s disease.
45. What are freckles (ephelis)?
These are common in Caucasians and Chinese
population. An ephelis is a common small
hyperpigmented macule of the skin that Freckle on lower vermillion border
represents a region of increased melanin
production. Ephelides are seen most often the epidermis, not by a local increase in the
on the face, arms, and back of fair-skinned, number of melanocytes.
blue-eyed persons, they may be associated No treatment is necessary for ephelides. The
with a strong genetic predilection (autosomal- use of sunscreen scan prevent the appearance
dominant). The skin discoloration is produced of new freckles and help prevent the darkening
by a relative excess of melanin deposition in of existing lesions.
7
Developmental Disturbances,
Physical and Chemical Injuries to
the Oral Cavity
1. Enumerate the exophytic anatomic Epidermoid and Pyostomatitis vegetans

structure. dermoid cysts
• Accessory tonsillar tissue Jaundice or icterus Lipoid proteinosis
• Buccal fat pads carotenemia
• Circumvallate papillae
Rarities
• Foliate papillae
Amyloidosis
• Genial tubercles
Lesions of sebaceous glands pseudoxanthoma
• Lingual tonsillar tissue
clasticum
• Palatine rugae
Psoriasis
• Palatine tonsils
• Palatine papillae Many potentially yellow lesions may not
appear yellow because the covering mucosa
• Retrocuspid papillae
masks their color. Normal fat covered by a thin
• Retromolar papillae
layer of mucosa appears yellow. Salivary gland
• Stensen’s papillae tissue infiltrated with fat appears yellow. This
• Sublingual caruncles condition occurs most often in the soft palate.
• Tongue Bone and salivary stones covered by a thin
• Uvula mucosa may impart a yellowish tinge to the
2. Enumerate yellow conditions of oral mucosa.
mucosa. 3. What is caviar tongue?
Fordyce’s granules Fibrin clot A varicosity, a distended vein, is a common
Superficial abscess Superficial nodules of occurrence in the oral cavity, especially in older
tonsillar tissue individuals. It may also result from partial
Yellow hairy Acute lymphonodular blockage of the vein proximal to the distension.
tongue pharyngitis The varicosities most frequently observed by
Lipoma Lymphoepithelial cyst the clinicians are superficial, painless, and
131
bluish; they appear somewhat congested and microscopic examination the tract is lined with
accentuate the shape and distribution of the stratified squamous epithelium that continues
vessel. The most frequent site is the ventral into the vermilion tissue of the lip. Mucous
surface of the tongue. gland ducts may empty into the sinus; as a
When many of the sublingual veins are result, mucous frequently can be milked from
involved, this condition is called caviar tongue the tract.
(phlebectasia linguae).
Differential Diagnosis
4. What is ankyloglossia? What is partial The commissural lip pit especially must be
ankyloglossia? What is classification? differentiated from the congenital lip pit,
Ankyloglossia (more commonly called “tongue- which is seen on the vermilion border of the
tie”) is a congenital anomaly characterized by lower lip but not at the commissures. The
an abnormally short lingual frenum, which congenital lip pit, however, is extremely rare,
may restrict tongue tip mobility. It is defined occurring in approximately 1 of 2 billion births.
as a limitation of the possibilities of protrusion
and elevation of the tip of the tongue due to Management
either the shortness of the frenulum or the The commissural lip pit is asymptomatic and
genioglossus muscle or both. The problems requires no treatment.
associated with it are trouble in breastfeeding,
dental caries malocclusion, gingival recession,
and restricted alveolar bone growth in
children. Mostly tongue tie presents as partial
ankyloglossia from tongue tip to base of
tongue.
Clinically acceptable, normal range of free
tongue  16 mm
Class I: Mild ankyloglossia = 12–16 mm
Class II: Moderate ankyloglossia = 8–11 mm
Class III: Severe ankyloglossia = 3–7 mm
Class IV: Complete ankyloglossia = <3 mm
Class I and II cases are self-correcting, thus
wait and watch along with speech therapy.
Class III and IV surgical therapies are desirable.
5. What is commissural oral pit and what
is its significance?
The commissural lip pit is a relatively common
developmental disorder, although there is
disagreement concerning its incidence. The
commissural lip pit may be bilateral or
unilateral. Unilateral pits occur as often on the
right as on the left side of the mouth. The pits
are located at the angles of the mouth, with the
tracts diverging dorsolaterally into the cheek.
They range in size from a shallow dimple to a
tract measuring 4 mm in length, and the tissue
is slightly raised around the opening. On
Developmental Disturbances, Physical and Chemical Injuries to the Oral Cavity 133
6. What is caliber-persistent artery? • Nontoxic thyroid enlargement in a person

A caliber-persistent artery is a common vas- with blepharochalasis, recurring edema of
cular anomaly in which a main arterial branch the upper eyelid leads to sagging of the lid
extends up to the superficial submucosal at the outer canthus of the eye.
tissues without a reduction in its diameter. This drooping may be severe enough to
Similar to oral varices, caliber-persistent interfere with vision. Both the double lip and
arteries are seen more frequently in older blepharochalasis usually occur abruptly and
adults. This suggests that their development simultaneously, but in some cases they develop
may be an age-related degenerative pheno- more gradually. The nontoxic thyroid enlarge-
menon in which there is a loss of tone in the ment occurs in as many as 50% of patients with
surrounding supporting connective tissue. Ascher’s syndrome and may be mild in degree.
The caliber-persistent artery occurs almost The cause of Ascher’s syndrome is not certain
exclusively on the lip mucosa. Either lip may autosomal dominant inheritance has been
be affected, or some patients have bilateral suggested in some cases.
lesions or lesions on both lips. The average
patient age is 58 years and the gender ratio is 9. In which conditions double chin appear-
nearly equal. The lesion presents as a linear, ance seen?
arcuate or papular elevation that ranges from Genetic predisposition for same, submental
pale to normal to bluish in colour. Stretching space infection often produces a swelling
the lip usually causes the artery to become below chin giving double chin appearance.
inconspicuous. The unique feature is pulsation— Inframyloid variety of dermoid cyst, achondro-
not only vertically but also in a lateral direction. genesis, adipose tissue distribution with
However, usually it is not possible to feel a familial partial lipodystrophy, in the treatment
pulse in a caliber-persistent artery with gloved of Cl III in surgical orthodontics setting back
fingers. The lesion is usually asymptomatic of chin often leads to drooping of soft tissues
being discovered as an incidental finding and with hyperactivity of mentalis muscle
during an oral examination, rarely a patient leads to double chin appearance.
may notice a pulsatile lip nodule. A few cases
have been associated with ulceration of the 10. What is retrocuspid papilla?
overlying mucosa. In addition, a couple of It is a fibroepithelial pink papulae (less than
examples have been found adjacent to labial 5 mm in diameter) on attached gingival usually
squamous cell carcinomas, although this is bilaterally lingual to mandibular canines.
probably coincidental. The prevalence in 25% to 99% in children and
The ulcer is attributed to continual pulsation young adults and drops to 6% to 19% in older
from the large artery running parallel to the adults suggesting that it is a normal anatomic
surface. Ligation of artery appears successful. variation disappears with age.
7. What are ectopic lymphoid tissue?
Lymphoid tissue appears yellow or yellow-
white with dome-shaped elevations, asympto-
matic. Ectopic locations are posterolateral
aspect of tongue (lingual tonsil), soft palate,
floor of mouth and tonsillar pillars.
8. What is Ascher’s syndrome?
Ascher syndrome is characterized by a triad at
features:
• Double lip
• Blepharochalasis
11. What are clinical presentations of

fissured tongue?
Three presentations are commonly seen:
1. A prominent median groove as a sole mani-
festation
2. A prominent median groove with accessory
grooves radiating laterally at right angles
to the median groove
3. Multiple grooves arranged in irregular
circinate pattern
12. What is Cupid’s bow lip?
Developmental disorder of lip exhibiting
double lip appearance. The lip is divided into
two by horizontal fissure. However, it is not
prominent when lip is in relaxed position.
Involved upper lip is tensed, the double lip
resembles “Cupid’s bow’’.
13. What is protostylid?
A protostylid is a supernumerary cusp located
on the mesial half of the buccal surface on the
upper and lower molars. These may be seen on
primary molars and permanent molars. They
are more common on primary molars.
14. What are nonmetric dental traits? 16. What is Stafne’s bone cyst? What are the
Cusp of Carabelli, protostylid, central accessory other names of it?
cusp, variations in the cusp number and Stafne’s bone defects are usually presented as
number of roots are all termed “nonmetric asymptomatic radiolucency below mandibular
dental traits”. The nonmetric features are canal between molar teeth and angle of
recorded visually in terms of presence, mandible. These defects are static in nature
absence, degree of development or expression containing ectopic salivary tissue. These are
of these features. incidentally found on radiographs. These may
be unilateral occasionally bilateral, sometimes
15. What are different variations in cuspal in anterior mandible and even in ramus con-
morphology of teeth? taining portion of parotid. The two proposed
1. Cusp of Carabelli: It is an accessory cusp mechanisms are:
located on the palatal surface of the mesio- 1. Failure of normal bone formerly
palatal cusp of maxillary molar. More occupied by cartilage
prominent on first molar and then less 2. Localised pressure atrophy of adjacent
prominent on second and third molars. It is surface of salivary gland.
seen in permanent and deciduous dentition.
The form may vary from a definite cusp to The other names are Stafne’s bone defects,
small intended pit and fissure. Protostylid Stafne’s bone cavities, static bone cyst, pseudo-
is analogous accessory cusp on mandibular cyst, lingual mandibular defect, and lingual
deciduous or permanent molars. salivary gland depression.
2. Talon’s cusp: It is a well-delineated additio-
nal cusp that is located on the surface of an
anterior tooth and extends at least half the
distance from cementoenamel junction to
incisal edge. It is common on lingual sur-
faces of lateral incisors and central incisors.
Rarely facial talons are also seen. These may
seen in association with Rubinstein-Taybi
syndrome, Mohr syndrome, Ellis-van
Creveld syndrome, and even in Sturge-
Weber’s syndrome.
3. Dens evaginatus: It is a cusp like elevation
of enamel located on the central groove or
lingual ridge of the buccal cusp of premolar
or molar teeth. It is also called central
tubercle, occlusal pearl, Leong’s premolar
(tuberculated premolar) frequently, it is
seen in association with shovel-shaped
incisors, affected incisors demonstrate
prominent lateral margins, creating a
hollowed lingual surface that resembles
scoop of shovel. Typically the thickened
marginal ridge converge at cingulum.
Maxillary lateral and central incisors most
commonly affected.
17. What are different types of amelogenesis affected teeth. However, if the two teeth are not
imperfecta? equally affected, the score for the less affected
It is the term applied to number of rare geneti- tooth is recorded. When teeth are scored; the
cally disorders of enamel formation which examiner should start at the higher end of the
affect both primary and permanent dentition, index, and eliminate each score or category
without any systemic disturbances. There are until he or she arrives at the present condition.
three major types: Hypoplastic, hypocalcified, If there is any doubt, the lower score should be
hypomaturation. However, Witkop described recorded.
fourth type as amelogenesis imperfecta with Normal (0): The enamel represents the usual
taurodontism. translucent semivitriform type of structure.
The surface is smooth, glossy, and usually of a
Hypoplastic pale, creamy white colour.
This is due to defects in the secretary process Questionable (0.5): The enamel discloses slight
of ameloblasts resulting in thin or pitted aberrations from the translucency of normal
enamel. Thin enamel of normal calcification. enamel, ranging from a few white specks to
It varies from localized pitting of enamel to a occasional white spots. This classification is
general diminution of enamel formation with used in those instances where a definite
lack of interproximal contacts. diagnosis of the mildest form of fluorosis is not
warranted and a classification of ‘normal’ not
Hypocalcified Type justified.
This is due to inability of crystallites to nucleate Very mild (1.0): Small, opaque, paper white
properly causing abnormal crystallite growth areas scattered irregularly over the tooth, but
and decreased mineral enamel content. not involving as much as approximately 25%
Enamel is of normal thickness but with low of tooth surface. Frequently included in this
radiodensity, low mineral content, and is classification are teeth, showing not more than
therefore soft and quickly lost exposing the or about 1–2 mm of white opacity at the tip of
dentine. It shows great variability and enamel the summit of the cusps of bicuspid or second
of cervical portion of teeth may be highly molars.
mineralized. Mild (2.0): The white opaque areas in the
enamel of teeth are more extensive, but do not
Hypomaturation Type involve as much as 50% of tooth.
Normal amounts of enamel matrix that is Moderate (3.0): All enamel surfaces of the teeth
deficiently mineralized. Enamel is as radio- are affected and subject to attrition show
dense as dentine and has a characteristic wear. Brown stain is frequently a disfiguring
mottled brown, yellow-white appearance, and feature.
easily chips away from dentine. Snow capped
Severe (4.0): All enamel surfaces of the teeth
teeth are variations which show varying
are affected and hypoplasia is so marked that
proportions of incisal and occlusal aspects of
the general form of the tooth may be affected.
crowns, have an opaque white appearance.
The major diagnostic sign of this classification
18. What is Dean’s fluorosis index? is discrete or confluent pitting. Brown stains
Dean’s fluorosis index modified criteria are widespread and teeth often present a
(1942): Classification criteria corroded-like appearance.
Procedure 19. What are hypodontia and oligodontia?
To obtain Dean’s fluorosis index, the Hypodontia—a commonly used term to
examiner’s recording is based on the two most describe the absence of one to six teeth and is
most common dental developmental anomalies eruption, malformed teeth, early exfoliation
in human. The absence of more than six teeth and noninflammatory gingival enlargement.
excluding third molars, is called ‘oligodontia’. It This is seen in both dentition with little female
is also called ‘severe hypodontia’. Oligodontia predominance. Their shape is markedly
is usually a part of syndrome, and seldom seen altered, being generally very irregular in
as an isolated entity. These are classified as appearance, often with evidence of defective
isolated (non-syndromic) or syndromic mineralization. Pulpal necrosis is common due
hypodontia or oligodontia. to long pulpal horns and clefts in dentin.
20. What are the other symptoms associated Radiographic Features
with hypodontia and oligodontia? The radiographs are uniquely characteristic,
Dental malposition, periodontal damage, lack showing a marked reduction in radiodensity
of alveolar bone height, esthetic and functional so that the teeth assume a ‘ghost’ appearance.
impairment are well-known symptoms. Both the enamel and dentin appear very thin
21. What are the syndromes associated with and the pulp chamber is exceedingly large. The
hypodontia and oligodontia? enamel and dentin layer often is not evident.
Short roots and open apices are seen.
Ectodermal dysplasia, Down’s syndrome,
Ellis-van Crevald syndrome, cleft lip and 24. What are shell teeth?
palate, hemifacial microsomia, Van der Woude Dentinogenesis imperfecta type II is called
syndrome. shell teeth. Shell teeth demonstrate normal
22. When tooth is called congenitally thickness enamel in association with extremely
missing tooth? thin dentin and dramatically enlarged pulps.
The thin dentin may involve the entire tooth
Congenitally missing teeth are defined as those
or be isolated to the root. This rare abnormality
teeth that fail to erupt in oral cavity and remain
has been seen most frequently in deciduous
invisible in the radiograph, there is no previous
teeth in the presence of dentinogenesis imper-
history of extraction or trauma which implies
fecta. The alteration may be unassociated with
that this is caused by disturbances during the
dentinogenesis imperfecta as an isolated
early stages of tooth development.
finding in both dentitions and demonstrate
23. What are ghost teeth? normal tooth shape, coloration, a negative
This is an unusual, uncommon, nonhereditary, family history, and diffuse involvement. In the
developmental dental anomaly in which one isolated variant slow but progressive root
or several teeth in a localized area are affected resorption occurs.
in an unusual manner (i.e. extensive adverse 25. What are the other names of dentino-
effects on formation of enamel, dentin and genesis imperfecta?
pulp). Apparently the maxillary teeth are
Hereditary opalescent dentin, Capdepont’s
involved more frequently than the mandibular,
teeth.
the most frequently affected teeth being the
maxillary permanent central incisor, lateral 26. Enumerate the conditions in which
incisor, and cuspid. In the mandible, the same enlarged pulp chambers are seen.
three anterior teeth are most often affected. Regional odontodysplasia, dentinogenesis
Ipsilateral involvement of both arches and bila- imperfecta, taurodontism and trichodento-
teral changes in same jaw have been reported. osseous syndrome.
Clinical Features 27. What is abfraction?
The ghost teeth (regional odontodysplasia) The term abfraction derived from the Latin
exhibit either a delay or a total failure in verb frangere. Fregi, fractum (to break) is used
to describe a special form of wedge-shaped 28. What is meth mouth?

defect at the cementoenamel junction (CEJ) of Methamphetamine is central nervous system
a tooth (2). Such lesions observed on a single stimulant. A very common and visible sign of
tooth or on non-adjacent teeth are hypothesized long-term meth use is extreme tooth decay also
to be the result of eccentrically applied occlusal known as meth mouth. Users with meth
forces, leading to tooth flexure rather than to mouths have often blackened, attrition, cracks,
be the result of abrasion alone abfraction, erosion, stained and rotting teeth that often
appears as wedge-shaped defects limited to the cannot be saved. Meth damages blood vessels
cervical area of the teeth, and may closely and decreases blood flow to all parts of body.
resemble cervical abrasion or erosion. Clues to Meth users have xerostomia or meth mouth.
the diagnosis include defects that are deep,
narrow, and V-shaped (which do not allow the 29. What is myospherulosis?
toothbrush to contact the base of the defect), It is also called paraffinoma. It is a unique
and often affect a single tooth with adjacent foreign body reaction which results from
unaffected teeth. placement of topical antibiotic in a petroleum
In addition, occasional lesions are sub- base in surgical site. It is an inflammatory
gingival, a site typically protected from abra- granulomatous lesion resulting from the action
sion and erosion. The lesions are seen almost of lips substances on extravasted arythrocytes.
exclusively on the facial surface and exhibit It may occur in soft tissue or bone and para-
a much greater prevalence in those with nasal sinuses. The area is asymptomatic and
bruxism. A higher frequency is noted in the may show swelling and radiographically
mandibular dentition, presumably because circumscribed radiolucency in extraction site.
the lingual orientation makes them more It is treated by surgical removal of foreign
susceptible to the concentration of tensile material and affected tissue.
stresses at the cervical regions.
30. Enumerate the conditions causing

palatal perforations.
Palatal perforation can be defined as a com-
munication between the nasal cavities and the
oral cavity.
1. Developmental conditions: During the
sixth week of prenatal period, palatal
shelve coalescence to form the hard palate.
Failure to this integration results in cleft
palate. Some syndromes, maternal alcohol
consumption and cigarette smoking, folic in his/her palate. Due to bone resorption
acid deficiency, corticosteroid use and anti- a previously impacted canine may emerge
convulsant therapy are some causative in the form of a palatal perforation. An
agents for this abnormality. orthopantomograph can easily reveal the
2. Infectious: There are some infections result- impacted tooth.
ing in palatal perforation. In leprosy, tertiary 31. What are the lesions associated with
syphilis, tuberculosis, rhinoscleroderma, electrogalvanism?
naso-oral blastomycosis, leishmaniasis,
Oral galvanism observed in persons having
actinomycosis, histoplasmosis, coccidiomy-
metal fillings of diverse electrical potentials in
cosis and diphtheria. The palatal roof may
teeth that are either next to each other or oppo-
be perforated.
site to each other. Saliva serves as conductor
3. Autoimmune: There are some autoimmune through which mild conductor passes and
diseases which results in palatal perfora- creating an appropriate environment for ion
tion. Examples are lupus erythematous, exchange, this causes electrogalvanism and
sarcoidosis, Crohn’s disease and Wegener’s electric current. This may result in pain that can
granulomatosis. be reduced by applying varnish. It is called
4. Neoplastic: Many tumors can extend from galvanic keratosis, it is due to weak electric
maxillary sinus or nasal cavity and per- current from dissimilar restorative metal, non-
forate the palate. Although these neoplasms scrapable lesion disappears on removal of
usually form a mass, but in advance cases restorations.
perforation of palate may occur in course
Electrogalvanic lesions consist of chronic
of disease or even following treatment.
gray patches or ulcerations at the site of two
Minor salivary gland malignancy adenoid
dissimilar metallic dentures.
cystic carcinoma is reported to cause palatal
perforation. Other malignancies like nasal Electrogalvanic or mercury contact allergy
T-cell lymphomas, carcinoma, melanoma, perhaps should be considered an entity
etc. separate from leukoplakia. The two types of
clinical lesions that a microgalvanic current
5. Drug related: Palatal perforation due to
from dissimilar metal restorations can produce
cocaine abuse is a well-known situation.
on adjacent gingivae, tongue, or buccal
Other drugs (heroine, narcotics) can be
mucosa are: (1) Keratotic plaque lesions like
responsible for palatal perforation.
leukoplakia, and (2) a variation that mimics LP.
6. Iatrogenic: Sometimes following a tooth
Electrogalvanism has been found to be
extraction an oroantral fistula remains.
associated with carcinoma cases developed
Other procedures such as tumor surgery
from oral leukoplakia, glossodynia.
(maxillectomy), corrective surgeries (e.g.
septoplasty) or intubation can cause palatal 32. What are the injuries likely to happen
perforation. with the misuse of cotton in oral cavity?
7. Traumatic origin: Case reported with ani- 1. Cotton roll stomatitis (cotton roll burn,
mal injury, ingestion of hot foods (thermal cotton roll ulcer, cotton roll injury): Cotton
injury). Tantrum oris. rolls are used during restorative and endo-
8. Miscellaneous: Midline nonhealing granu- dontic procedures. Oral mucosa can adhere
loma. Rhinolith can result in palatal perfora- to dry cotton rolls, and rapid removal of the
tion. Patients with psychologic problems rolls from the mouth often can cause stripp-
may present with a fictitious palatal per- ing of the epithelium in the area. Clinically,
foration. Sometimes an elderly edentolous the lesions appear as painful erosions
denture wearer complains of a perforation covered with a whitish pseudomembrane
and may heal within 4–6 days. Clinically, it 2. Lesion on tongue: Oral lesions also can
is similar to acetylsalicylic acid burns. occur from performing cunnilingus,
2. Mucosal injury: Caustic materials (e.g. resulting in horizontal ulcerations of the
sodium hypochlorite) can leak into the lingua frenum. As the tongue is thrust
cotton roll and be held in place against the forward, the taut frenum rubs or rakes
mucosa for an extended period, with across the incisal edges of the mandibular
mucosal injury resulting from the chemical central incisors. The ulceration created
absorbed by the cotton. The affected mucosa coincides with sharp tooth edges when the
may be red and painful with superficial tongue is in its most forward position. The
erosions and heals spontaneously within lesions resolve in 7 to 10 days but may recur
4–6 days. The use of the rubber dam can with repeated performances. Linear fibrous
dramatically reduce iatrogenic mucosal hyperplasia has been discovered in the
burns. same pattern in individuals who chronically
perform the act.
33. What are oral lesions associated with
3. HSV: HSV1 is common in pharynx and
orogenital sexual practices?
intraoral sites, while HSV2 is common in
The orogenital sexual practices are common, genital area and skin below the waist. The
although these are considered illegal in many changing sexual practices have made both
jurisdictions. These acts are almost universal lesions common in oral cavity and below
amongst homosexual males and females. waist.
Even though the frequency of orogenital
4. Gonococcal pharyngitis: More common in
sexual practices is as high as 90% in married
male homosexuals and lesions show mixture
heterosexual couples especially younger age,
of signs of inflammation, edema, vesicula-
the frequency of associated traumatic oral
tion, ulceration, and pseudomembranes.
lesions is surprisingly low.
5. HPV associated oral and oropharyngeal
Clinical Features cancers: These may be seen in frequent
1. Lesions on palate: It is the most common sexual and orogenital sexual contact
lesion. This lesion is described as sub- especially in younger patients who are non-
mucosal palatal hemorrhage secondary to smokers.
fellatio. The lesions appear as erythema, 6. Molluscum contagiosum: To oral partner
petechiae, purpura or ecchymosis of the soft in orogenital sex.
palate. The areas are often asymptomatic No treatment is required, and the prognosis
and resolve without treatment in 7 to 10 days. is good. Palatal petechiae can be prevented
Recurrences are possible with repetition of through the use of less negative pressure and
the inciting (exciting) event. The erythro- avoidance of forceful thrusting and abstinence
cytic extravasation is thought to result from of act. Smoothing and polishing the rough
the musculature of the soft palate elevating incisal edges of the adjacent mandibular teeth
and tensing against an environment of can minimize the chance of lingual frenum
negative pressure. ulceration.
8
Systemic Manifestations in Oral
Cavity and Traumatic Lesion
1. Define oral medicine. of pain is referred to as ‘fifth vital sign’.

It may be defined as a branch of dentistry that However, some authors do recommend ECG,
deals with the relationship between oral and oxygen saturation and tobacco use as fifth vital
systemic diseases and also with the diseases sign. These are taken daily or only once in a
that are not manifested orally week. However, in critically ill-patients the
or machines are attached.
It is the specialty of dentistry that is con- 3. What is evidence-based dentistry?
cerned with the oral health care of medically
American Dentist Association (ADA) defines
compromised patient and with the diagnosis
it as an approach to oral health care that
and nonsurgical management of medically
requires the judicious integration of systematic
related disorders or conditions affecting the
assessment of clinically relevant scientific
oral and maxillofacial region
evidences, relating the patient’s oral and
or
medical conditions and, history with the
Oral medicine is that specialty of dentistry
dentist’s clinical expertise, and the patient’s
concerned with the basic diagnostic pro-
treatment needs and preferences.
cedures and techniques useful in recognizing
the disease of the oral tissues of local and 4. Enumerate pregnancy associated oral
constitutional origin, and their medical and paraoral changes.
management. The degree to which the associated changes
2. What are vital signs? Enumerate various occur is partly related to the previous health
vital signs. Which is fifth vital sign? and the effectiveness of preventive procedures
Vital signs represent the real significance of life. performed by pregnant woman.
It can be defined as body’s physiological status 1. Caries, gingivitis, and periodontal disease:
and provide information critical to evaluating Tooth mobility is associated with increased
homeostatic balance. Temperature, pulse, hormone levels when it is not associated
respiratory rate along with blood pressure with periodontitis, the condition is reversible.
reading are known as vital signs. Assessment 2. Xerostomia.
141
3. Enamel erosion: May be seen when gastric

acids present in the vomitus may erode the
lingual surfaces of anterior teeth. Most
common in first trimester.
4. Pregnancy-induced gingivitis: Increase in
metabolism of estrogens by gingival may
increase sensitivity to local irritants like
plaque and food debris causing inflamma-
tion. Increased synthesis of prostaglandins
results sensitivity to inflammation. 7. Emerging evidence has shown that
5. Pregnancy tumor: Granuloma gravidum periodontal disease may be associated with
usually develops in second trimester preterm, low birth weight (LBW) babies.
resolves after delivery. Histologically, 8. Recurrent aphthae may stop or even
pyogenic granuloma closely resembles. It become severe during pregnancy.
occurs on gingiva, lips, tongue, and buccal 5. What are the causes of premature loss of
mucosa. It is seen commonly on facial teeth?
aspects of upper anterior teeth, excision not
Trauma (avulsed teeth), aggressive periodontitis
needed unless it impedes mastication or
(premature alveolar bone loss), acrodyania,
hinders routine dental care.
immunocompromised states (AIDS, leukemia,
6. Chloasma gravidarum is the tanned mask
chemotherapy), diabetes, especially juvenile
seen on the cheeks, nose, and infraorbital
onset (increased susceptibility of infection and
areas of pregnant, light-skinned women
severity of periodontitis), osteomyelitis (bone
during the latter half of pregnancy. It is
destruction, loosening of teeth), cyclic or
occasionally accompanied by a diffuse
chronic neutropenia (increased susceptibility
browning of the oral mucosa. The pigmen-
to infection, premature bone loss), Langerhans
tation slowly disappears after delivery. The
cell histiocytosis (premature alveolar bone
increased level of adrenocorticotropic
loss), dentin dysplasia type 1 (rootless teeth),
hormone (ACTH) during pregnancy is
regional odontodysplasia (ghost teeth),
thought to account for the increased
Papillon-Lefèvre syndrome (premature peri-
melanocyte activity.
odontitis), Down’s syndrome (premature peri-
odontitits), hypophosphatasia (lack of ementum
production), scurvy (vitamin C deficiency),
Ehlers-Danlos syndrome, agranulocytosis.
In teenagers it is indication of underlying
destructive process of bone, leukemia, histo-
cytosis X or benign neoplasm.
6. What is halitosis? Enumerate the diffe-
rent causes of halitosis.
Halitosis is a term used to describe a noticeably
unpleasant odour exhaled in breathing. The
other names are fetor oris, breath malodour,
foul breath. The cause may be oral/non-oral.
Oral malodour is the term used to describe
odour from the oral cavity. It is classified
as genuine halitosis, pseudohalitosis and
halitophobia. Pseudohalitosis is the condition
Systemic Manifestations in Oral Cavity and Traumatic Lesion 143
Not associated with disease Associated with disease

Morning breath Oral/paraoral structure: Periodontal disease, xerostomia
Medications, mouth breathing (associated with underlying disease), gingivitis, stomatitis,
Aging, poor denture hygiene glossitis, cancer, candidiasis, parotitis
Fasting/starvation GI disorders
Tobacco, foods like onion, garlic, Gastro-esophageal reflux, hiatus hernia, cancer
meats, alcohol Nasal
Rhinitis, sinusitis, tumors, foreign bodies
Pulmonary bronchitis, pneumonia, TB, cancer
Psychiatric
Delusions
Other causes
Diabetes, uraemia, hepatic disease, blood dyscrasias,
rheumatologic diseases, dehydration, and fever, etc.
where malodour is not perceived by others but variable number of fungiform papillae of
patient always complains of its existence. tongue. It is also called lie bumps, tongue
Halitophobia is psychosomatic halitosis or torches. The suggested causes are local
imaginary bad breath associated with irritation, stress, GIT diseases, hormonal
psychiatric disorder. fluctuation, URTI, viral infection, topical
From oral cavity: Poor oral hygiene, hypersensitivity to foods, and drinks or oral
poor hygiene of prosthesis, oral infection hygienic products.
(candidiasis, pericoronitis, dry socket), oral
Three patterns have been documented.
ulcerative/erosive lesions
Nasal cavity: Nasal infections, polyps, 1. It is localized and involves one to several
sinusitis. Dietary considerations—volatile fungiform papillae that become enlarged
sulphur containing foods (garlics, onions), and present as elevated papules that are
hydrogen sulphide red, may demonstartae yellow ulcerated
cap. These are common on anterior portion
Salivary gland: Xerostomia
of tongue, with mild to moderate pain
Obstruction of airflow: Tonsils, infections
resolves spontaneously within hours to
Systemic diseases: Bronchial/pulmonary week.
infection, renal failure.
2. Involvement is more generalized and
7. What is oral allergy syndrome? affects more papillae, tip, and lateral
Swelling of lips, tongue and palate, throat portion may be involved. Fever and cervical
along with oral pruritis and irritation, some- lymphadenopathy may be seen. Resolution
times associated with other allergic clinical in week, rarely recurrence.
features including rhino conjunctivitis, urticaria 3. More diffuse involvement. Papillae are
and even anaphylaxis has termed oral allergy asymptomatic, elevated white to yellow
syndrome. It seems to be precipitated by fresh papules called papulo keratotic variant.
foods including apples in people who have
been sensitized to cross-reacting allergens in 9. What are the different types of glossitis?
pollens particularly birch. What are Moeller’s glossitis and Hunter’s
8. What is lingual papillitis? What are the glossitis?
different patterns of it? Glossitis is a condition refer to an inflammation
Common disease in which affected individuals of the tongue; it may be caused by injury,
experience clinical alterations which involve infection, allergy reaction. All these causes can
be inducing glossitis with varying severity.

Bacterial or viral infections (including oral
herpes simplex).
Mechanical irritation or injury from burns,
rough edges to teeth or due to appliances, or
other trauma.
Exposure to irritants such as tobacco,
alcohol, hot food or spices.
Allergic reaction to toothpaste, mouthwash.
Disorders such as iron deficiency anemia,
pernicious anemia, and other vitamin B
deficiencies, oral syphilis and others.
Yeast infection, dry mouth associated with
connective tissue disorder, such as Sjögren
studies. Occasionally glossitis can be inherited.
Moeller’s and Hunter’s glossitis is used
to describe the condition associated with Bald tongue
vitamin B12 and pernicious anemia.
11. What is chloroma?
10. Describe various changes occurring in It is granulocytic sarcoma and called chloroma.
tongue in various anemias. Granulocytic sarcomas are composed of a
localized collection of immature myeloid cells
Iron deficiency The tongue is often described as and are considered to be specific lesions of
anemia red and bald with glazed and dry AML or the onset of a blast crisis in chronic
appearance. The tongue may myelogenous leukemia (CML). Localization in
have waxy appearance and the oral cavity is rare. Granulocytic sarcoma
glossitis. was described for the first time by burns in
Pernicious Soreness, severe pain, itching or 1811. In 1873, the King dubbed ‘‘chloroma”
anemia burning of tongue. Atrophy of because of its green colour to the cut.
lingual papillae with some com-
plaining of painful glossitis. 12. What is Quincke’s disease?
Beefy red tongue is characteris- Angioedema or angioneurotic edema is also
tics. If the colour is less beefy red called Quincke’s disease. It is a diffuse
and surface is smooth, then indi- edematous swelling of the soft tissues that most
cations that pernicious anemia is commonly involves the subcutaneous and
disappearing or its mild form. submucosal connective tissues but may affect
Glossitis and atrophy of papillae gastrointestinal and respiratory tract to result
occur more common with perni- fatally. It is characterized by the relatively
cious anaemia and less often
rapid onset of soft, nontender tissue swelling,
with iron deficiency anemia.
which may be solitary or multiple.
Megaloblastic Initially the tongue is fissured/
anemia lobulated eventually becomes 13. What is Chvostek sign (Chvostek-Weiss
smooth flabby, atrophic. sign)?
Depapillated beefy red tongue It is given by Frantisek Chvostek in 1876. The
(Hunter’s glossitis/Moeller’s Chvostek sign is one of the signs of tetany seen
glossitis), altered sensation of
in hypocalcemia. It refers to an abnormal
tongue is characteristic.
reaction to the stimulation of the facial nerve.
Chvostek I phenomenon: Contracture of test may be seen in hypocalcemia and hypo-

facial muscles produced by tapping on the magnesemia. Occlusion of the brachial artery
facial nerve at a specific point which is located causes flexion of the wrist and metacarpo-
0.5 to 1 cm below the zygomatic process of the phalangeal joints, hyperextension of the fingers
temporal bone, 2 cm anterior to the ear lobe, and flexion of the thumb on the palm produc-
and on a line with the angle of mandible. ing the characteristic posture called main
Chvostek II phenomenon: It can be d’accoucheur.
produced by tapping on different location of The patients with positive Trousseau’s sign
the face. The point is located on the line joining may also experience paresthesia of fingers,
the zygomatic prominence and corner of muscular fasciculations or twitches of the
mouth, one-third of distance from the zygoma. fingers and a sensation of muscular cramping
In both instances the response is twitching or stiffness.
of the muscles supplied by facial nerve on 15. What is pathognomonic sign? What are
that side. This is because of hypocalcemia the different pathognomonic signs?
(i.e. from hypoparathyroidism, pseudohypo-
Pathognomonic (patho means disease, gnoma
parathyroidism, hypovitaminosis D) with
means signature, pathognomonic is signature
resultant hyperexcitability of nerves. Though
of the disease), especially distinctive or char-
classically described in hypocalcemia, this
acteristics sign of the disease or pathological
sign may also be encountered in respiratory
condition on which a diagnosis is made) or a
alkalosis, such as that seen in hyperventilation,
pathognomonic sign is a sign whose presence
rickets, diphtheria, measles, scarlet fever,
means that a particular disease is present be-
whooping cough, and myxedema.
yond doubt.
14. What is Trousseau’s sign? • Ptregyoid sign which is pathognomonic for
Named after Sir Armand Trousseau, a French TMJ pain origin. The examiner faces the
physician (1801–1867), it is a test for latent patient and to examine the right side faces
tetany in which carpal spasm is induced by the tip of little finger to the above and
inflating a sphygmomanometer cuff on the slightly behind maxillary tuberosity. If the
upper arm to a pressure exceeding systolic patient winces the sign is positive and same
blood pressure for 3 minutes. A positive is done for left side. It has been described
by Frost (1972).
• Pterygoid and greenstick fractures in
adults are almost pathognomonic for osteo-
malacia.
• Hemarthrosis for hemophilia.
• Exophthalmos for hyperthyroidism.
• Chvostek sign and Trousseau signs for
hypocalcemia.
• Subperiosteal erosions, especially of the
middle phalanges are almost pathogno-
monic for hyperparathyroidism, which are
the recalcitrant benign giant cell lesion of
the jaws.
• In fact, the maxillary enlargements resulting
in prominent cheek bones and anterior
displacement of the incisors produce a
characteristic “rodent” facies, which when
coupled with the sinus hypoplasia is • Pathognomonic sign for necrotizing fasciitis
pathognomonic of thalassemia. of head and neck dusky, purplish discolora-
• A round, radiopaque enlargement of the tion of skin, small purplish patches with
condyle with an anterior radiopaque ill-defined borders, necrosis of fascia, and
projection along the lateral pterygoid gangrene of overlying skin.
tendon. This radiographic picture is • Slight digital pressure on the periphery of
pathognomonic for an osteochondroma. a parulis may force a drop of pus from the
• Specifically the clinician should form a sinus opening and this is almost pathog-
strong impression of central hemangioma nomonic.
(CH) when encountering a pumping tooth • Oral lesions in varicella zoster are charac-
(a tooth that can be pushed apically and teristic and pathognomonic prodrome
then rebounds to its original position) or followed by unilateral vesicular eruptions
localized gingival bleeding around a loose soon ulcerates.
tooth coupled with radiographic evidence • Peutz-Jeghers syndrome shows perioral
of bony change in the region. This pigmentation.
impression may be further strengthened • Wash-leather slough on floor is pathogno-
when large quantities of blood are easily monic of gummatous ulcer.
aspirated from the area. • Slip sign in subcutaneous lipoma, the edges
• Soft, dark tooth structure that can be pene- are well-defined and when pressed away,
trated by dental explorer or sharp instru- it sleeps away.
ment clinically is pathognomonic sign for • The presence of oral and perioral gonor-
caries or tooth decay. rhea/syphillis is pathognomonic for sexual
• Hairy leukoplakia is almost pathogno- abuse.
monic for HIV. • The gingiva between teeth is missing or
• Pseudomembranes on tonsils, pharynx punched out is characteristic for ANUG.
and diphtheria are pathognomonic for
diphtheria. 16. What is prodromal symptom? Enumerate
various prodromal symptoms.
• Strawberry gums is red-puplish granular
gingivitis—a rare but pathognomonic sign A prodrome is an early symptom (or set of
of Wegener’s granulomatosis. symptoms) that might indicate the start of a
disease before specific symptoms occur or it
• Painful local rash for herpes zoster.
is a symptom that may be the first indication
• Measles show Koplik’s spot.
of disease. It is derived from Greek word pro-
• In the early vesicular stage, pathognomonic dromos which indicates forerunner of the event.
features include the ballooning of the
epithelial cells is pathognomonic for Neuralgia in the prodrome stage of zoster
intraoral herpes lesions. is followed by vesicles and ulcers similar in
appearance to those caused by herpes simplex.
• The presence of numerous neurofibromas
Because the lesions follow a nerve distribution,
or a plexiform type of neurofibroma is
they extend to the midline and stop.
characteristically pathognomonic for NF1
(neurofibromatosis 1 or von Reckling- Recurrent aphthous ulcers: These may
hausen’s disease. begin as prodromal burning, itching or string-
• The pathognomonic features, such as small ing 24 to 48 hours before the ulcer begins (little
purple or red flat papules on extensor symptoms).
surfaces, particularly the elbows and joints Mumps: They may have headache, chills,
of the hand (Gottron’s papules). These are moderate fever, pain below ear, which lasts for
pathognomonic for dermatomyositis. 1 week. The child usually has a nonproductive
cough, photophobia due to conjunctivitis, and diagnosis, therapy of diseases or for the
often a discharge or crusting around the eyes. modification of physiological function”.
This set of signs and symptoms is often called The author makes a distinction between an
the prodrome because it precedes any skin adverse effect (adverse outcome attributed to
rash. Oral lesions called ‘Koplik spots’ also an action of the drug), and an adverse event
appear during this prodrome and are (adverse outcome that occurs when a patient
pathognomonic of the disease. Koplik spots is on the drug but that may not be caused by
appear as flat, erythematous maculas with tiny the drug). An adverse drug event includes the
white “salt crystal” centres. following:
Primary herpes simplex infections: May be 1. Harm caused by a drug (commonly
preceded by fever, headache, nauseas, malaise known as adverse drug reaction)
and lymphadenopathy. These symptoms may 2. Harm caused by appropriate drug use
be useful to differentiate from vesiculobullous (usually referred to as a side-effect)
lesions of oral cavity. 3. Medication errors.
Secondary herpes (herpes labialis): May
show tingling, burning or pain at the site. These can be classified as:
Erythema multiforme lesions: May have 1. Salivary gland disorders: Xerostomia,
fever, headache, general malaise. ptyalism, salivary gland pain, discoloration
Dermatitis herpetiformis: May have of saliva.
burning sensation before the lesion occurred. 2. Oral ulceration: Nonspecific ulcerations,
Acute radiation syndrome: May have aphthous ulcerations, fixed drug eruptions,
anorexia, nausea, vomiting, diarrhoea, weak- mucositis, pemphigoid like reactions,
ness, fatigue. pemphigus, erythema multiforme, lupoid
Rubella: May have Forchheimer‘s sign reactions.
which refers to an enanthem of red macules 3. Oral malodor
or petechiae confined to the soft palate in 4. White lesions: Lichenoid reactions, oral
one-fifth of patients. candidiasis, black hairy tongue
Syncope: May not have prodormal 5. Taste ulcerations
symptoms. 6. Mucosal pigmentation
17. What is adverse drug reaction? What are 7. Teeth discoloration
the various manifestations of adverse 8. Swellings: Gingival and mucosal swellings.
drug reactions in the oral cavity?
An adverse drug reaction is defined by 18. Enumerate various drug associated oral
Edwards and Aronson in 2000 as “an lesions.
appreciably harmful or unpleasant reaction, Common reactions produced in the oral cavity
resulting from an intervention related to the are stomatitis, ulceration, necrosis, hemorrhage,
use of a medicinal product, which predicts gingival hyperplasia, pigmentation, altered
hazard from future administration and salivary function and altered taste sensation.
warrants prevention or specific treatment The most common allergic reaction is
or alteration of the dosage regimen or erythema multiforme producing ulcers in
withdrawal of the product.” mouth with pain and discomfort. Followed by
or anaphylactic stomatitis, intraoral fixed drug
An adverse drug reaction is defined by reactions, lichenoid drug reactions, and lupus
WHO as “a response to a drug which is noxious erythematous like eruptions, pemphigus
and unintended, and which occurs at doses like eruptions and nonspecific like vesi-
normally used in man for the prophylaxis, culoulcerative lesions. Stevens-Johnson’s
syndrome, toxic epidermal necrolysis, Inedentulous individuals, the mylohyoid

medication-induced mucositis. ridge, and the crestal bone are the more com-
A number of different medications cause monly affected sites, apparently because of
oral mucosal lesions that do not appear to be denture pressure. In dentate areas, any of the
allergic reactions but rather represent a toxic teeth may be involved in what will look like
side-effect of the medication. These mucosal advanced periodontal disease.
lesions can present as nonspecific ulcers, Clinically, contact drug reactions produce a
erosions or may resemble erosive lichen soft, spongy, red attached gingiva. They may
planus. They do not necessarily appear also affect to a lesser degree the labial mucosa,
immediately after the patient begins taking the tongue, and commissures. The gingiva and
medication. tongue are reported to have a dull, burning
Some drugs become bound to cell mem- sensation.
branes in one or many organs as part of their 19. What are morbilliform drug reactions?
mechanism of action or their elimination. If, These are also called maculopapular or
through sensitization, the drug has stimulated exanthematous drug reactions. Symmetric
antibody production by the coupling of anti- erythematous macules/papules which may
body to the antigen fixed to the cell membrane, become confluent. Oral mucosa may show
the drug in question may cause cell lysis. This erythema or lichenoid damage. These are seen
type of reaction, which may be very severe from less than week after starting treatment
and cause extensive tissue destruction, is until several weeks after discontinuation of
thought to be the mechanism responsible for drug. Topical steroids and antihistaminics
erythema multiforme and, although less may be used. The most common drugs are anti-
severe, so called lichenoid drug reaction. It has biotics, antiepilectics, allopurinol, NSAIDs,
been known to produce a hemolytic anemia antianxiolytics, antihypertensives, diuretics.
when the drug is fixed to red blood cell Generalised morbilliform reactions are com-
membranes. mon with ampicillin and amoxicillin. Viral
While any drug can cause a systemic drug infections may increase the incidence. It
reaction, some drugs historically have is tenfold common in HIV patients. This is
produced a higher incidence than others. The often the initial presentation of more serious
following substances have the highest reactions including toxic epidermal necrolysis,
incidence of these reactions: hypersensitivity syndrome, and serum
1. Levothyroxine sodium sickness.
2. Gold salts 20. What are fixed drug eruptions?
3. Allopurinol This is peculiar phenomenon whereby one or
4. Colchicine more inflammatory patches appear at the same
5. Methyldopa cutaneous or mucosal site on each occasion that
6. Nifedipine (procardia) the patient ingests a culprit drug. The time may
vary from 2 to 24 hours. Common sites are geni-
7. Penicillin (particularly ampicillin)
talia, torso, hands, feet, face, and intertriginous
8. Codeine areas, i.e. axilla and groin. Common drugs are
9. Propranolol. NSAIDs, tetracyclines, chlorpromazine, and
Patients with drug-induced avascular calcium channel blockers, sulfonamides,
necrosis of bone will present with exposed barbiturates, analgin, and chlorhexidine.
white- or yellow-colored bone, either in the The oral lesions appear as localized areas
maxilla or the mandible that is obviously of erythema and edema commonly seen on
nonvital. labial mucosa and can later develop into
vesiculoulcerative lesion even mouth ulcera- although the roots of developing teeth are
tions and post-inflammatory pigmentation. stained dark black. The dental discoloration
It can be seen as manifestations of oral remains (because of the extensive involvement
hypersensitivity reaction. Primary treatment is of dentin) even though the cutaneous staining
withdrawal of the drug and avoidance in fades, after the discontinuation of medication,
future. Potent topical corticosteroids may be 1. Atropine, antidepressants, antihistaminics,
given to avoid further complications and post- opioid analgesics can cause reduced
inflammatory pigmentation. salivary flow and may be causative factor
The third generation antihistamine levo- for carious destruction, the most common
cetirizine was reported in a case of FDE involv- tooth discoloration.
ing the oral (lower lip and tongue), and genital 2. Sucrose containing oral medication such as
tissues (glans penis). Use of acetaminophen cough syrups or nutritional supplements
was reported to result in erythematous and can cause caries.
papular FDEs on the hard palate and skin; 3. Tetracycline in the affected teeth can cause
naproxen and oxicams have caused lesions on bright yellow to dark brown discolorations
the lips and fluconazole has caused lesions of and, in UV light showing a bright yellow
the palatal mucosa and oral bullae. fluorescence.
4. Chlortetracycline causes gray-brown dis-
21. Enumerate drug-induced oral reactions. coloration and oxytetracycline causes
These reactions are: yellow.
Hyposalivation/xerostomia, lichenoid reaction/ 5. Minocycline hydrochloride appears to bind
lichen planus, aphthous-like ulcers, bullous preferentially to certain types of collagenous
disorders, pigmentation, fibrovascular hyper- tissues (e.g. dental pulp, dentin, bone, etc.).
plasia, keratosis/epithelial hyperplasia, Once in these tissues, oxidation occurs and
dysesthesia, osteonecrosis of the jaws, infec- may produce the distinctive discoloration.
tion, angioedema, and malignancy. Additionally blue-gray appearance on
palate or anterior alveolar mucosa that
22. Name the different medications associa-
represents the black bone showing through
ted with tooth discoloration.
the thin, translucent oral mucosa.
Clinically evident tooth discolorations can be 6. Chlorhexidine gluconate, liquid prepara-
seen due to different medications that become tions of iron salts and some antibiotics in
incorporated into the developing tooth. The liquid form and essential oils can cause
severity of the alterations is dependent on extrinsic staining.
three factors, i.e. the time of administration, the
7. Fluoride causes intrinsic staining.
dose and the duration of the drug’s use. The
discolorations may be in the form of white spots, Suggested aesthetic solutions include
yellow to dark brown and gray generalised restorations, full crowns, external bleaching of
discoloration. These stains may be extrinsic vital teeth, internal bleaching of nonvital teeth,
and intrinsic. The other effects of drugs on teeth bonded restorations, composite build-ups, and
include physical alteration of tooth structure laminate veneer crowns.
and changes in tooth sensations. 23. What are oral manifestations of renal
Several patterns of staining are noted in the disease?
dentition. Fully erupted teeth typically reveal Ammonia like taste and smell, stomatitis,
a blue-gray discoloration of the incisal, three- gingivitis, decrease in salivary flow, xerosto-
fourths with the middle one-third being maxi- mia, parotitis. Early symptom and particularly
mally involved. The exposed roots of erupted in morning. Uremic fetor and ammonical
teeth demonstrate a dark green discoloration, odor is due to high concentration of urea in
the saliva and is subsequent breakdown to Uremic Frost

ammonia. Salivary urea levels may correlate White plaques occasionally on skin and rarely
well to BUN, but no fixed relationship. Uremic on oral mucosa. Residual area crystals left on
stomatitis. It occurs BUN level >150 mg/dl. skin after perspiration evaporates/decreased
Resolves with medical treatment. It is regarded salivary flow.
as chemical burn or general loss of tissue
resistance and inability to withstand normal/ 24. What are care oral health considerations
traumatic influences. Erythemopultaceous in renal disesaes?
form—red mucosa covered by thick exudate Elective dental care should be deferred until
and pseudomembrane. Ulcerative form—frank recovery. No contraindications if peritoneal
ulcerations with redness and a pultaceous dialysis. During surgery meticulous technique
coat. should be followed. Wound by primary closure
and use of local hemostatic aids (cellulose).
Elective procedures should be done on
nondialysis days, avoid on dialysis day.
Timing early in the dialysis cycle. Use of arm
on arteriovenous site I/M, I/V injections
should be avoided and BP checking should be
avoided. Avoid sitting, permit walking during
long procedures.
25. Which are the drugs avoided in renal
diseases?
Steroids, tetracyclines and nonsteroidal anti-
inflammatory agents, and aminogylcoside.
26. What care should be taken while manag-
ing the patients with renal failure,
kidney dialysis, and kidney transplants
in dental practice?
Consult nephrologist
Check and correct bleeding time
Need of antibiotic cover prior and need of
supplemental steroids
Drugs avoided—NSAIDs, aspirin, and
tetracyclines.
Procedures should be avoided on the day of
dialysis.
27. What are exophthalmos and proptosis?
Both these conditions describe abnormal
protrusion of eyeball. Proptosis is forward
displacement of organ while exophthalmos is
only related to eyes. Henderson reserves the
use of the word exophthalmos for those cases
of protrusion, secondary to endocrinological
dysfunction and indicates bilateral protrusion.
For example, thyroid dysfunction and Graves’
disease. Proptosis is axial protrusion of eyeball, 28. What care should be taken for patients
may be unilateral or bilateral. The aetiological with gastrointestinal disease in dental
basis of proptosis can include inflammatory, vas- practice?
cular, infectious, and cystic, traumatic. The pro- Routine dental treatment should be provided for
trusion is more in proptosis than exophthalmos. patients with inflammatory bowel disease and
ulcerative colitis by taking prior history. Aspirin
avoided and acetaminophen recommended.
Antibiotics and dietary supplements should
be taken 2 hours before after antacids.
Tetracycline should be avoided if patients
are on antacids like gelucil that contains
aluminium hydroxide as the absorption may
be prevented.
Oral fungal infections are likely to get
precipitated in long-term antibiotics.
29. What care should be taken in diabetic
patients in dental practice?
1. Morning appointments and preferably
short appointments as these patients are
more stable in morning.
2. Stable diabetics should take medicines as
prescribed while unstable diabetics require
physician’s guidance.
Exophthalmos in hyperthyroidism 3. Stress must be reduced. Use of analgesics
and/or other premedication should be
considered. Use of bathrooms during
procedures and availability of small snacks
will reduce stress, as the stress releases
endogenous epinephrine which leads to
mobilization of glycogen from liver
ultimately leading hyperglycemia.
4. Unstable diabetic patients should be covered
by antibiotics (amoxycillin/clindamycin are
the choices of drug) for invasive procedures.
Proptosis of left eye in leukemic patient 5. Need for dietician after procedure.
30. What is INR?
INR has been introduced in 1983. It is the ratio
of prothrombin time (PT) that adjusts for the
sensitivity of thromboplastin reagents, such
that normal coagulation profile is reported as
an INR of 1.0. This test evaluates the extrinsic
coagulation system and measures the presence
or absence of clotting Fs I, II, V, VII and X. Its
most common use is to measure the effects
of coumarin anticoagulants and reduction of
Right eye proptosis vitamin K dependant Fs II, VII, IX and X.
31. What is capillary fragility test? What are origin. Extrinsic origin is considered when it
the other names of it? State in which is caused by excessive consumption of acid
conditions it is positive. drinks and foods such as soft drinks, alcoholic
It is a nonspecific evaluation to measure beverages, acid fruit and prescription drugs for
capillary wall weakness and deficiencies in daily use. When caused by gastrointestinal
platelet number and function. An inflated disorders, such as those resulting from bulimia,
blood pressure cuff at specific pressure for a anorexia nervosa and gastroesophageal reflux,
fixed period of time produces increased it is considered of intrinsic origin. The acid
pressure and hypoxia in the capillaries distal action can cause erosion on palatal/lingual
to cuff. Decreased capillary resistance causes incisor surfaces, and occlusal and palatal/
capillary to rupture and leads to bleeding and lingual posterior tooth surfaces causing pain.
petechiae formation.
The blood pressure cuff in the arm is inflated
in midway between clients systolic and dias-
tolic blood pressure (but not more than
100 mm of Hg). Leave the cuff inflated for at
least for 5 minutes and observe at least 1 inch
distal to The cuff for formation of petechiae.
(The pre-existing petechiae are counted
additional.) Negative—no petechiae males 5 or
less petechiae, females 10 or less petechiae.
It is also called capillary fragility test, nega-
tive pressure test, Rumpel-Leede capillary
fragility test, dengue test, Hess test, vitamin C
test, etc.
The test is positive in purpura, vessel wall
defect, scurvy, liver disease, dengue fever,
factor VII deficiency, aplastic anemia acute
leukemia, chronic nephritis, decreased estrogen
level in postmenopausal woman, disseminated
intravascular coagulation, fibrinogen defi-
ciency, hereditary telangiectasia, drugs like 34. What is erosion? What are the different
long-term steroid use. types of erosion?
32. What is the difference between Cushing’s It is defined as the loss of dental hard tissue as
disease and Cushing’s syndrome? a result of chemical process not involving
Cushing’s syndrome is caused by excess bacteria. Erosion derived from the Latin verb
amount of glucocorticoid production and erodere, erosi (to gnaw, to corrode), Wuszm
Cushing’s disease is excessive cortisol is describes the process of gradual destruction
produced by excessive ACTH production. of the surface of something usually by
Cushing’s syndrome more commonly electrolytic or chemical processes.
noted. Clinical findings may be similar. Types of Erosion
33. What is perimolysis? 1. Regurgitation erosion
Perimolysis is a form of tooth erosion, charac- 2. Dietary erosion
terized by dental tissue demineralization 3. Industrial erosion
without bacterial involvement; that is, wear or or
mineral loss from the tooth surface caused by i. Extrinsic erosion
chemical agents, it can be of intrinsic or extrinsic ii. Intrinsic erosion
35. Enumerate the noncarious causes of chronic destructive process leading to tooth wear.
Number Terminology Causes of loss of hard tissue
1 Attrition Mechanical process involving tooth-to-tooth contact
2 Abrasion Mechanical process involving foreign objects or substances
3 Erosion Chemical etching and dissolution
4 Demastication Mechanical interaction between food and teeth
5 Abfraction Mechanical process involving tooth flexture by eccentric occlusal forces
6 Resorption Biological degradation
36. What are factitial injuries? In those cases with no underlying physical,
Self-induced lesions because of abnormal infectious, or allergic cause, psychotherapy may
habit, some psychological problem or even achieve resolution. Patient’s education regar-
accidental. They may overlap number of ding discontinuation of potentially causative
physical and chemical injuries or these are the habits or behaviour is important. Although for
oral lesions created by the patient that are not refractory cases (1) highly variable, protective
attributable to oral disease or accidental moisturizing preparations (topical petrolatum
trauma. These are difficult to diagnose as they jelly) and tacrolimus ointment (0.1%) once/
are to treat. twice daily may be effective.
The common type is gingival abrasion by 38. Name the various factitious disorders.
fingernail, obsessive tooth brushing, use of
The term factitious means willfully produced.
inappropriate aids to clean the teeth and burns
Factitious disorders are characterized by
caused by aspirin. Even self-extraction/auto-
intentionally produced or feigned psycho-
glossectomy are reported in schizophrenic.
logical or physical signs and/or symptoms in
Patient education and symptomatic treatment
order to assume a sick role in the absence of any
is the choice of treatment.
known external incentives for the behaviour.
37. What is factitious cheilitis? or
The cases of cheilitis arise from chronic injury Factitious disorders can be defined as
are termed factitious cheilitis, which is an mental disorder leading the patient to feign
unusual chronic condition of the lips multiple signs and symptoms for the purpose
characterized by crusting and peeling of of assuming sick role.
superficial epithelium often associated with
discomfort or burning. A marked female Classification of Factitious Oral Lesions
predominance is seen in cases of factitious (FOL) by Stewart and Kemohan
origin, with younger than 30 years. Mild cases Type A: Those superimposed on pre-existing
feature chronic dryness, scaling, or cracking of lesion.
the vermilion border of the lip and with
Type B: Involving injuries secondary to an
progression, the vermilion can become covered
established habit.
with a thickened, yellowish hyperkeratotic
crust that can be hemorrhagic or that may Type C: Unknown or complex aetiology.
exhibit extensive fissuring. 1. Munchausen syndrome by proxy refers to
This often starts from the centre of lower lip the condition where one person induces ill-
and spreads to involve whole of the lower lip ness in another for the purpose of indirectly
or both lips. No association with dermatologic satisfying his/her own unconscious needs.
and systemic cause but a few cases seen with HIV. Common mother causes injury to child.
Some authors also called it exfoliative 2. Gilles de la Tourette’s syndrome is a
cheilitis. neuropsychiatric syndrome characterized
by motor and vocal tic sudden, purposeless, lymphoma. Multiple sclerosis diabetes other
repetitive nonrhythmic stereotyped move- benign tumors radiotherapy osteomyelitis,
ments, e.g. eye twitching, throat clearing, abscess, dental related iatrogenic trauma,
grunting, barking, behavioural problems, extractions, mandibular surgery, implants, ill-
and self-mutilation. fitting dentures.
3. Trichotillomania is a type of compulsive 40. What is Frey’s syndrome?
behaviour. Pulling of hair out of root from
Frey’s syndrome, also known as auriculo-
scalp, eyebrows, eyelashes or pubic area
temporal syndrome, Baillarger’s syndrome,
and some other habits such as nail biting
Dupuy’s syndrome, is an unusual pheno-
and skin picking.
menon, which arises as a result of damage to
4. Autism shows speech difficulties, unusual the auriculotemporal nerve (due to parotid
behaviour. Various degrees of cognitive gland surgery, infection or trauma), and
impairment. Self-injury, e.g. strike his own subsequent reinnervation of sweat glands by
face, strike body surfaces against hard parasympathetic salivary fibres which leads to
surfaces like floor walls, self-biting, self- gustatory sweating.
scratching causing bruises, scratches which
The minor iodine starch test can be used to
can become infected.
delineate the extent of the lesion. The test is
5. Lesch-Nyhan syndrome is genetic disorder administered by applying an alcohol-iodine
affecting males. Self-injury or self-mutilation oil solution to the affected side of face. The
is a distinctive feature. Kidney problems solution is allowed to dry and lightly covered
affecting the level of uric acid in the body. with starch powder. The patient is given
6. Riley-Day syndrome shows reduced pain, a lemon candy for gustatory stimulus for
temperature sensations. Lack of tear pro- 10 minutes blue discoloration of the starch
duction, ulcer on lips, toe, finger, and iodine mixture is interpreted as a positive
unstable gait. finding.
39. What is numb chin syndrome? Initial management consist of topical
“Numb chin syndrome” (NCS) called “mental Anticholinergics (scopolamine, glycopyrolate,
neuropathy”, is a sensory neuropathy diphenamanil methyl sulphate or aluminium
characterised by hypoesthesia, paraesthesia or chloride).
less commonly pain over the chin in the region 41. What are different oral piercings?
supplied by the mental nerve and its branches.
It was first described by Charles Bell. It is often Intra and Perioral Piercing
caused by the presence of a metastatic tumor Body piercing is the act of puncturing or
in the mandible or the base of skull and cutting a part of the human body, creating an
represents advanced malignancy. Patients may opening in which jewellery may be worn. This
bite their lip inadvertently causing painless may be the reflection of cultural, religious,
ulcers. Symptoms are usually unilateral but spiritual practice, and even superstitious
up to a third may have bilateral symptoms. beliefs. Eyebrow, ear, ala of the nose, lip,
Since then, studies have reported a positive tongue, nipple, navel, and genitals are the areas
correlation linking neuropathies of the mental of piercing and are decorated with an
nerve to metastatic cancers. The most notable ornament for fashion.
are recurrent cancers in the breast, lung, and Oral piercing is a form of body art that involves
prostate, as well as leukemia and lymphoma; perforating various oral sites for beautification
however, the strongest relationship with numb by mostly metallic ornaments. The tongue and
chin syndrome has been with breast cancer and cheek may be pierced for religious purpose.
Various Specifications of Oral Piercing with diagnostic test like MRI, improper fit
• Mostly barbell types, often pierced in the of jewellery, gaging, and drooling.)
midline in the tongue towards lingual e. Perkins et al. have reported a case of
sulcus. Other most common sites are Ludwig’s angina, secondary to tongue
dorsolateral site of the tongue labial frenum piercing.
uvula and anterior tongue. f. Forked tongue also has been reported as a
• Other commonly used is ball shaped (94%), complication of tongue piercing.
cone shaped (4%).
Forked Tongue
• The materials used for fabrication are
Split tongue and bifid tongue are a rather recent
titanium acrylic steel and niobium.
addition to the art of body modification, with
a few associated publications. In this practice
Complications the anterior one-third of the tongue is split. This
Oral cavity contains millions of bacteria and has been performed slowly by pulling fishing
has a warm and moist environment. These line through a pierced hole and tightening the
bacteria without proper sterilization care may loop over a period of 3 weeks or using a surgical
migrate from the piercing wound to blood instrument or laser to quickly separate the two
stream and cause multiple complications, halves. Some form of cautery is necessary to
some of them may be life-threatening like prevent the halves from reuniting.
hematoma, septicemia, infective endocarditis, Another practice with unique or official
and toxic shock syndrome. manifestation is implantation of a form of
a. Complications during initial piercing pro- talisman (magical charm) called susuk (charm
cedure (loss of consciousness, bruising, needles, charm pins). This practice is common
swelling, bleeding, poor anatomical posi- in Southeast Asia, especially Malaysia,
tioning of piercing). Thailand, Singapore, Indonesia, and Brunei.
b. Primary post-operative complication The susuk is placed by a native magician or
(swelling, bleeding, tenderness, nerve medicine man termed bomoh and is thought
damage, gingival inflammation, metallic to enhance or preserve beauty, relieve pain,
taste). bring success in business, or provide protection
c. Secondary post-operative complications against harm. The majority of the individuals
(scar formation, kelioid formation, gingival with susuk are Muslims, although Islam
recession, periodontitis, gingival over- strictly prohibits black magic. Therefore, many
growth, periodontal and periapical ab- affected individuals will deny placement of
scesses, tooth mobility, tooth abrasions, and susuk, even when confronted directly with
sensitivity of the pulp because of galvanism, hard evidence.
calculus build-up). In most of the occasions piercing is done by
d. Complications that can occur any time non-medical individuals who do not have
(transmission and development of hepatitis adequate knowledge about sterilization and
C, B, tetanus, HIV candidiasis, infection, disinfection patients should be educated
cellulitis at piercing site, endocarditis, regarding the sequela and the potential
allergic reactions, choking aspiration or dangers of oral piercing. The dental examina-
swallowing of loose jewellery, interference tion should be done by removing oral piercing.
Section 2
Radiology
9. Radiology—Part 1
10. Radiology—Part 2
9
Radiology—Part 1
1. Define radiology. or
It is the medical speciality which embraces all X-rays may be defined as electromagnetic
the fields in which electromagnetic radiations radiation of wavelength 10–5 to 100 Å produced
are used or produced. by deceleration of high energy electrons
or and/or by electron transitions in the inner
It is defined as study and use of radiant orbits of atom.
energy including roentgen rays, radium, and 3. Define radiation.
radioactive isotopes as applied to medicine and
It may be defined as energy in the form of
dentistry.
waves or particles, emanating from its source
2. Define X-rays. through space in divergent straight lines.
A form of ionizing radiation; which is weight- However, radiation in the form of charged
less, neutral bundles of energy (photons) that particles may be deflected from its linear path
travel in a wave at the specific frequency with by electric and/or magnetic fields.
the speed of light; a beam of energy that has
4. Define roentgen.
the power to penetrate the substances and
record image shadows on photographic films It is unit of radiation exposure, i.e. amount of
also known as roentgen rays. ionizing radiations required to produce one
electrostatic unit of electricity in one mm3 at
or
0°C at standard atmospheric pressure.
Mechanically generated electromagnetic
radiation having an extremely short wave- 5. Define rad.
length of 1 to 10–3 Å and have the properties of Amount of radiation energy transferred to
penetrating various thicknesses of solids and mass.
producing secondary radiations by impinging
on material bodies, and of acting on photo- 6. Define rem.
graphic films and plates as light does It is the dose of any radiation to the biological
(Merriam-Webster). effect of that dose.
159
7. What is radiograph? What is ideal radio- 4. Position indicating device (PID): It is also
graph? called ‘spacer cone’. It is a device for setting
Radiograph is processed film or a radiograph the distance from focal spot and skin. It is
is actually a photographic recording produced made-up of plastic and lead lined. It is
by the passage of radiation through a subject conical, rectangular and round type.
onto a film, producing what is called a latent
image of the subject.
An ideal radiograph has been defined by
HM Worth as the one which has the desired
density or overall darkness and which shows
the part completely, without distortion, with
maximum detail and with the right amount of
contrast to make the detail fully apparent.
8. What are the components of dental X-ray
units?
1. Control panel: It is the part where the
circuit boards and controls that allow the
operator to adjust the correct setting for
each patient are located. It is the part where
the on and off switch is located, along with
selection of mA and kVp and electronic
timer. It is the portion of the X-ray machine
that houses the major controls. (1) Control panel, (2) extension arm, (3) tube head,
2. Arm assembly: It is attached firmly to wall (4) position indicating device (PID)
in the X-ray room. The flexible extension 9. What is the other name of exposure button?
allows the operator to position the tube
It is also called “Dead man exposure switch”.
head for various procedures.
It is called so as it acts as safety feature because
3. The tube head is where X-ray vacuum tube it is designated to permit radiation exposure
and step-up and step-down transformers while the switch is depressed. Release of the
are located. The tube head is made-up of switch must terminate the exposure. This
leaded glass and has unleaded window prevents the exposure for operator when enters
(aperture) from where the X-ray exits. It the radiation area.
is six inches long and one-half inch in
diameter often called a ‘coolidge tube’. 10. What are the diagnostic properties of
X-rays?
1. Travel in straight line.
2. Penetrate solid, liquid, and gases.
3. Can produce image on photographic plate.
4. Cause biological changes in living cells.
5. They show the property of fluorescence,
ionization, and absorption.
11. What are different uses of X-rays?
• Radiography: The main use of X-rays is in
medicine. A common application is in the
(1) Tube head, (2) position indicating device (PID), form of X-ray machines, which take photos
(3) vertical indicator scale of a patient’s body and teeth. X-rays easily
Radiology—Part 1 161
penetrate into low density substances but its position in the spectrum between the UV
do not pass through high density objects like rays and ordinary X-rays in electromagnetic
bone. This property helps to find the diseases spectrum. These are low energy X-rays and
like TB of lungs and fracture of bone. are produced by X-ray machines operating
• Radiotherapy: X-rays can also be used to 10–20 kV. These can be produced by special
kill cancer cells, but also kill healthy cells, Grenz machines. The HVL is less than 0.035 mm
so must be used with much care. In cancer Al. They are essentially absorbed between first
like diseases it is allowed to fall on affected 2 mm of skin. They are used for variety of
part of the body. inflammatory skin disorder.
• In detective department: X-rays are used
13. Which factors are concerned in X-ray
to detect contraband goods like gold, arm,
measurement?
etc. Hidden in sealed boxes or in body.
Other uses are in industry, at airports to The X-ray spectrums concerned with the
check customers and baggage. following four physical quantities in measure-
ment of X-rays:
• In engineering: X-rays are used to detect
cracks, flaws and air bubbles in the iron 1. Frequency 2. Wavelength
girders fitted in buildings and bridges. 3. Energy 4. Intensity
Accidents may be avoided by replacing
14. What is anode? What are different types
these defective girders.
of anodes? What are functions of anode?
• In trade: X-rays are used to distinguish
artificial diamonds from real diamonds, The positive terminal of an X-ray tube is called
presence of pearls in oysters and to test the the ‘anode’. Anodes are of two types:
homogeneity of rubber, and wool, etc. 1. Stationary anode: Square/rectangular
• Fluoroscopy: This allows doctors to see plate of tungsten 2/3 mm thick embedded
moving images of the internal structures of in large copper.
patients. The patient stands between an 2. Rotatory anode: The purpose of rotating
X-ray source and a fluorescent screen anode is to spread the heat produced during
and a large number of images are taken to an exposure over the large area of anode as
form a short film. These are often used to it increases the total target area. It serves
investigate problems with the digestive three important functions: (i) It provides a
system. complete circuit for purposes of accelerating
• In laboratories, spectroscopy and crystallo- the electrons, (ii) it houses the target
graphy: X-ray diffraction is also very material, and (iii) it helps to cool the tube.
important in spectroscopy and as a basis
for X-ray crystallography. The diffraction
of X-rays by a crystal where the wavelength
of X-rays is comparable in size to the
distances between atoms in most crystals
is used to disperse X-rays in a spectrometer
and to determine the structure of crystals
or molecule.
• Sterilization: For tinned foods.
12. What are Grenz rays?
These are also called ‘Bucky rays’. These were
discovered by Sir Gustav Bucky in 1923. Grenz
is German word for boundary and refers to
15. What is cathode? What are the elements

of cathode and functions of each?
Cathode is negative terminal of X-ray tube.
There are two elements of cathode: Motion
1. Filament
2. Connecting wires. The cathode may be
referred to as filament.
Filament serves as source of electron. The
filament is made up of tungsten wire 0.2 mm
diameter that is coiled to form a vertical spiral
of 0.2 cm diameter and 1 cm or less in length.
Connecting wires supply voltage (10 V) and
Sudden stop
amperage.
Electrons striking an anode target of high
atomic number causes sudden deceleration or
stoppage of rapidly moving electrons, which
produces heat and X-ray energy.
17. What is Edison effect?
The tungsten wire is heated some electrons
in the metal acquire enough energy that moves
them from the surface of metal. This escape
is thermionic emission. The electron cloud
surrounding the filament produced by
thermionic emission is called Edison effect.
18. What is stator and rotor?
The stator: The stator is the induction-motor
electromagnet that turns the anode and is the
16. Enumerate the factors that are needed for only part of the cathode or anode assemblies
production of X-rays. that is located outside the vacuum of the glass
envelope. If the stator fails, the rotor will cease
The things needed for production of X-rays are:
to turn the anode, resulting in immediate
1. Source of electron
2. Motion—high voltage potential to move
electrons,
3. Sudden stop.
Source of electrons
melting of a spot on the target that will damage size is 1 × 3 mm2. The anode is angled at 20° to
the anode. the central ray of electron beam (it may vary
The rotor: The rotor is located inside the stator from 6° to 20° according to various tube manu-
and inside the glass envelope. It is composed factures), making the effective focal spot
of a hollow copper cylinder attached to the smaller, i.e. 1 × 1 mm2. If the anode angle is
anode disk and affected by the electromagnetic made smaller, the effective focal spot is smaller.
field of the stator, causing the anode to turn. The effective focal spot is the beam projected
19. What is line focus principle? onto the patient. As the anode angle decreases,
the effective focal spot decreases.
The Benson line focus principle (angle of
truncation) explains the relationship between Thus, the line focus principle helps to
the anode surface and the effective focal spot resolve the following issues:
size. It is developed in 1918. 1. Heat dissipation, and
Tilting the anode surface so that there is an 2. Sharp image by having smaller effective
angle between the surface and the X-ray beam focal spot with heat capacity of large
spreads the heat over a larger area while focal spot.
maintain the smaller focal spot for the sharper
images is called ‘line focus principle’. The limitations of line focus principle are
The focal spot is the area of the target upon the area covered by the beam reduces with the
which the electron beam impinges and actual target angle and anode heel effect.
20. What is heel effect? length within target. This is called ‘heel effect’
X-rays produced within anode travel in all (results in higher X-ray intensity at cathode end
directions (isotropic) and intensity of emergent and lower intensity at anode end).
beam is not uniform because some part is The magnitude of heel effect depends on
absorbed in focal spot itself. X-rays produced anode angle, source to image detector (SID)
within anode must pass through a portion of distance and field size. To reduce heel effect the
target and are therefore attenuated on their anode angel is increased, SID is increased and
way out of target. The target is usually tungsten field size is decreased. The effect is increased
(Z = 74), which has attenuation properties when the target angle is reduced.
similar to lead (Z = 82), the attenuation is The heel effect can be taken advantage by
greater in anode direction than cathode keeping the denser part of body towards
direction because of the difference in the path cathode side and thinner side towards anode
side.
21. What is off focal radiation?
The electrons can rebound and interact with
other areas of anode other than focal areas.
These areas can produce X-rays too. This is
called off focal radiation. A diaphragm is
placed between the tube and collimator
reduces off focal radiation.
22. What is focal spot?

The focal spot is the area on the target to which
the focusing cup directs the electrons from the
filament.
or
The focal spot is the area on the target to
which the focusing cup directs the electrons
and from which X-rays are produced. Orit
is the apparent source of X-rays from the tube.
2. High melting point (3370°C) which helps

to withstand the high temperature
produced.
3. High thermal conductivity which helps in
dissipating heat into copper stem.
4. Low vapour pressure at high temperatures
helps in maintaining the vacuum in the tube
at high operating temperatures.
5. All metals expand when heated but at
different rates. The bonding between
tungsten and copper provides technical
23. What factors determine the size of focal problems as the coefficient of expansion for
spot? both metals are different. Ultimately, it is a
Size and also shape of focal spot is determined good material for absorption of heat and
by the size and shape of the electron beam for rapid dissipation of heat from the target
which is ultimately determined by filament area.
shape, dimensions of filament tungsten coil, 27. What are the other materials used in
position of filament in focusing cup, construc- anode?
tion of focusing cup and electric field created
In addition to tungsten, molybdenum or
between anode and cathode are the factors for
graphite are layered under the tungsten target.
size of focal spot. If the focal spot is too big,
These materials are less dense materials than
sharpness of image will be lost while if the focal
tungsten which makes easier to rotate anode.
spot is too small, then the anode will get too hot.
Molybdenum also has high melting point
24. What are the characteristics of X-ray while graphite backed anodes can double the
beam? heat loading capacities without increasing
Quantity of beam and quality of beam are the wear to bearings.
two terms describes characteristics of beam.
Quantity describes the number of photons 28. What is space charge and space charge
while quality describes the energy of photons. effect?
Space charge: The electron emitted from the
25. What is intensity of X-ray beams?
tungsten filament in the immediate vicinity of
It is defined as number of photons in the beam filament form a small cloud, this collection of
multiplied by energy of each photon in beam. negatively charged electrons forms space
The intensity is measured in roentgen per charge.
minute (R/min, or C/kg in SI system). It
Space charge effect: The cloud of negatively
depends upon the kVp, tube current, target
charged electrons tends to prevent the
material, and filtration.
other electrons from being emitted from the
26. Why tungsten is used as a target in X-ray filament until they have acquired sufficient
tube? thermal energy to overcome the force caused
The target is made of tungsten, a material that by the space charge. This tendency of space
has several characteristics of an ideal target charge to limit the emission of more electrons
material. from the filament is called ‘space charge
1. It has a high atomic number (74) which effect’. The space charge effect limits X-ray
makes it more efficient for production of tubes to maximum mA range of 1,000 to
X-rays. 1,200.
29. What is transformer? What is step up, anode circuit when the exposure button is
step down, and autotransformers? pressed. Located in tube head.
An electromagnetic device for changing Autotransformer: A voltage compensator
the alternating current coming into the corrects minor fluctuations in current flowing
machine. Required to decrease or increase the through the wires.
ordinary 100 V current that enters the X-ray 30. What is attenuation of X-ray?
machine. Attenuation is the reduction in the intensity of
Step down transformer: This decreases the X-ray beam as it traverses matter by either
voltage from the wall outlet to approximately absorption or deflection of photons from the
just enough to heat the element and form an beam. It depends on quality and quantity of
electron cloud. photons in X-ray beam. The intensity of X-ray
beam is the product of quantity and energy of
Step up transformer: Increases voltage as photons so it depends on both quality and
required. Begins to flow through the cathode quantity of beam.
31. What is beam hardening effect? 5. Collimation: When the X-rays are directed
It refers to the effect of filter on a polychromatic at patient only 10% give useful information
X-ray beam containing a range of X-ray photon while 90% are responsible for scattered
energies. Beam energy is the preferential loss radiation. Scattered radiation produces fog.
of low energy photons. It does not occur with Collimation reduces size of X-ray beam and
monochromatic X-ray beams. ultimately the volume of irradiated tissue—
qualitative and quantitative.
32. What are beam restrictors? 6. Target–patient distance: Intensity of X-ray
Beam restrictors are the device attached to the beam (the number of photons per cross-
X-ray tube housing, to regulate the size and sectional area) at a given point is inversely
shape of X-ray beam. They are: proportional to square of distance from the
1. Aperture diaphragms (sheet of lead with source of radiation—quantitative.
a hole) The factors found on X-ray machine are:
2. Cones and cylinder 1. Tube voltage
3. Collimators. 2. Exposure time
33. What are the factors controlling X-ray 3. Tube current
beam? 34. What is inverse square law?
X-ray beam may be modified by altering the It states that the intensity of radiation is
beam exposure duration (timer), exposure rate inversely proportional to the square of the
(mA), energy (kVp and filtration), shape distance from the source of radiation. The
(collimation) and intensity (target–patient intensity of an X-ray beam at a given point
distance), these can be divided into qualitative (number of photons per cross-sectional area per
and quantitative factors. unit exposure time) depends on the distance
1. Tube voltage (kVp): As kVp increases, it of the measuring device from the local spot.
results in increase in efficiency of convert- The reason for this decrease in intensity
ing electron energy into photons. Increas- is that the X-ray beam spreads out as it moves
ing kVp will increase: (i) The number of from the source.
photons generated, (ii) mean energy of pho- The relationship is as follows:
tons, (iii) maximal energy of photons. High I1 (D2 )2
energy (short wavelength) are preferred as =
I2 (D1 )2
they have greater penetrating power— where I is intensity and D is distance.
qualitative and quantitative. Therefore, if a dose of 1 gray (Gy) is measured
2. Exposure time(s): When the time of at a distance of 2 m, a dose of 4 Gy will be found
exposure is doubled, the number of photons at 1 m, and 0.25 Gy at 4 m.
generated are doubled. Thus, it increases
the number of photons and controls the
quantity of exposure. The range of photon
energy is not changed—quantitative.
3. Tube current (mA): It is directly proportio-
nal, so doubling the tube current will
double the number of photons produced.
The quantity is increased—quantitative.
4. Filtration: Aluminium filters used will
remove the long wavelength photon with
less penetrating power—qualitative and
quantitative (reduces the quantity).
Other example is position indicating device Purpose of filtration is to remove soft, low
(PID) is changed from 8 inches to 16 inches, the energy, long wavelength X-rays from the
source to receptor distance is doubled and the beam.
resultant beam is one-fourth as intense and if Consequently, to reduce patient dose, the
the PID is changed from 16 inches to 8 inches, less-penetrating photons should be removed.
the resultant beam is four times more intense. This can be accomplished, in part, by placing
35. What is filtration? an aluminium filter in the path of the beam. The
The removal of soft, low energy, long wave- aluminium preferentially removes many of the
length X-rays from beam is called filtration. lower energy photons with lesser effect on
the higher-energy photons that are able to
Although X-ray beam consists of a spectrum
penetrate to the film. In determination of the
of X-ray photons of different energies, only
amount of filtration required for a particular
photons with sufficient energy to penetrate
X-ray machine, kVp and inherent filtration of
through anatomic structures reach the image
the tube and its housing must be considered.
receptor (usually film) are useful for diagnostic
radiology. Those that are of low energy (long Inherent filtration consists of the materials
wavelength) contribute to patient exposure that X-ray photons encounter as they travel
(and risk) but do not have enough energy to from the focal spot on the target to form the
reach the film. usable beam outside the tube enclosure. These
materials include the glass wall of the X-ray A collimator is beam restrictor. It defines the
tube, the insulating oil that surrounds many size and shape of X-ray field that emerges from
dental tubes, and the barrier material that X-ray tube. A collimator is a metallic barrier
prevents the oil from escaping through the with an aperture in the middle used to reduce
X-ray port. The inherent filtration of most the size of the X-ray beam and therefore the
X-ray machines ranges from the equivalent
of 0.5 to 2 mm of aluminium.
Total filtration is the sum of the inherent
filtration plus any added external filtration
supplied in the form of aluminium disks placed
over the port in the head of the X-ray machine.
Governmental regulations require the total
filtration in the path of a dental X-ray beam
to be equal to the equivalent of 1.5 mm of
aluminium to 70 kVp, and 2.5 mm of aluminium
for all higher voltages.
Aluminium and copper are used in volume of irradiated tissue within the patient.
compound filter. Collimation does not change the energy or
A dental X-ray machine operating at 50 to number of X-rays in X-ray beam that reach the
69 kVp should have at least 1.5 mm equivalent film. It just limits size and shape of beam.
Al filtration, whereas machine operating Round and rectangular collimators are
70 kVp or more should have 2.5 mm Al most frequently used in dentistry. Dental
equivalent filtration. X-ray beams are usually collimated to a circle
23/4 inches (7 cm) in diameter or it is colli-
mated such that useful beam does not exceed
2.75 inches in diameter. Its functions are as
follows:
1. The size of film is reduced, ultimately the
volume of irradiated tissue and indirectly
reducing the scattered radiation.
2. Reduces exposure by reducing the size of
beam.
3. Film quality is increased by improving the
contrast.
• A round collimator (diaphragm) is a thick
plate of radiopaque material (usually lead)
36. What is collimation and collimator? with a circular opening centred over the port
in the X-ray head through which the X-ray
Collimation is the term used to indicate
beam emerges. Typically, round collimators
shaping of the X-ray coming from the tube head
are built into open-ended aiming cylinders.
into a column or beam of X-ray.
It produces a beam that is 2.75 inches in
or diameter, considerable larger than size of
It is process of confining and restricting the 2 films. Main disadvantage is typically it
X-ray beam to given area. produces large pneumbra at periphery of
or beam.
Collimation means restriction of the cross • Rectangular collimators further limit the
sectional area of the beam. size of the beam to just larger than the size
Dentsply rinn universal collimator attached to long round BID
of 2 X-ray films. It is important to reduce X-ray beam. A rectangular collimator exposes

the beam to the size of the film to reduce 60% less tissue than circular collimator.
further unnecessary patient exposure. • Tubular collimator is simply a tube lined
Some types of film-holding instruments with or a radiopaque material.
also provide rectangular collimation of the • Slit collimator used in OPG machine.
37. What are the uses of aluminium in X-ray

system?
Margraph long rectangular BID Aluminium is used as:
1. It is used material to filter X-ray beam.
2. As a reference material to measure the
penetrating ability (HVL) of X-rays.
38. What is HVL and TVL?
HVL (half value layer) is that thickness of
specified material which will reduce the inten-
sity of X-radiation to half its original value.
Increase in penetrating ability of a radiation
increases its HVL. It is also called half value
layer thickness, half value thickness (HVT).
TVL is the thickness of stated medium that
Collimator side—left long, round BID. Middle short will reduce the intensity of narrow beam of
round BID, right rectangular, long BID smallest X-rays to exactly one-tenth of its original value.
39. What is timer? What are different types
of timers?
Timer is the device into high voltage circuit
to control the duration of X-ray exposures
(length of exposure). The switch is like dead
man type which means it has to be conti-
Rectangular collimation showing less radiation
nuously depressed for X-ray production.
exposure than round collimator. There are four types of exposure timers:
Rectangular collimation reduces the dose fivefold 1. Mechanical timers: Mainly used in single
to circular one.
phase generator circuit. The accuracy and
reproducibility is poor rarely used today.
2. Electronic timers: The length of exposure
is determined by the time required to
change the capacitor through the resistance.
The electronic timer controls the length of
time that the high voltage is applied to the
tube and therefore the time during which
tube current flows and X-rays are produced.
It is set by turning the selector knob,
depressing the marked push button or
touching a keypad.
3. Photo timers: The actual amount of radia- Bitewing View

tion transmitted through the patient is Bitewing (interproximal) views are used to
measured. It terminates the exposure record the coronal portions of the maxillary
when the voltage receptor has received a and mandibular teeth in one image. Size 2 film
preselected X-ray exposure. Three types of is normally used in adults; the smaller size 1 is
photo timers are: (i) Ionization chamber, (ii) preferred in children. In small children, size 0
solid state diodes, (iii) scintillations with may be used. A relatively long size 3 is also
photomultiplier tube. available. Bitewing films often have a paper tab
4. Pulse counting timers: It uses technology projecting from the middle of the film, on
of voltage pulse counting to control the time which the patient bites to support the film. This
of short exposure technique. In this high tab is rarely visualized and does not interfere
frequency oscillations are generated by the with the diagnostic quality of the image. Film-
oscillation in quartz crystal. holding instruments for bitewing projections
5. mAs timer: For any particular X-ray tube are also available.
and kV the radiation exposure is controlled
by tube current and exposure time. The Occlusal View
mAs timer does it automatically and it The size 5 film occlusal film is more than three
terminates the exposure as soon as the times larger than size 2 film (57 × 76 mm). It is
desired mAs has passed through the X-ray used to show larger areas of the maxilla or
tube and into the condenser. mandible than may be seen on a periapical film.
The timer serves to regulate the duration of These films are also used to obtain right-angle
the interval that the current will pass through views to the usual periapical view. The name
the X-ray tube. derives from the fact that the film is usually
Time settings of less than a second may be held in position by having the patient bite
indicated on fractions and impulses. lightly on it to support it between the occlusal
surfaces of the teeth.
New machines are accurate to 1/100 sec
intervals. Time determines the duration of
exposure. Dimensions
Type-size number mm in
40. Enumerate various types of intraoral
Periapical
films and the dimension of each film 1.00 21 × 32 4/5 × 11/4
pack. 1.0 22 × 35 7/8 × 13/8
1.1 24 × 40 15/16 × 19/16
Periapical View 1.2 31 × 41 11/4 × 15/8
Periapical views are used to record the crowns, Bitewing (interproximal)
roots, and surrounding bone. Film packs come 2.00 21 × 32 4/5 × 11/4
in five sizes: 2.0 22 × 35 7/8 × 13/8
1. For small children (22 × 35 mm); 2.1 24 × 40 15/16 × 19/16
2.2 31 × 41 11/4 × 15/8
2. Which is relatively narrow and used for
2.3 27 × 54 11/16 × 2
views of the anterior teeth, adult anterior
Occlusal
(24 × 40 mm);
3.4 57 × 76 21/4 × 3
3. The standard film size used for adults
(31 × 41 mm). Note: The digit at the left of the decimal point
represents the use of the film (periapical, bitewing, or
4. Relatively long size bitewing (54 × 27 mm) occlusal). The digits on the right indicate the size of
5. Occlusal film (57 × 76 mm). the film (00, 0, 1, 2, 3, or 4)
41. What are the sizes of bitewing films?

Size 0: (For children) 22 mm × 35 mm
Size 1: For adult (anterior teeth) 24 mm × 40 mm Size 0: Children’s film
Size 1: Narrow anterior periapical film
Size 2: For adult (posterior teeth) 31 mm × 41 mm Size 2: Adult regular for posterior periapical and bitewing
Size 3: For adult (for all posterior teeth of one Size 3: Longer in use
side in one film) 27 × 54 mm. Size 4: Occlusal film
42. What are the differences between screen and nonscreen films?
Characteristics Direct exposure film Indirect exposure film
Exposed by Only X-rays Mainly by visible light
Used Without screens With screens
Emulsion layer Thick Thin
Image formation In deep Superficially
Processing time More Less
Resolution More Less
Characteristic curve No apparent shoulder region in Shoulder region in useful
useful density range density range
Screen artifact No May be possible
Exposure dose More Less
Uses Orbit and extremities radiography General radiography
and industrial radiography
43. What is composition of X-ray film? supporting material onto which the emul-
X-ray film has four basic principal components: sion is coated.
1. Film base Cross-section of Double Emulsion Film
2. Adhesive layer 1. Film base: It is a flexible piece of polyester
3. Film emulsion plastic (polyethylene terephthalate—the
4. Protective layer. The emulsion, which is thickness is 0.18 to 0.2 mm or 0.007 inches),
sensitive to X-rays and visible light, records the function of the film base is to support
the radiographic image. The base is a plastic the emulsion. The base must have the
silver halide crystals store energy from

which they have been exposed and react
with the chemicals in the processing tank
to form a black (radiolucent) region on
the film. Those crystals which are not
been stuck they wash off during process-
ing. Iodide is added to ultraspeed film
because its large diameter (compared
with bromine) disrupts the regularity of
the silver bromide crystal structure,
thereby increasing its sensitivity to
X-radiation. The photosensitivity of the
silver halide crystals also depends on the
presence of trace amounts of a sulphur-
containing compound. In addition, trace
amounts of gold are sometimes added to
silver halide crystals to improve their
sensitivity. In the manufacture of film,
proper degree of flexibility to allow easy the silver halide grains are suspended in
handling of the film. The semi-clear film a surrounding vehicle that is applied to
base (cellulose acetate) is uniformly both sides of the supporting base. The
translucent and casts no pattern on the vehicle composed of gelatinous and
resultant radiograph. Some believe that a nongelatinous materials, keeps the silver
base with a slight blue tintometrics image halide grains evenly dispersed. To ensure
quality by emphasizing the contrast. The good adhesion of the emulsion to the film
film base must also withstand exposure to base, a thin layer of adhesive material is
processing solutions without becoming added to the base before the emulsion is
distorted and do promote easy handling applied. During film processing, the
and provides strength. vehicle absorbs the processing solutions,
2. Adhesive layer (subcoating, substratum, allowing the chemicals to reach, and
subbing layer): A thin layer added on both react with the silver halide grains.
sides of film before emulsion is added and b. Gelatin: It must be uniform in thickness
serves to adhere the emulsion and to base. (0.0002–0.0004 inch 5–10 Mu microns). It
This layer is mixture of gelatin and film base. is composed of cattle bone and used to
3. Film emulsion: It is homogeneous mixture suspend and disperse the millions of
of silver halide grains (sensitive to X-radia- microscopic halide crystals over base
tion and visible light), and a vehicle matrix during film processing. Gelatin absorbs
(gelatin and nongelatin material). Each the silver halide crystals and allows the
emulsion layer is about one thousand of an chemicals to enter and react with halide
inch thickness. crystals.
a. Halide crystals: Halides are compounds 4. Protective coat (super coat, antiabrasive
of halogen such as chlorine, bromine, and layer): An additional thin layer of vehicle
iodine. The silver halide grains are (tough coating of hard protective gelatin)
composed primarily of crystals of silver is added to the film emulsion as an overcoat;
bromide in dental X-ray films (80–99%) this barrier helps protect the film from
and to a lesser extent silver iodide damage by scratching, contamination, or
(1–10%). During radiation exposure the pressure from rollers when an automatic
processor is used. It is also less likely to

pick-up dirt. It is treated to achieve anti-
static behaviour. It should not be too hard
to prevent penetration.
Film base is 0.007 inch while protective coat.
Emulsion and adhesive layer on either side
is 0.0005 inch.
44. What is coating weight?
Coating weight is the amount of silver halide
crystals in emulsion. The screen and non- 3. To maintain the film in close, uniform
screen films consist of silver bromide as main contact with both screens during the
constituent. Nonscreen films have higher exposure.
coating weight than screen film. The consi-
4. To protect the intensifying screens from
deration is important to obtain silver in
physical damage.
recovery process.
48. What are the properties of cassette? How
45. What is safe film? the care of cassette is taken?
The film base is made up of acetate polyester The properties are:
which is not easily inflammable, then the film
a. Weight: It should be light for easy
is called safe film or safety film.
manipulation.
46. What are the differences between single b. Robust structure: Cassettes in daily use are
emulsion film and double emulsion subject to considerable stress and wear.
film? Screens may fail to maintain contact with
the film or leakage of light at the edges can
Characteristic Single Double occur. Cassettes deserve and should have
coated coated stringent care in handling.
Emulsion layer One side Both side c. i. Nonflexible: So as not to allow the film to
Patient radiation dose More Less bend.
Noncurl back layer Present Absent ii. Flexible cassettes: For panoramic machines.
Radiographic detail More Less
Flexible cassettes are necessary for the
Average gradient (G) Very less More
Parallax effect No Yes
specialized equipment associated with
Contrast Less More panoramic radiography. They are moun-
ted within a simple envelope of plastic
47. What is cassette? What are functions of material, folded at one end and fastened
cassettes? with press buttons or velcro of conventio-
A flat, light-tight container in which X-ray films nal design. The cassette is attached to a
are placed for exposure to ionizing radiation drum and is rigid for the duration of the
and usually backed by lead to eliminate the exposure.
effects of back scatter radiation, containing d. Size: Slightly larger than the X-ray beam
front and back intensifying screens. and area to be radiographed.
Cassettes are used in association with e. Ease of operation.
intensifying screens and screen films. They 49. How the care of cassettes is taken?
have related functions: Treated with care X-ray cassettes and inten-
1. To contain a film sifying screens are good for years of hard
2. To exclude light work.
Their general care is aimed at the avoidance faults are observed, ascribable to damage
of rough handling by all who use them. of some kind, e.g. cracks in the intensifying
It is helpful to mark each cassette with screens or light leaks. Screens come with a
identifying numerals which are inconspicuous, sticker indicating the film speed and this sticker
that makes it easy to eliminate, if radiographic is placed on the outside of the cassette.
50. Enumerate the errors in loading and uses of cassette and useful hints to avoid them.
Problem Cause How to correct Useful hints

Overall grayness or Damaged cassette Tape edges of soft Cassettes should be
blackness along one edge (light leak) or filmcassette, replace inspected regularly for
or corner of film (fog) exposed to light damaged hard cassette light tightness
Little or no image is Screens reversed Replace screens Dull surface of screen
visible on film properly should face film, not shiny
White streaks on image Damaged (scratched) Handle screens Use screen cleaning
screens carefully solutions and soft cloth to
clean screens
Black marks, round Static electricity Avoid too rapid Use of antistatic mats or
clusters or lightning bolt removal humidifier can reduce
of film from cassette static
Multiple images Double exposure Remove film from Store unexposed and
cassette after each exposed cassettes
exposure separately
51. What are intensifying screens? is related to their speed: The slower the speed
Early in the history of radiography, scientists of a screen, the greater is its resolving power
discovered that various inorganic salts or and vice versa. Intensifying screens are not
phosphors fluorescence (emit visible light) used intraorally with periapical or occlusal
when exposed to an X-ray beam. The intensity films because their use would reduce the
of this fluorescence is proportional to the X-ray resolution of the resulting image below that
energy absorbed. These phosphors have been necessary for diagnosis of much dental disease.
incorporated into intensifying screens for use
Composition
with screen film. The sum of the effects of the
X-rays and the visible light emitted by the Intensifying screens are made of a base
screen phosphors exposes the film in an supporting material, a phosphor layer, and a
intensifying cassette. protective polymeric coat. In all dental applica-
tions, intensifying screens are used in pairs, one
Function on each side of the film, and they are positioned
The presence of intensifying screens creates an
image receptor system that is 10 to 60 times
more sensitive to X-rays than the film alone.
Consequently, use of intensifying screens
means a substantial reduction in the dose of
X-radiation to which the patient is exposed.
Intensifying screens are used with films for
virtually all extraoral radiography, including
panoramic, cephalometric, and skull projec-
tions. In general, the resolving power of screens
inside a cassette. The purpose of a cassette is blue-sensitive films. The speed and resolution
to hold each intensifying screening contact of a screen depend on many factors including:
with the X-ray film to maximize the sharpness • Phosphor type and phosphor conversion
of the image. Most cassettes are rigid, but they efficiency
may be flexible. • Thickness of phosphor layer and coating
weight (amount of phosphor/unit volume)
Base
• Presence of reflective layer
The base material is mostly of card, polyester • Presence of light-absorbing dye in phosphor
and plastic that is about 0.25 mm thick. The binder or protective coating
base provides mechanical support for the other
• Phosphor grain size.
layers. In some intensifying screens the base
is also reflective; thus it reflects light emitted Fast screens have large phosphor crystals
from the phosphor layer back toward the X-ray and efficiently convert X-ray photons to visible
film. This has the effect of increasing the light light but produce images with lower resolu-
emission of the intensifying screen. However, tion. As the size of the crystals or the thickness
it also results in some image “unsharpness” of the screen decreases, the speed of the screen
because of the divergence of light rays reflected also declines but image sharpness increases.
back to the film. Some fine detail intensifying Fast screens also have a thicker phosphor
screens omit the reflecting layer to improve layer and a reflective layer, but these properties
image sharpness. In other intensifying screens also decrease sharpness. In deciding on the
the base is not reflective, and a separate coating combination to use, the practitioner must
of titanium dioxide is applied to the base consider the resolution requirements of the
material to serve as a reflecting layer. task for which the image will be used. Most
dental extraoral diagnostic tasks can be
Phosphor Layer accomplished with screen-film combinations
that have a speed of 400 or faster.
The phosphor layer is composed of phosphore-
scent crystals suspended in a polymeric binder. Protective Coat (super coat)
When the crystals absorb X-ray photons, A protective polymer coat (up to 15 Jlm thick)
they fluorescence. The phosphor crystals often is placed over the phosphor layer to protect the
contain rare earth elements, most commonly phosphor and provide a surface that can be
lanthanum and gadolinium. Their fluorescence cleaned. A strong, smooth, protective layer of
can be increased by the addition of small cellulose acetate is used. The intensifying
amounts of elements such as thulium, niobium, screens should be kept clean because any
or terbium. Some rare earth compounds are debris, spots, or scratches may cause light
efficient phosphors. In the energy range spots on the resultant radiograph. This layer
typically used in dental radiography, a pair of is—resistant to abrasion, moisture protecting
rare earth intensifying screens absorbs about the fluorescent layer, minimal thickness
60% of the photons that reach the cassette after reduces image sharpness.
passing through a patient. These phosphors are
about 18% efficient in converting this X-ray 52. How the care of intensifying screens is
energy to visible light. Rare earth screens taken?
convert each absorbed X-ray photon into about Screens are easily damaged. Their fluorescent
4,000 lower-energy, visible light expose the film. emission will be affected if the active surface
Different phosphors fluorescent in different is soiled even slightly. Screens must thus be
portions of the spectrum. It is important to kept clean, otherwise light photons will be
match green-emitting screens with green- prevented from reaching the screen and
sensitive films and blue-emitting screens with creating an image and the screen in that area
will appear clear. Dirt will also create “high” cassette which is failing to maintain contact
spots which will create wear. Screens are best between the intensifying screens.
cleaned with antistatic solution (at least once 3. Screens which are old or cracked can be
in 6 months). Use a damp cloth and rub gently. seen to have fairly mottled appearance and
Ensure that the screen is dry before closing the this will be reproduced on radiographs.
cassette, otherwise the gelatin on the surface When this is noticed it is time to discard
of the screens will stick together. Never leave the screens.
the cassette open as it will accumulate dirt and 53. What are the speeds of intensifying
dust on the screen. Avoid touching of screen screens?
and keep the film processing area free of dirt.
1. Fast screens (lanex): Rare earth thick layer,
Check for proper screen film contact before
and relatively large crystals used, maxi-
exposure. The foam supporting the screens
mum speed is attained but with some
should be intact and is capable of holding
sacrifice in definition. They use gadolinium
screen closely with films.
or lanthum phosphors.
Procedure 2. Slow screens: Standard slow screens or
1. Choose a clean location to clean screens. high definition screens—a thin layer and
2. Moisten a lint-free wipe with a small relatively small crystals are used; detail is
amount of commercially available screen the best, but speed is slow necessitating a
cleaners and antistatic solutions. Mild soap higher dose of ionizing radiation. They use
and water solution and 70% of isopropyl calcium tungstate phosphors.
alcohol may be used as an alternative, but 3. Medium screens-standard: Medium thick
screen cleaners and antistatic solutions layer of medium-sized crystals in order to
must be used. provide comprise between speed and
3. Clean, dry screen avoid excess pressure. definition.
4. Use a second lint-free wipe inside and clean 54. What are the factors of regular inspection
the frame (single screen). of intensifying screens?
5. Stand the cassettes on edge to dry. 1. Intensifying screens in a flat cassette may
6. UV light is used to inspect dust, dirt parti- come loose and should be reattached im-
cles. mediately. Loose screens are an invitation
to error in the darkroom. It is easy, when
Regular Inspection loading a cassette, to slip the film on top of
1. The screens in a flat cassette may come loose both screen if they are unattached.
and should be reattached immediately. 2. The felt pad or foam rubber in the back of
Loose screens are an invitation to error in the cassette may have become in secure or
the darkroom. It is easy, when loading a worn. This can result in failure of the
cassette, to slip the film on top of both intensifying screens to maintain uniform
screen if they are unattached. contact with the film and this causes a
2. The felt pad or foam rubber in the back of localized area of unsharpness on the
the cassette may have become insecure or radiograph, due to the spread of fluorescent
worn. This can result in failure of the light between the screens and the emulsion.
intensifying screens to maintain uniform There is nothing that can be done for a
contact with the film and this causes a cassette which is failing to maintain contact
localized area of unsharpness on the between the intensifying screens.
radiograph, due to the spread of fluorescent 3. Screens which are old or cracked can be
light between the screens and the emulsion. seen to have fairly mottled appearance and
There is nothing that can be done for a this will be reproduced on radiographs.
When this is noticed it is time to discard 7. This is covered with a thin transparent
the screens. super coat consisting of gelatin. The
As they are sold in pairs, there is a little to purpose of the latter is protective, and is
be done except to replace both screens in very thin and care is always required in
the cassette. (Like one glove on its own, it handling intensifying screens to avoid any
may subsequently never have a match.) kind of abrasion.
55. What are functions of intensifying 8. The flexibility of the material is important
screen? to allow the screen to bend without
cracking—an intensifying screen of this
1. Reduce the patient's exposure to radiation.
type is used in the panoramic cassette.
2. It reduces blurring of the image due to
subject movement by shortening the 58. What are grids? Mention their functions.
exposure time. When an X-ray beam strikes a patient, many
3. It reduces geometric blur by making it of the incident photons undergo compton
possible to use a small focus X-ray tube. interactions and produce scattered photons.
4. This makes possible use of portable X-ray Typically, the number of scattered photons in
tube and extend the life of X-ray tube. the remnant beam that reach the film is two to
5. Increase the contrast of radiograph. four times the number of primary photons that
56. What is luminescence? do not undergo absorption. The amount of
Luminescence is the emission of light from a scattered radiation increases with increasing
substance bombarded by radiation. These are subject thickness, field size, and kVp (energy
of two types: Fluorescence and phosphore- of the X-ray beam). These scattered photons
scence. produce fog on the film and reduce the subject
contrast. By virtue of function and composition,
Fluorescence means that luminescence is
grids and collimators are same but differ by
excited only during the period of irradiation
location.
and will terminate at completion of the X-ray
exposure. The phosphors in intensifying The grid is placed in front of patient. It
screens produce fluorescence. allows the parallel rays and absorbs the
scattered rays. The problem is it forms its own
Phosphorescence is after glow. The irradiated
shadow and the problem can be overcome by
material continues to emit light for a time after
moving the grid.
cessation of exposure to radiation and will
continue to produce an image which you do
Function
not want.
The function of a grid is to reduce the amount
57. What are the characteristics of intensify- of scattered radiation exiting a subject that
ing screen? reaches the film.
1. An intensifying screen consists of a base of The grid, which is placed between the
polyester or cellulose triacetate similar to subject and the film, preferentially removes
radiographic film. the scattered radiation and spares primary
2. This base must be radiotransparent. photons; this reduces non-imaging exposure
3. It must be chemically inert. and increases subject contrast.
4. It must combine characteristics of tough-
ness and flexibility. Composition
5. It should neither curl nor discolour with age. A grid is composed of alternating strips of a
6. The base is first coated with a reflective radiopaque material (usually lead) and strips
layer of titanium dioxide to bounce light of radiolucent material (often plastic). When
back onto the film. secondary photons generated in the subject are
scattered toward the film, they are usually growth and development of the facial region
absorbed by the radiopaque material in the use of a grid usually is not indicated because
grid. This occurs because the direction of the improved contrast does not aid in
the scattered photons deviates from that of the identification of anatomic landmarks.
primary beam, and consequently they cannot
59. Enumerate the various ways to eliminate
pass through the parallel plates of the grid.
gagging.
Focussed grids are used most often. In a
focussed grid the strips of radiopaque material Gagging is also called retching which refers
are all directed toward a common point, the to strong involuntary effort to vomit. It is
focal spot of the X-ray tube, some distance protective mechanism. It is caused by stimula-
away. Because the lead strips are angled tion of sensitive tissues of palate.
toward the focal spot, their direction coincides
with the paths of diverging photons in the Causes—Psychogenic Stimuli
primary X-ray beam. The lead strips absorb the These are stimuli which originate in mind and
scattered photons as their paths diverge from causes the gag stimuli even the film is not
those of the primary photons. A focussed grid placed in mouth. The psychic stimuli can
can be used only within a range of distances be overcome by conditioning the patient
from the focal spot where the alignment of lead appropriately.
strips closely coincides with the path of the
diverging X-ray beam. The range of distances Tactile Stimuli
is specified on the grid. Grids are manufactured These stimuli originate when the film is
with a varying number of line pairs of touched at soft palate, retromylohyoid space
absorbers and radiolucent spaces per inch. and lateral posterior third molar region. The
Grids with 80 or more line pairs per inch do ninth nerve or glossopharyngeal nerve covers
not show objectionable grid lines on the image. the reflexes. The gag reflex is problem
The ratio of grid thickness to the width of the especially taking upper and lower molar
radiolucent spacer is known as the grid ratio. region radiographs.
The higher the grid ratio, the more effectively 1. Attitude—dental radiographer must be
scattered radiation is removed from the X-ray confident. Every effort should be made to
beam. Grids with a ratio of 8 or 10 are preferred. avoid gagging. If the patient gags the film
To compensate for the absorbing materials should be removed and assured that gag
in the grid, the exposure required when a grid reflex is less in patients who are relaxed
is used is approximately double that needed and comfortable and explain in short the
without a grid. Therefore, grids should be used procedure.
only when the improvement in diagnostic 2. Never suggest gagging—one should not
image quality is sufficient to justify the added use term gagging so that patients have
exposure. For example, with lateral cephalo- psychogenic stimuli.
metric examinations made for assessing the 3. Keep the exposure factors and tube
placement ready before placing the film in
mouth.
4. The patient should take deep breath and
asking the patient to concentrate on breath-
ing when image receptor is in position or
divert patients mind by asking him to
count the numbers or making yoga (anulom
vilom), patient is asked to look fixedly at
one point in room or asked to bite hard on • The shape of teeth and relation to surround-
bite plate. ing structures is more accurate.
5. The patient is asked to swallow im- • The technique used with aiming ring the
mediately before insertion. alignment of X-ray beam is simplified.
6. Ask the patient to gargle with ice cold • Head position is not critical as paralleling
water and patient sucking a local anaes- instrument and aiming ring will take care
thetic lozenge before attempting the of alignment of X-ray beam.
position of image receptor or xylocaine • Eliminates the need of predetermined
ointment or spray. angulation.
7. Salt is placed on patient’s tongue. • The image will have same shape of tooth
8. Place image receptor flat position as in but will have a little magnification, i.e.
occlusal film and giving steep downward slightly larger than actual tooth size.
angulation. • The shadow of the zygomatic buttress
9. Use of film holders as when patient bites appears above the apices of the molar teeth
the floor of mouth is relaxed. and it does not superimpose on apices of
10. Stephen Cohen said, ask the patient not to maxillary molar teeth because central ray
blink, if the patient does not blink when is perpendicular to long axis of molars and
film and sensor is kept in patient’s mouth, enters below level of zygomatic arch.
the sense of gagging is eliminated and • The periodontal bone levels are well-
remove the film or sensor as soon as represented.
possible the procedure is over. • The periapical tissues are accurately
11. If everything fails, go for extraoral radio- shown with minimal foreshortening or
graph. elongation.
60. What are the other names of paralleling • The crowns of the teeth are well-shown
angle technique? enabling the detection of proximal caries.
It is also known as extension cone paralleling • The horizontal and vertical angulations of
(XCP) technique, right angle technique, long the X-ray tube head are automatically
cone technique. determined by the positioning devices if
placed correctly. These film holding devices
61. What are the fundamental rules of
are useful in contour chairs or if patients
paralleling angle (right angle) technique?
are treated in supine positions, as in these
The rules are: positions it is difficult to place occlusal
1. The film is placed in mouth that is parallel plane parallel to floor.
to long axis of tooth. • The X-ray beam is aimed accurately at the
2. The central ray is directed perpendicular centre of the film, all areas of the film are
to both long axis of tooth and plane of irradiated and there is no coning off or cone
tooth. cutting.
62. What are advantages of long cone or • Reproducible radiographs are possible at
paralleling angle technique? different visits and with different operators
• When performed accurately the image and ultimately easy to standardize.
formed has linear and dimensional • The relative positions of the film packet,
accuracy to help valid diagnosis, with less teeth and X-ray beam are always main-
dimensional distortion, i.e. geometrically tained, irrespective of the position of the
accurate images and true lateral image of patient’s head. This is useful for some
tooth. patients with disabilities.
• Dose reduction in paralleling technique. • Positioning of film is comfortable and

The vertical angulation in paralleling patient friendly as the film does not
technique is either +10 degrees as compared impinge on tissues.
to vertical angulation of +45 degrees com- • Positioning in all areas of mouth can be
pared to short cone bisecting angle techni- reasonable, easily achieved.
que. The lack of extreme vertical angulation • Simple and quick as does not require film
reduces the exposure to the thyroid gland holders.
and lens of eye because they are in no longer • Radiographs can be taken with low output
path of primary beam. X-ray machines.
• It is easier to standardize and serial com- • No anatomical variation restrictions. The
parison of radiographs have a greater film can be angled to accommodate the
validity. (Important in assessing alveolar different anatomical variations.
bone levels after periodontal surgeries.)
63. What are the disadvantages of paralleling 65. What are the disadvantages of bisecting
angle technique? angle technique?
Positioning of the film packet can be very • It represents the dimensional distortion,
uncomfortable for the patient, causes dis- because the film and long axis of tooth are
comfort, particularly for posterior teeth, often not parallel.
causing gagging. In children it is difficult. • Harder to position X-ray beam—since
• Positioning the holders within the mouth the film holders are not used, it is difficult
can be difficult for inexperienced operators. to visualize where the X-ray beam directed.
• The anatomy of the mouth sometimes • Film less stable—as it is used with finger
makes the technique impossible, e.g. a chances of moving are more.
shallow, flat palate. • The radiopaque image of zygomatic arch
The apices of the teeth can sometimes appear is often superimposed on apices of maxil-
very near the edge of the film: lary molars, making diagnosis difficult.
This happens because the point of entry of
• Positioning the holders in the lower third
central beam is along zygomatic arch.
molar regions can be very difficult.
• The technique cannot be performed • To implement the Cieszynski’s rule of
satisfactorily using a short focal spot to skin isometry in multirooted teeth, the central
distance (i.e. a short spacer cone) because ray must be directed differently for diffe-
of the resultant magnification. rent roots.
• The holders need to be autoclavable or • The alveolar ridge is positioned coronally
disposable. than its usual position.
• The objection is to long cone PID also • Cone cut chances are more.
because they are difficult to operate in short • Incorrect vertical angulation (elongation/
operatory, longer exposure time may make foreshortening) and incorrect horizontal
patients movement. angulation (overlapping).
• Difficult to place —when extremely long • Less useful in periodontal diseases as levels
roots and rubber dam in place. are poorly represented.
64. What are the advantages of bisecting • It is difficult to obtain reproducible views.
angle technique? • The crowns are often distorted, difficult to
• The proper technique represents the image detect proximal caries.
of tooth with correct linearly, i.e. same • The buccal roots of premolars and molars
length of tooth is formed on radiograph. are often foreshortened.
66. What are differences between long cone paralleling and short cone bisecting angle
technique?
Bisecting Paralleling
TFD 6–8 inch 16–18 inch
The size of cone
Object film distance Touches the tooth Away from the tooth
Position of the film Filmat angle Film parallel to long axis of tooth
Central ray Angulated Parallel

Patient’s exposure
More Exposure is reduced

67. What is the modification of paralleling

angle technique?
Walton has given modification of paralleling
angle technique in which the central ray is
directed perpendicular to the film but not the
teeth. This helps to overcome the disadvantages
of paralleling angle technique. This technique
is useful for following situations:
1. Shallow palatal vault
2. Maxillary tori
3. Extremely long roots
2. In children when difficulty in placing image
4. Uncooperative
receptor intraorally.
5. Gagging patients.
69. What is Le master technique?
68. What is modification of bisecting angle In Le master’s technique a cotton roll is placed
technique? between the film and the palate so that the film
The image receptor is placed in mouth in is moved away from the teeth. The vertical
occlusal plane (flat) and the position of X-ray angulation is then reduced and the central ray
tube head is adjusted accordingly. This is directed from below the zygomatic process
technique is used for: of maxilla to prevent its superimposition on the
1. To avoid gagging dentoalveolar structures.
technique is developed in 1952. The steps are

as follows:
1. The film is places as far back as possible
and the patient is asked to bite gently.
2. To make angle prominent the head is tilted
downwards and forwards.
3. The central ray is perpendicular to film.
Impacted third molars are visualized in
buccal and lingual plane. The other name
is Rita-Manuer technique.
71. What is umbra and penumbra?
The word penumbra is derived from two Latin
words pene means almost and umbra means
shadow. The region of complete image is called
umbra. Penumbra is the region of partial
70. What is Donovan’s technique? illumination that surrounds the umbra or
For studying of mandibular third molar complete shadow. It is also called geometric
impaction this technique is used. This unsharpness or edge gradient.
72. What is latent image? interact primarily with the bromide ions by
Film emulsion consists of photosensitive compton and photoelectric interactions.
crystals containing primarily silver bromide These interactions result in the removal of an
suspended in a vehicle and layered on a thin electron from the bromide ions. By the loss of
sheet of transparent plastic base. Some crystals an electron, a bromide ion is converted into a
also contain small amounts of silver iodide. neutral bromine atom. The free electrons move
These silver halide crystals also contain a few through the crystal until they reach a sensitivity
free silver ions (interstitial silver ions) in the site, where they become trapped and impart a
spaces between the crystalline lattice atoms. negative charge to the site.
The crystals are chemically sensitized by the
addition of trace amounts of sulphur compounds,
which bind to the surface of the crystals. The
sulphur compounds play a crucial role in image
formation. Along with physical irregularities
in the crystal produced by iodide ions, sulphur
compounds create sensitivity sites, the sites in
the crystals that are sensitive to radiation.
The negatively charged sensitivity site then

attracts positively charged free interstitial
silver ions.
Each crystal has many sensitivity sites,

which begin the process of image formation by
trapping the electrons generated when the
emulsion is irradiated. Exposure to radiation
chemically alters the photosensitive silver
halide crystals to produce the latent image.
Processing the exposed film in developer
and fixer converts the latent image into the
visible radiographic image. When the silver
halide crystals are irradiated, X-ray photons
When a silver ion reaches the negatively reached the film, and dark (radiolucent) areas
charged sensitivity site, it is reduced and forms of the film that were struck by many photons.
a neutral atom of metallic silver.
The sites containing these neutral silver

atoms are now called latent image sites.
This process occurs numerous times within The process repeats and is also called Gurney-Mott
a crystal. The overall distribution of latent hypothesis
image sites in a film after exposure constitutes 73. What is parallex?
the latent image. Film processing converts the
Parallex results from an apparent change in
latent image into one that can be visualized.
position or size of a subject when it is viewed
The neutral silver atoms at each latent image
from a different perspective. This causes loss
site render the crystals sensitive to develop-
of image unsharpness due to double emulsion.
ment and image formation. The larger the
The images recorded on each side may vary
aggregate of neutral silver atoms, the more
because of the divergent nature of X-ray beam.
sensitive the crystal is to the effects of the deve-
The use of intensifying screens also causes
loper. Most latent image sites that are capable
parallex distortion because light from one
of being developed in an optimally exposed
screen may cross the film base and reach the
film have at least four or five silver atoms.
emulsion on the opposite side. The problem
Developer converts silver bromide crystals
with neutral silver atoms deposited at the
latent image sites into black, solid silver
metallic grains. These solid silver grains
block light from a view box. Fixer removes
unexposed, undeveloped silver bromide
crystals (those without latent image sites),
leaving the film clear in unexposed areas. Thus,
the radiographic image is composed of the 1 and 3—the two sides of emulsion,
light (radiopaque) areas, where a few photons 2 and 4—the horizontal lines are parallex
can be solved by incorporating dyes that the area and to exhaust the heat from the dryer
absorb light. Parallex is seen more in wet films. and moisture from the drying films. Also, a
comfortable room temperature helps maintain
74. What is darkroom?
optimal conditions for developing, fixing, and
The darkroom should be convenient to the washing solutions. If supplies (including
X-ray machines and dental operatory and unexposed X-ray film) are to be stored in the
should be at least 4 × 5 feet (1.2 × 1.5 m). One of darkroom, ventilation is doubly important
the most important requirements is that it because temperatures of 90°F or higher can
should be lightproof. To accomplish this, a cause a generalized increase in density (film
light-tight door or door less maze (if space fog) on the film.
permits) is used. The door should have a lock
to prevent accidental opening, which might 75. What is safe light?
allow an unexpected flood of light that can It is defined as a darkroom lamp with one or
ruin opened films. The room must be well- more color filters to screen out rays that can
ventilated for the comfort of those working in affect the photosensitive film. Safe lights
allow darkroom workers to handle the photo-
sensitive materials under limited illumination.
It consists of light source (combusting gas or
other fuel, incandescent light bulbs, fluorescent
light tubes) and filter to limit the range of
wavelengths that are used for illumination.
X-ray films are not sensitive to the entire
spectrum of visible radiation. They are sensi-
tive to only UV blue, green emission and not
sensitive to radiations in certain bandwidth of
radiations in blue, green areas. If we use low
lightning filters through colour filters, the film
is safe.
Type of Filter
This should be compatible with the color
sensitivity of film used, i.e. blue, green or
ultraviolet.
• Condition of filters: Scratched filters
should be replaced.
• Wattage of the bulb: 15 watt bulb is used
when direct illumination is used while
25 watt bulb is used when facing the ceiling.
The pre-exposed films are 8 times sensitive
than unexposed films so these should be
kept for less time under safe light.
• Their distance from the work surface:
Ideally they should be at least 1.2 m (4 ft)
away from working place.
• Overall safety (i.e. their fogging effect on
film): The simple quality control measure
for doing this is known as the coin test or
penny test.
76. What is penny test?

It is also called coin test or safe light test.
The following simple penny test can be
4. Develop the test film as usual. If the image
used monthly to evaluate for fogging caused
of the penny is visible on the resultant film,
by inappropriate safe lighting conditions.
the room is not light-safe for the particular
1. Shut all lights and start safe light. film tested. Each type of film used in the
2. Open the packet of an exposed film and office should be tested to measure the
place the test film in the area where the integrity of the darkroom.
films are usually unwrapped and clipped Note: Coin test can also be performed to
on the film hanger. assess the amount of light transmission
3. Place a penny on the film and leave it in through the safety glass of automatic
this position for the approximate time processors by performing the test within the
required to unwrap and mount a full- processor under the safety glass under the
mouth set of films, usually about 5 minutes. normal daylight conditions.
77. How the coin test can be performed for 78. What are the contents of developing
automatic processors? What is other test solution?
performed to test the safety of automatic The developing solution contains four compo-
processor? nents, all dissolved in water:
The coin test can also be used to assess the 1. Developer: The primary function of the
amount of light transmission through the developing solution is to convert the
safety glass of automatic processors by exposed silver halide crystals into metallic
performing the test within the processor under silver grains. This process begins at the
the safety glass under the normal daylight latent image sites, where electrons from
loading conditions. the developing agents are conducted into
The other test is: the silver halide crystal and reduce the cons-
1. Unwrap two unexposed films: Expose one tituent silver ions (approximately 1 billion
to light. to 10 billion) to solid grains of metallic
2. Process both the films in automatic proces- silver. Two developing agents are used
sor. in dental radiology: A pyrazolidone-type
3. Check the results. compound, usually phenidone (1-phenyl-
4. If the unexposed film appears clear and dry, 3-pyrazolidone), and hydroquinone (para-
and if the film exposed to light appears dihydroxybenzene). Phenidone serves as
black and dry, the automatic processor is the first electron donor that converts silver
functioning properly. ions to metallic silver at the latent image
5. If the unexposed films do not appear clear site. This electron transfer generates the
and dry and film exposed to light does not oxidized form of phenidone. Hydro-
appear black and dry, the corrections must quinone provides an electron to reduce the
be made before the films are processed. oxidized phenidone back to its original
active state so that it can continue to reduce forms stable, water soluble complexes with
silver halide grains to metallic silver. silver ions, which then diffuse from the
Unexposed crystals, those without latent emulsion. The clearing agent does not
images are unaffected during the time have a rapid effect on the metallic silver
required for reduction of the exposed grains in the film emulsion, but excessive
crystals. fixation results in a gradual loss of film
2. Activator: The developers are active only density because the grains of silver slowly
at alkaline pH values, usually around 10. dissolve in the acetic acid of the fixing
This is achieved with the addition of alkali solution.
compounds (activators) such as sodium or 2. Acidifier: The fixing solution contains an
potassium hydrozide. Buffers are used to acetic acid buffer system (pH 4 to 4.5) to
maintain this condition—usually sodium keep the fixer pH constant. The acidic pH
bicarbonate. The activators also cause the is required to promote good diffusion of
gelatin to swell so that the developing thiosulphate into the emulsion and of silver
agents can diffuse more rapidly into the thiosulphate complex out of the emulsion.
emulsion and reach the suspended silver The acid fixing solution also inactivates any
bromide crystals. carryover developing agents in the film
3. Preservative: The developing solution emulsion, blocking continued development
contains an antioxidant or preservative, of any unexposed crystals while the film is
usually sodium sulphite. The preservative in the fixing tank.
protects the developers from oxidation by 3. Preservative: Ammonium sulphite is the
atmospheric oxygen and thus extends their preservative in the fixing solution, as it is
useful life. The preservative also combines in the developer. It prevents oxidation of the
with the brown oxidized developer to pro- thiosulphate clearing agent, which is uns-
duce a colorless soluble compound. If not table in the acid environment of the fixing
removed, oxidation products interfere with solution. It also binds with any colored
the developing reaction and stain the film. oxidized developer carried over into the
4. Restrainer: Bromide, usually as potassium fixing solution and effectively removes it
bromide and benzotriazole are added to the from the solution, which prevents oxidized
developing solution to restrain develop- developer from staining the film.
ment of unexposed silver halide crystals. 4. Hardener: The hardening agent most often
Although bromide and benzotriazole used is aluminium sulphate. Aluminium
depress the reduction of both exposed and complexes with the gelatin during fixing
unexposed crystals, they are much more and prevent damage to the gelatin during
effective in depressing the reduction of subsequent handling. The hardeners also
unexposed crystals. Consequently, the reduce swelling of the emulsion during the
restrainers act as antifog agents and final wash. This lessens mechanical damage
increase contrast. to the emulsion and limits water absorption,
79. What are the contents of fixing solution? thus shortening drying time.
Fixing solution also contains four components, 80. What are the components of automatic
all dissolved in water: processors? What are functions of each?
1. Clearing agent: After development the film, 1. The processor housing: Encases all the
emulsion must be cleared by dissolving and components of automatic processor.
removing the unexposed silver halide. An 2. Film feed slot: An opening of the outside
aqueous solution of ammonium thiosulphate of processor housing used to insert the
(hypo) dissolves the silver halide grains. It unwrapped film in the processor.
3. Rollers for transporter: Consists of series radiograph. Farmer’s reducer, a well-known

of rollers driven by constant speed motor reducer composed of:
that operates through gears, chains or belts. Mix solution A: Plain hypo as follows: Sodium
These functions: (i) Primarily to move the thiosulphate 480 grams (equal to 1–1/2 cups)
film through developing solutions. (ii) The water at 70°F to make 2 litres mix farmer’s
motion of rollers keeps the solutions reducer.
agitated. (iii) The solution exchange is
Solution B: Ferricyanide as follows: Potassium
achieved in emulsion, as the roller press on
ferricyanide 38 grams (equal to 2 tablespoons
emulsion forcing solution out and again it
and 1 teaspoon) water at 70°F, 500 ml.
is refilled by next solution. (iv) The top
rollers at the crossover point between the 82. What are factors considered in image
developer and fixer tanks remove rapidly attributes of radiograph?
the developing solution minimizing the risk Following factors are considered in image
of carrying the developer into fixer. attributes of radiograph:
4. Developer compartment: Holds the deve-
1. Density
loper solutions.
2. Contrast
5. Fixer compartment: Holds the fixer solu-
tion. 3. Detail/resolution
6. Water compartment: Holds the circulating 4. Sharpness
water. 5. Speed
7. Drying chambers: Used to hold the wet 6. Latitude
films to make it dry 7. Noise
8. Replenished pump and solution: Used to
maintain proper solution concentration and 83. What is radiographic density?
levels automatically. The overall degree of darkening of an exposed
9. Film recovery slot: It is an opening at the film is referred to as radiographic density or
outside of processing housing where the overall blackness produced on radiographic
dry, processed film emerges out of auto- film. An image that is neither too dark nor too
matic processor. light when seen on viewing monitor is said to
have correct radiographic density. Density is
81. What is cutting reducer? primarily controlled by varying mAs usually
Farmer’s solutions were previously called by increasing or decreasing exposure time.
cutting reducer. It is used to lighten the kVp and SID do affect but are not used to
control the same. This density can be measured 84. Define radiographic contrast.
as the optical density of an area of an X-ray film Radiographic contrast is a general term that
where optional density is given as follows: describes the range of densities on a radio-
Optical density It = Log10 I0 graph. It is defined as the difference in densities
between light and dark regions on a radio-
where I0 is the intensity of incident light (e.g. graph. Thus, an image that shows both light
from a view box) and it is the intensity of the and dark areas has high contrast. This is also
light transmitted through the film. Thus, the referred to as a short grey scale of contrast
measurement of film density is also a measure because a few shades of grey scale are present
of the opacity of the film. With an optical between the black and white images on the
density of 0, 100% of the light is transmitted film. A radiographic image composed of only
with a density of 1, 10% of the light is trans- light grey and dark grey zones has low
mitted with a density of 2, 1% of the light is contrast, also referred to as having a long grey
transmitted, and so on. scale of contrast. The radiographic contrast of
Film is of greatest diagnostic value when an image is the result of the interplay of subject
density is between 0.6 and 3.0. contrast, film contrast, and scattered radiation.
Low density light radiograph

Low contrast
High density, dark radiograph High contrast

85. What is relationship between radio- 89. What is film lattitude?

graphic contrast and density? It is a measure of the range of exposures that
When the contrast is changed, density is also can be recorded as distinguishable densities on
altered. However, when only the density is a film. Wide latitude can record a subject with
changed, the contrast remains unchanged. The a wide range of contrast. Useful when both
reason is: hard and soft structures have to be recorded,
• mA is the prime controlling factor for e.g. lateral cephalograms.
density, has no effect on contrast. Latitude of CCD and CMOS detectors is
• kVp which is the prime controlling factor greater than film. PSPs have larger latitudes.
for contrast, also affects density. 90. What is radiographic noise?
Working rule: For every 10 kVp increase, It is the appearance of uneven density on a
mA must be halved. uniformly exposed film. The causes are:
1. Radiographic mottle
86. What is resolution? 2. Radiographic artifact
It is the ability of the radiograph to record 91. What is static electricity? What are the
separate structures that are close together. effects of static electricity on film called?
Measured by radiographing an object made
It refers to development of an electric charge
up of series of lead strips with alternating
due to friction. This goes on exposing the films,
spaces of same thickness. They are arranged in
which is common on extraoral radiograph and
an increasing order of lines and spaces/mm.
rare on intraoral radiographs. These are star
Resolution is the highest number of line
burst, smudge, grassroot, tree branch or
pairs/mm that can be distinguished on the
lightning bolt.
radiograph with low power magnification.
Naked tree markings on the radiographs are
Indirect films have 5 line pairs/mm. Direct
a result of electrical discharges that do not
films have 20 line pairs/mm.
produce any visible light.
87. What is sharpness? Smudge type static electrical markings are
It is the ability of the radiograph to define an caused because of low potential charges which
edge precisely. Slower the film speed, smaller produce visible light.
the grain size, better the sharpness. Intensifying
screens decrease sharpness, avoided by close
contact between screen and film. In dental
radiographs, structures closer to the film are
sharper than structures away from the source.
Therefore, the lingual/palatal cusps will
appear sharper than the buccal cusps.
88. What is radiographic speed?
Radiographic speed refers to the amount of
radiation required to produce an image of a
standard density. Expressed as the reciprocal
of exposure in RA ‘fast’ film requires less
exposure to achieve the same density as
compared to a ‘slow’ film . Film speed depends
on the size of the AgBr crystals and their silver
content, bigger the crystals, faster the film.
Speed can be increased by processing at higher
temperature but this causes graininess and fog.
92. What is SLOB rule? What are the other • The objects (which has to be separated from
names of SLOB technique? buccal and lingual) and the film are kept
This technique separates and identifies the on fixed position.
facial and lingual structures. It is described by • The tube head is moved for radiograph.
Clark in 1910. The rationale for this procedure • The resultant radiograph shows the buccal
derives from the manner in which the relative objects moved away from the central ray of
positions of radiographic images of two projection while lingual object is moving
separate objects change when the projection towards the same direction of projection
angle at which the images were made is (hence same lingual and opposite buccal).
changed. If the tube is shifted and directed at The other names are BOR (buccal object
the reference object (e.g. the apex of a tooth) rule), BOMM (buccal object moves most),
from a more mesial angulation and the Clark’s rule, Walton’s projection, cone image
object in question also moves mesially with shift technique, and parallax technique.
respect to the reference object, the object lies Examination of a conventional set of full-
lingual to the reference object. Alternatively, mouth films with this rule in mind demon-
if the tube is shifted mesially and the object strates that the incisive foramen is indeed
in question appears to move distally, it located lingual (palatal) to the roots of the
lies on the buccal aspect of the reference central incisors and that the mental foramen
object: lies buccal to the roots of the premolars.
(a)
(b)
(a) Shows an IOPA of RO object placed lingually to apical area of mandibular second premolar with ideal
horizontal angulation, (b) Shows the tube head is moved mesially and central ray directed distally showing
the mesial movement of RO object which depicts its lingual position
(a)
(b)
(a) Shows an IOPA of RO object placed bucally to apical area of mandibular second premolar with ideal
horizontal angulation, (b) Shows the tube head is moved mesially and central ray directed distally showing
the distal movement of RO object which depicts its buccal position
(a) (b) (c)
(a) Shows red is buccal object, yellow is lingual object with ideal horizontal angulation, (b) Showing distal
movement of tube head with central ray mesially moving the buccal object moves (red dot) in opposite
direction more than the lingual object (yellow dot) showing little, (c) Shows mesial movement of tube head
with central ray directed distally showing the buccal object (red dot) moving more and lingual with a
little change
(a) Shows IOPA showing normal incisor positions and impacted canine using ideal horizontal angulation,
(b) The central ray moved distally and image of impacted canine has moved along with it distally indicating
palatal impaction of canine.
93. What is panorama? What are the other 95. What are the indications of panoramic
names of panoramic radiography? radiography?
Panorama is an unobstructed view, it is also Indications of panoramic radiography are as
called bird’s view, and extensive view. Panora- follows:
mic radiography is also known as pantomo- • For initial examinations of new patients in
graphy or rotational radiography, rotational all age groups that can provide insight or
panoramic radiography, orthopantomo- idea in determining other projections and
graphy [OPG], dental panoramic tomography other screening.
[DPT], and panora. It is named after the • To evaluate the cause of multiple missing
panoramic X-ray machine. teeth or unerupted teeth.
94. What are the ten steps in panoramic • To assess the pathological conditions below
radiography? complete and partial dentures (retained
teeth/roots)
1. Load cassette.
• As part of an orthodontic assessment where
2. Set exposure factors.
there is a clinical need to know the state of
3. Remove patients jewellery, place apron on
the dentition and the presence/absence of
patient.
teeth.
4. Ask the patient to bite on bite rod.
• To assess tooth development especially in
5. Adjust chin tilt. mixed dentition period.
6. Position the side guides. • As attaining a larger field size than possible
7. Ask the patient to stand up straight right. with periapical.
8. Ask the patient to swallow, place the • To assess bony lesions or an unerupted
tongue in the roof of mouth and hold still. tooth that are too large to be demonstrated
9. Expose the film. on intraoral films and to attain larger field
10. Process the radiograph. size than is possible.
• Prior to dental surgery under general anaes- 4. The roots of maxillary and mandibular teeth
thesia. are readily visible with minimal distortion.
• As part of an assessment of periodontal 5. Magnification is equal on both sides of
bone support where there is pocketing midline.
greater than 5 mm.
98. What is tangential effect?
• Assessment of third molars, at a time when
consideration needs to be given to whether This is a characteristic effect of roentgen rays.
they should be removed or not. By using normal exposure parameters if the
structure is at right angle to central ray they will
• Fractures of all parts of the mandible except
be visible only if the structure is of sufficient
the anterior region.
density or thickness.
• Antral disease—particularly to the floor,
The tangential effect of X-rays renders
posterior and medial walls of the antrum.
clearly visible in the irradiated space only those
• TMJ disease—TMJ dysfunction syndrome,
hard tissues with either high density or
to investigate disease within joint, to
significant thickness:
investigate pathological conditions affect-
ing condylar heads, fracture of condylar 1. Flat surface structures: The bony lamellae
head and/or neck, condylar hypo/hyper- would not be visible unless they are parallel
plasia. to central ray. The cancellous bone, only a
• Destructive diseases of the articular sur- portion bone will be visible.
faces of the TMJ.
• Vertical alveolar bone height as part of
preimplant planning.
• Asymmetries of jaws and face.
• Painful or asymptomatic swellings of jaws.
• When intraoral radiography is not possible
(e.g. severe trismus, gagging).
96. How the dose in panoramic radiography
is reduced compared to full mouth X-rays
with periapical and bite wing radio-
graphs?
In panoramic radiology the dose of radiation Only basal portion of mandible is seen because of
to the patient is 10 times less than full mouth transverse tangentially by central ray
survey using round BID and E+ film and it is
4 times less than 4 bite wings using long, round,
and BID with E+ film.
The panoramic dose is equal to that of four
bite wings using the long, rectangular BID and
E+ film.
97. How does the normal panoramic radio-
graph look like?
1. The mandible is U shaped.
2. Position of condyles: (a) About an inch
inside the edges of film and one-third of
way down from the top edge of film.
3. The occlusal plane exhibits a slight curve Zygomatic bone within radiolucency of maxillary
or smile line upwards. sinus (6, 7) encountered tangentially.
2. Curved surface structures: Basal portion of Addition Effect

mandible only seen as a tangential effect, The structure of interest lose clarity due to
temporal surfaces of zygomatic bone in summation of radiopaque objects, e.g.
maxillary sinus. 1. Mandibular anterior region by vertebrae.
99. What is summation effect? In children and adolescent this imposition
These are characteristic effects on radiographs is less disturbing as the hydroxyapetite
by roentgen rays. The central ray along its content is low. As the age advances the
traverse through tissues penetrates various addition effect is increased and even cannot
objects and superimposes such objects upon be manipulated by changing kV setting or
each other and portrays the third dimension slowing speed of electrons.
on two-dimensional radiograph. There are two 2. The parts which are closer to image receptor
types of summation effect, namely addition are superimposed by both sides of the
and subtraction effects. In both effects the mandible. This especially in asymmetrically
clarity is lost by different mechanisms. patients can lead to addition effects.
No. 2 is representing addition effect

3. The foreign bodies, normal and patho- central ray in maxillary anterior region
logical structures outside the plane of focus. which obscures the images.
The hairpins, necklace, eyeglasses, earrings,
sialoliths, and calcified lymph nodes can
obscure the diagnosis.
2. The shadow of epipharynx (if patient

improperly takes deep breath and holds
breath before exposure) as a radiolucency
Radiopacity by piercing tongue on ascending mandible creates radio-
lucency.
The earring with ghost image
3. Osteolysis can be misdiagnosed by air

containing external auditory meatus on
mandibular condyle (circumscribed sub-
traction effect).
Radiopacity caused by metal zipper's placed

on woman dresses, necklace
In this way the rays while travelling

encounters soft tissues, osseous structures, and
other radiopaque objects the ray is weakened
or diminished by such material and ultimately
the object shadow is with less radiation inten-
sity, producing circumscribed shadowing.
Subtraction Effect
The clarity is lost because of over radiation. 100. What is burn out effect?
1. If dorsum of tongue is not pressed against This is due to improper positioning of tongue
the palate air containing space results, it during projection. The roots of maxillary teeth,
promotes the uninhibited penetration of the structures of the maxilla, the boundaries of
nasal and maxillary sinuses are not properly 102. How the ghost image of cervical spine is
visible because of air. The air is negative reduced on panoramic radiograph?
contrast substance and is obliterating it. The The ghost image of cervical spine is avoided
radiation over-radiates that area and ulti- by asking the patient to sit straight or asked to
mately the structures are effected from final stand straight and the neck also straight,
results. This is called burnout effect. extended rather than slouched during
exposure. If the patient is slouched, the X-ray
beam traverses several cervical vertebrae.
103. What points are considered in the overall
assessment of panoramic radiograph?
Divide panoramic radiograph into 6 zones:
Zone 1: Dentition
Zone 2: Nose sinus
Zone 3: Mandibular body
Zones 4 and 6: Four corners; condyles and
hyoid
Zone 5: Ramus spine
Zone 1: Dentition
• Teeth should be arranged with a smile-like
upward curve posteriorly and separated
from each other.
• Anterior teeth should be neither too large
nor so narrow.
101. Which is the anatomic ghost seen on
panoramic radiograph? • Posterior teeth should not be larger or
smaller on one side than the other.
The ghost image of cervical spine is seen on
radiograph.
Zone 2: Nose sinus

• Images of inferior turbinates and their
surrounding air spaces should be contained
within nasal cavity.
• Soft tissue of nasal cartilage should not be
seen.
• Hard palate shadow and sometimes ghost
images of palate must be within maxillary
sinus.
• Tongue must be in contact with hard palate.
Zone 3: Mandibular body 104. Enumerate some of the useful panoramic

• Inferior cortex of mandible should be errors.
smooth and continuous. 1. Too for forward positioning: To visualize
• Double image or ghost image of body of nasal fossa and sinus. This results in an
hyoid should be absent in this area. improved image of nasal cavity and
• Midline area should not be overly enlarged maxillary sinus. Useful in detection of sinus
superiorly-inferiorly. disease, extension of disease into nose, and
deviated nasal septum.
Zones 4 and 6: Four corners; condyles and
hyoid
Zone 4:
• Contains condyles bilaterally.
• Should be more or less centred within this
zone.
• Should be of equal in size and on same
horizontal plane.
Zone 6: 2. Chin too low: To visualize anterior
• Contains body of hyoid. maxillary teeth.
• Should appear as a double image equal in
size bilaterally.
• Should not spread across the mandible.
3. Chin too high: To visualize anterior

mandibular teeth.
Zone 5: Ramus spine
• Ramus of mandible should be of the same 105. Classify panoramic errors.
width bilaterally. 1. Loading and uses of cassettes
• Spine should not superimpose on ramus. 2. Exposure errors
• When present distance between spine and 3. Positioning errors
ramus should be same bilaterally. 4. Errors during exposure
106. What are the exposure errors during panoramic radiography?
Problem Cause How to correct Hints

Light, pale film with Too little exposure Increase mA or kVp Rule out, worn out or
a few dark areas or use next higher reversed screens
settings on machine
Dark film with loss of Too much exposure Decrease machine Do not confuse with
details, amalgams and settings film fogging which is
unexposed areas overall grayness to film
are still clear
White opacities on film; Ghosts of metal Remove prior to Watch out for
little or no image is visible Jewellary exposure necklaces
on film
White opacity in palate Tongue bar Remove prior to Image is projected high
exposure onto palate instead of in
floor of mouth
White opacity at bottom Lead apron above colour Adjust and properly Watch for bunching at
of film shaped like line and X-ray beam place the apron back of neck
inverted “V” or “sharkfin”
107. Enumerate the panoramic positioning errors.

1. Anterior positioning errors

Anterior teeth blurry, too Patient biting too far Make sure anterior Make sure mandibular
small and narrow, spine forward on bite rod teeth are located in incisors are in groove
visible on sides of film grooves on rod also, and bite rod is not
being bent forward
Anterior teeth blurry and Patient is biting too Make sure anterior If anterior teeth are
wide, ghosting of mandible, far back on rod or teeth are located in missing, use
spine, and condyles close not at all grooves on rod edentulous guide
to edge of film
2. Chin tilt errors

Roots of lower incisors Patient’s chin is Reposition using Make sure patient does
blurry, mandible- tipped too far down proper guidelines for not have unusual
shaped like a “V”, too much that machine, such occlusal plane
smile line, condyles at top as ala-tragus line orientation
of film, spine forms arch
Maxillary incisors blurry, Patient’s chin is Reposition using Make sure bite rod
hard palate superimposed tipped too far up proper guidelines remains seated in its
on roots, flat occlusal plane, for that machine such guide
mandible is broad and flat, as ala-tragus line
condyles at edge of film
3. Head twist error

Teeth are wide on one Patient’s head is Reposition using Make sure patient does not
side, narrow on other side twisted in machine proper guidelines try and look towards
of midline; ramus is wider causing midline for that machine technician, but straight
on one side than the asymmetry ahead. Always use front-
other; uneven pattern of surface mirror on
blurring throughout arch; machine to check
nasal structures not clear alignment
Condyles are not equal Patient’s head is Reposition using Make sure patient’s head
in height, nasal rotated in machine proper guidelines remains level through
structures distorted (tipped) for that machine ears
4. Slumping errors
White tapered opacity Ghost of spinal Have patient take a Do not allow patient to
in middle of image column due to step forward and reach forward into
(Washington slumping straighten neck machine; then make
monument shape) step forward
Dark vertical line Cassette hit Straighten neck as Have patient keep
extending from top to shoulder and above. Check apron elbows tucked into
bottom edge of film temporarily stopped for interference sides
5. Errors during exposure

White vertical line on film Cause exposure Hold exposure Modern machines will
running from top to stopped briefly, button down return to start position if
bottom edge of film probably due to firmly during this happens
letting go of exposure button exposure
Images of springs or Cassette was placed Label tube side; Left and right will
rectangular radiolucencies in machine backwards place lead foil be reversed on
visible on film “X” on back side film if this happens
of cassette
6. Processing errors

Thin, washed-out images Depleted chemistry Replenish more Consider X-OMAT
frequently processor
Fogged film, overall Improper filter in Use red filter or You can use cardboard
grey or very dark film daylight loader cover viewing area to cover filter area while
on daylight loader loading panoramic film
108. List common factors that need to consi- of maxilla. It should be distinguished from
der during panoramic exposure. vertical septate, reinforcement webs and
posterior wall of maxillary sinus. The posterior
Factors to consider Exposure setting
region behind this line may be misinterpreted
Obese patient with Use the next highest as available bone for implants.
kVp or mA setting On skull radiograph and PA projections it
Large bone structure Use the next highest
represents the tangentially viewed greater
kVp or mA setting
Patient with small bone Use the next lower
wing of sphenoid. Panoramic innominate line
structure kVp or mA setting indicates infratemporal surface of zygomatic
Patient that is edentulous Use the next lower bone.
kVp or mA setting The three pathological processes affecting
the innominate line, namely destruction,
hyperostosis, and expansion.
109. What is innominate line? What are the
patterns of innominate lines? There are four patterns on radiographs:
It is a thin vertical radiopaque line on pan- • No visualization
oramic radiographs in the posterior third of • Visualization of whole length
antrum. The line is an artifact corresponding • Visualization of upper half
in its lower half to the posterior surface of the • Visualization of lower half
zygomatic process of maxilla and in its upper Lower half innominate line is confused with
half to the posterior surface of frontal process bone tips of blow out fracture.
110. What is tomography and zonography? more efficient at recording photon energy
Tomography is a general term for a technique than conventional films. It is nearly
that provides a distinct image of any selected following 50% compared to F speed films.
plane through the body, while the images of • Film images and films are obtained much
structures that lie above or below are blurred. more quickly and time is saved and
Narrow angle tomography, which uses consultation can be expedited.
an angle of less than 10° is called zonography • Simultaneous availability of images at
because a relatively thick zone of tissue (up to multiple sites without additional exposure.
25 mm) is sharply imaged, it is particularly useful • No need for conventional processing, thus
when subject contrast is low because of little avoiding all processing film faults and the
difference in physical density between adjacent hazards associated with handling the
structures. Because subject contrast is low in chemical solutions.
soft tissue, zonography is the preferred tomo- • Ultimately processing expenses are saved.
graphic technique when soft tissues are imaged. • No need to store films and darkroom
111. What is digital imaging? space.
Digital imaging is the art of making digital • No film degradation/no lost films.
images—photographs, printed texts, or artwork • Easy storage and archiving of patient infor-
through the use of a digital camera or image mation and incorporation into patient
machine, or by scanning them as a document. records.
Digital imaging uses sensors instead of a films. • Easy transfer of images electronically
It requires low exposure time in comparison (teleradiology).
to conventional radiography and image is • Image enhancement and processing.
displayed on computer almost instantly Current software packages allow several
without any need for chemical processing. image enhancement techniques including:
112. What are advantages of digital radio- – Inversion (reversal)
graphy over conventional radiography? – Alteration in contrast
Advantages over conventional film-based – Embossing or pseudo 3-D
radiography – Magnification
• Lower dose of radiation required as both – Automated measurement
types of digital image receptors are much – Pseudo-colorization.
113. What is a sensor? layer is also added. The scintillators used are
It is the key component of digital imaging gadolinium oxybromide and caesium iodide.
system. It is a technology used to record the 118. Where CCDs are used?
electronic images. A sensor consists of light
CCDs are involved in many aspects of every-
sensitive elements arranged in a regular grid
day life. They are used in video cameras for
of rows and columns. A rectangular two-
home use and those set-up to automatically
dimensional grid of sensor elements form a
trap speeders on British highways, hospital
pixel.
X-ray imagers and high speed oscilloscopes,
114. What is analog to digital conversion? and digital cameras used as quality control
At each pixel of the sensor, absorption of X- rays monitors.
generate small voltage. Analog to digital 119. How does CCD work?
conversion takes place in two steps:
When silicone atoms are exposed to radiation,
1. Sampling: A small range of voltage values X-ray photons provide energy to electrons in
are grouped together as a single value. valence band thus releasing them to the
2. Quantization: Every sampled signal is conduction band. This results in “electron
assigned a value. hole” charge pair—electron in conduction
These values are stored in computer and band and hole in valence band. Number of
represent an image. These values range from these electron hole charge pairs formed is pro-
0 to 255 where 0 represents black and portional to the amount of exposure received.
255 represents white. All the values in between Electrons in the conduction band are attracted
0 and 255 represent different shades of grey. towards the most positive potential in the
device resulting in formation of “charge
115. What is the meaning of ‘digital’ in digital
packets”. These charge packets represent latent
imaging?
image site for CCD. Each charge packet
‘Digital’ in digital imaging represents the represents one pixel. To read the image, each
numeric format of the image content and its row of pixel charges is transferred from one
discreteness. pixel to next in “bucket brigade” fashion.
116. What are the different digital image When charge reaches at the end of each row, it
detectors? is transferred to a readout amplifier and
The different digital image detectors are: transmitted as a voltage to analog to digital
convertor located within or connected to the
1. Charge coupled device (CCD)
computer.
2. Complementary metal oxide semicon-
ductor (CMOS) 120. What is pixel size range for CCD?
3. Photostimulable phosphor (PSP) For CCD pixel size ranges from 20 microns to
4. Bulk charge modulated device (BCMD) 70 microns. Smaller the pixel size, more
5. Thin film transistor (TFT) expensive is the manufacturing of CCD.
6. Flat panel detector (FPD)
121. What are the advantages of CCD in
117. What is charge coupled device (CCD)? comparison to conventional film
Sir George Smith and Willard Boyle on imaging?
October 17, 1969 first mapped out CCD. CCD 1. Image can be seen on the computer screen
is a first direct digital imaging receptor that was almost instantly. There is no time lag
used for intraoral imaging. It uses thin wafer between exposure and image display.
of silicone for image recording. As CCD is more 2. As no film processing is done, darkroom is
sensitive to light than X-rays, scintillating not required.
3. As no chemicals are used for processing, computed radiography, and radiolumino-

disposal of those hazardous chemicals is graphy.
eliminated.
126. What is the principle of PSP?
4. As low exposure time is required in com-
parison to conventional imaging, resultant PSP absorb and store energy from X-rays and
absorbed dose to the patient is also less. then release this energy as light when
stimulated by other light of appropriate
5. Image manipulation is possible for better
wavelength.
interpretation.
6. Teletransmission is easily possible. 127. Explain the working of PSP.
122. What are the disadvantages of CCD PSP is made of europium doped barium fluoro-
in comparison to conventional film halide. Barium fluorohalide forms a crystal
imaging? lattice and europium creates imperfections in
1. In comparison to conventional films, CCD this lattice.
sensors are very expensive. When exposed to radiation, valence
2. Sensors are bulky in comparison to the films electrons in europium absorb energy and are
and results in patient discomfort. released to conduction band. In conduction
3. Active area of sensor is smaller than its total band these electrons are trapped in halogen
surface area. vacancies known as “F centres”. In PSP these
4. Life expectancy of CCD sensor is unpredic- F centres represent latent image site. On
table and mainly depends on its handling. exposure to light, trapped electrons in F centres
5. Blooming artefact—blooming is similar to release energy in the form of green light and
allowing too much light through a viewer go back to the valence band. This green light is
box, blinding the operator and washing out detected by photomultiplier tube and is
radiographic information in the excessive converted into electrical energy. These voltage
bright image. In CCD this blooming occurs signals are sent for analogue to digital con-
by excess charge leakage to other pixel. vertor and digital image is formed.
123. What is complementary metal oxide 128. What is the function of photomultiplier
semiconductor? tube in PSP?
The construction and working of CMOS is Red filter at the photomultiplier tube
similar to CCD, only difference is in the way selectively removes the stimulating light.
in which pixel charges are read. In CMOS each Green light released from trapped electrons
pixel is isolated from its neighbouring pixel is detected and converted to voltage in
and is directly connected to a transistor. photomultiplier tube.
129. What are the safety precautions for use
124. What are the advantages and disadvan-
and storage of PSP plates?
tages of CMOS over CCD?
1. Before exposure, PSP plates should be
CMOS has low manufacturing cost in
erased to eliminate “ghost images” from
comparison to CCD. The disadvantages of
prior exposures. This can be done by
CMOS are that it has small active area for image
flooding the plate with a bright light source.
acquisition and the sensors may not perform
Most of the times, the processing system is
well in low light condition.
incorporated with automatic plate erasing
125. What are the other names for photo- lights. For intraoral plates, phosphor side
stimulable phosphor radiography? of the plate can be placed on dental view
Other names for photostimulable phosphor box for 1–2 minutes to erase it.
radiography are digital luminescence radio- 2. Erased plates should be kept in light-tight
graphy, storage phosphor radiography, containers.
3. For intra-oral plates, sealable polyvinyl 132. What are flat panel detectors?
envelopes impervious to oral fluids and FPDs are currently used in cone beam
light are used for packaging. computed tomography (CBCT). They provide
4. For extraoral plates, conventional cassettes relatively large matrix areas with pixel sizes
without intensifying screens can be used. less than 100 microns and allow direct digital
Some manufacturers provide extraoral imaging of larger areas of body.
plates with cassette.
5. A semi-dark environment is recommended 133. What are the types of flat panel dete-
for plate handling. ctors?
6. Red safelights found in most darkrooms are FPDs are of two types: Indirect FPD and direct
not safe for exposed PSP plates as they are FPD.
more sensitive to red light spectrum. Indirect FPDs are sensitive to visible light.
130. What are the advantages of PSP intra- Intensifying screens with gadolinium or
oral plate over CCD sensor? caesium are used to convert X-rays to visible
PSP intra-oral plate does not have electric cord light. Use of intensifying screens makes
attached to it like CCD sensor so placement of indirect FPDs more efficient but leads to image
PSP plate in oral cavity is easy. Also, PSP plates unsharpness.
have less thickness than CCD sensor so they Direct FPDs use a photoconductor material
are more comfortable to the patient. like selenium due to which there is more
efficient absorption of X-rays providing higher
131. What are the disadvantages of PSP intra-
resolution.
oral plate over CCD sensor?
In case of CCD, image is displayed on com- 134. What is spatial resolution?
puter screen almost instantly after exposure. Spatial resolution is capacity for distinguishing
In case of PSP, the plates have to be processed fine details. It is measured in units of line
through the system so it takes more time in pairs per millimetre. For IOPA film resolution
comparison to CCD. Also since PSP plates are is 20 lp/mm, for OPG it is 5 lp/mm, for most
less thick in comparison to CCD sensor, they digital systems resolution is more than
can get damaged easily. 7 lp/mm and for CT resolution is 12 lp/mm.
10
Radiology—Part 2
1. What is Aunt Minnie phenomenon? 3. What are Campbell’s lines?

It was coined by famous radiologist Ben Felson. These are the lines to be seen on occipitomental
The Aunt Minnie phenomenon in radiology is radiograph.
a phenomenon of correctly identifying a Line 1: Joins the two zygomaticofrontal
disease process by its unique radiological sutures. It runs along the superior orbital
presentation. Aunt Minnie represents an margin on each side and centrally across the
abnormality which looks like one that the region of glabella. This is check for any
evaluator has seen before or been told about. separation of the zygomaticofrontal suture and
It will be difficult to recognize new findings look at the integrity of the superior orbital
using this approach. Cousin Harry represents margin.
an abnormality which the evaluator has not
Line 2: It is traced from the zygomatic arch. It
seen for a long time, but would like to see while
follows the zygomatic bone and continues
uncle Fred represents an abnormality which is
along the inferior orbital margin across the
often present.
frontal process of maxilla and lateral wall of the
2. Enumerate the radiographic techniques nose through the septum. It then follows a
to visualize posterior border of maxillary similar course on the other side. Check the
sinus. zygomatic arch fractures, then compare the
Posterior wall separates the maxillary sinus transverse width of the frontal process
from pterygoplatine fossa. Posterior border of of maxilla and vertical dimensions of the
maxillary sinus is visualized in IOPA of zygomatic bones on the left and right sides.
posterior maxillary areas, lateral occlusal A symmentry indicates fracture. Look for
view, panoramic X-rays, submentovertex break in continuity of the inferior orbital
view, lateral cephalogram view. Although PA margin, particularly at the junction of inner
Waters view being best projection to visualize third and outer two-thirds. A downward
sinuses the posterior wall cannot be seen blow out fracture of the orbit may be seen
on it. (tear drop sign).
210
Line 3: Starts at the condyle of the mandible

and traces across the mandibular notch and
coronoid process to the lateral wall of maxillary
antrum. It continues through the medial wall
of the antrum or lateral wall of the nose at the
level of the nasal floor and follows a similar
course on opposite side. Check the continuity
of the maxillary antral walls and look for any
depression of the orbital floor.
Line 4: Follows the occlusal curve of the upper
and lower teeth. Check for evidence of
mandibular fractures. Specific views are
indicated for diagnosis.
Line 5: It is also called Trapnel’s line, which
traces the line of lower border of the mandi.
4. What is tear drop sign?

Blow out fracture of inferior orbital margin.
This injury occurs when an object (e.g. ball) hits
the eye rather than zygoma. The contents of the
orbit are pushed down through orbit since it is
weakest point.
The inferior rectus muscle is trapped
causing diplopia on upward gaze. The classical
appearance on X-ray is ball of proptosed tissue
described as “tear drop” appearance.
If this sign is observed, the patient is not
supposed blow through nose.
5. Which projections are used to visualize replaced by cicatrix produced by granula-

coronoid process? Which is the best tion tissues and so they are even difficult
projection? to palpate also. Examination of thyroid
Panoramic view, PNS, SMV, PA mandible, gland by USG is possible to detect
transpharyngeal view. PNS is the best metastasis from oral cancers.
projection. 7. What is foramen of Stensen and Scarpa
6. Enumerate the uses of ultrasound imag- contain?
ing in oral and maxillofacial region. A little behind the central incisor teeth and in
It is an easy method to detect noninvasive and the line of median palatine suture there is a pit
soft tissue related diseases in oral and called foramen incisivum. At the bottom of this
maxillofacial regions. may be seen openings of small canals ranging
1. Normal anatomical structures: It is in from one to four. These are arranged in two
particular in the oral and maxillofacial pairs—one being placed side by side and the
region in analyzing normal and abnormal other is placed in median plane, one forward
anatomical structures, as Doppler images and one behind.
associated with the B-mode can provide Foramen of Stensen is one which is arranged
vascular information associated with in side by side and transmits the greater
morphology of soft tissues. palatine arteries which ascend to reach the
2. In salivary gland diseases: The examina- nasal cavities. The foramen of Scarpa is the pair
tion done by ultrasonography can clearly
identify the presence or absence of mass-
like lesions and hence readily detect and
diagnose salivary gland-related diseases.
3. In lymph node diseases: The above-
mentioned property of mass detection by
USG helps in detection of lymph node
pathology.
4. Ultrasound with fine needle aspiration
biopsy: The accuracy of this procedure is
been shown to be relatively high in spite of
noninvasive procedure.
5. Interventional radiology using fine needle
aspiration by USG: The resolution of
Ranulas and plunging Ranula occurred
after administration of sclerotherapeutic
agents under ultrasound guidance.
6. Diagnosis in tongue lesions: In tongue can-
cer US imaging is often used to accurately
estimate tumour size or thickness and to
define adequate resection margins with
tumour extension and deep infiltration.
7. Diagnosis of metastatic lymph nodes:
Metastatic cervical lymph nodes are seen
better than CT. It is difficult to palpate the
remaining lymph nodes in neck after cancer
treatment because the normal tissues are
which is present in front and behind open into

left and right nasal cavities respectively, pass
left/right nasopalatine nerves respectively.
8. What are stalagmites of maxillary sinus?
Stalagmites are found on caves formed by
percolating water. Antral floor sometimes
show radiopacities that are small osseous
excrescences and small bony masses resemble
like stalagmites. They are formed on floor of
antrum and seldom reach 3 mm height, are
white masses. Differantiation from root tip has
to be done as root tip shows shadow of pulp with prominent depression in midline of the
canal. labial mental area. This pseudolesion on
panoramic radiograph is called presidents
9. What is president’s tumor?
tumor.
In the past president of US was retiring from
the office and as a part of administrative 10. What is cervical burnout?
process of the retiring the president was It is a radiolucent band at the neck of teeth
scheduled for an extensive physical examina- radiographically appearing as radiolucent
tion including a dental check-up and had areas at mesial and distal surfaces at neck,
undergone panoramic X-ray. There was a cervical portion of tooth and crest of alveolar
radiolucency observed at the root apices of ridge. It is an artifact caused by less absorption
anterior teeth in lower jaw. The consultants of X-ray in that area. In the cervical area there
who observed all this radiolucency agreed that is less tissue for X-ray beam to pass through
the nature of the radiolucency is pathologic. and it leads less accentuation of X-ray beam,
The intraoral radiographs taken in this hence no opaque shadow is cast. Additionally,
area appeared completely normal and this contrast of radiopaque enamel, dentin and
panoramic radiolucency seen in individuals alveolar bone also give perception.
11. Enumerate the differentiating points of cervical burnout and cervical caries.
Cervical burnout Cervical caries
The cause of radiolucency – It is an artifact due to less It defects in enamel and cementum.
attenuation of X-ray beam.
– Anatomic differences shape
of CEJ and various root
configurations.
Clinically Normal Capitation
Exposure factors It is increased when exposure Not necessarily associated.
is greater and contrast is more
Affected teeth Usually, all teeth on radiograph It may be associated with affected
are affected specially smaller tooth.
premolars.
Condition of alveolar bone Mostly the alveolar bone If associated with cemental caries, the
intacts as it is one of the factors recession is present and alveolar bone
for appearance. loss may be seen.
CEJ Knife edge at CEJ is intact. Knife edge at CEJ is affected.
Contd.
Contd.
Cervical burn out Cervical caries
Associated with restoration It is increased adjacent to It can be seen nearby the metallic
metallic restoration. prosthesis but the amount of radio-
lucency is not affected by the presence.
Location Nearer to alveolar crest Nearer to contact point.
Shape Band shaped in anterior teeth Mostly saucerized and irregular
or wedge (triangular) shaped, shaped.
in posterior teeth. The triangle
becomes less apparent towards
the centre of tooth.
Borders Well-demarcated Diffuse
Bounded above by enamel cap Apparently no upper and lower
or restoration and below by the demarcating borders.
alveolar bone.
Defect in angulation Seen when horizontal Seen horizontal angulation is correct.
angulation is incorrect.
Changing angulation With different angulation the It does not show change.
defect may not be seen.
12. What is Mach band effect? 13. How Mach band effect differentiated
This is an optical illusion, described by Sir Ernst from actual carious lesion?
Mach in 1865. It occurs within retina and results When there is confusion regarding differentiat-
from physiological process of lateral inhibition. ing Mach band from an actual carious lesion.
It occurs at the junction of two regions of The following experiment is done:
differing radiodensity. It is experienced upon 1. The radiograph under consideration is care-
viewing the enamel dentinal junction. The fully examined for the negative Mach band
enamel margin immediately adjacent to DEJ is effect.
white, whereas the dentin tends to black. 2. The opaque card is used to cover the enamel
The uniformly dark shade meets uniformly of the radiograph (light shade) if Mach
light shade (dentin meets enamel in radio-
graph), the dark shade (dentin) appears more
darker and light shade (enamel) appears even
more lighter as they appear DEJ (interface).
This edge enhancement phenomenon does not
result from actual density change in film
emulsion but from lateral neural inhibitory
interactions within the eye of the beholder. The
light shade which is brighter, is called positive
Mach band effect while darker appearance of
dark shade is called negative Mach band effect.
The negative Mach band effect may show (a) (b) (c)
fictitious Mach band effect resembling caries Figure showing Mach band effect: (a) Dark shade
(common in incisors, canines, premolars less meets light shade as dentin meets enamel,
frequently and to the least extent in molars). (b) Unmasking by putting an opaque object will make
The Mach band effect generally extends 0.5 mm to disappear the dark shade, (c) It will again appear
below the DEJ. after unmasking.
band effect, i.e. radiolucency disappears even lateral extraoral X-ray and tracing can
then it is positive Mach band effect, but if be done, which was originally advocated
radiolucency does not go off, then that is by Sir George Winter. Three imaginary lines
active carious lesion. are drawn which are known as ‘Winter’s lines’.
14. What is Wolff's law? White line corresponds to the occlusal plane.
It has been stated by Sir Julius Wolff in late 1800s. The line is drawn touching the occlusal sur-
It states that the number and the distribution faces of first and second molar and is extended
of bony trabeculae are dependent on the strains posteriorly over the third molar region. It indi-
and stresses to which the bone is subjected. cates the difference in occlusal level of second
and third molars. It indicates depth of impaction.
or
Every change in the form and function of Amber line represents the bone level. The
bones or of their function alone is followed by line is drawn from the crest of the interdental
certain definite changes in the configuration in septum between the molars and extended
accordance with mathematical laws. posteriorly distal to third molar or to the
ascending ramus. This line denotes the alveolar
For example, when the tooth is removed, the
bone covering the impacted tooth and the
bone from which tooth has been removed
portion of tooth not covered by the bone.
appears to have less strain as compared to the
bone if tooth is present, ultimately the bone in Red line is drawn perpendicular from the
this area appears to be radiolucent and the amber line to an imaginary point of application
trabeculae less organized. of the elevator. It indicates the amount of bone
that will have to be removed before elevation,
15. What are Winter lines? i.e. the depth of the tooth in bone and the
These are called war lines of Winter. The difficulty encountered in removing the tooth.
position and depth of an impacted third molar Howe said that 1 mm increase in length causes
can be assessed by taking intraoral X-ray or three times difficulty.
If the length of red line is 5 mm or less, then A sclerotic margin is a wide, radiopaque
the tooth can be conveniently removed. If the border of reactive bone that usually is not
length is more than 5 mm, it has to undergo uniform in width. This may be seen in
extraction under GA or with sedation. periapical cemental dysplasia and may
indicate a very slow growth rate or potential
16. How the caries is classified on radio-
for the lesion to stimulate the production of
graph?
bone. Unilocular lesions display well-defined
E0—No visible radiographic caries lesion sclerotic border. Most chronic inflammatory
E1—Lesion in outer one-half of enamel. bony lesions demonstrate sclerotic border
E2—Lesion in the inner one-half of enamel which reflects the reaction of surrounding
D1—Lesion in outer one-third of dentin trabecular bone to inflammation. Some
D2—Lesion in middle one-third of dentin malignant lesions may demonstrate sclerotic
border.
D3—Lesion in inner one-third of dentin.
17. What are sclerotic and corticated border?
Name conditions in which sclerotic and
corticated borders are seen.
A corticated margin is a thin, fairly uniform
radiopaque line of reactive bone at the
periphery of the lesion. This is commonly seen
in cyst. Lobulated and multilocular lesions
corticated with scalloping.
18. What are diagnostic criteria of odonto-

genic and nonodontogenic lesions on
radiograph?
If the epicentre of the lesion is above the inferior
alveolar canal, it is suggestive that the lesion is
probably composed of odontogenic tissue.
For example, residual cyst, radicular cyst.
The cartilaginous lesions originate in

condyle.
If the epicentre of the lesion is below the 19. What are the characteristics of neural and
inferior alveolar canal, it is less likely to be vascular lesions?
odontogenic origin and mostly nonodonto- Neural neoplasms cause expansion in more
genic in nature, e.g. Stafne’s bone cyst. concentric fashion creating fusiform shape
The neural and vascular lesions have the while vascular lesions increase the girth of the
epicentre in the inferior alveolar canal. canal down the entire length and often a shape
into serpiginous form.
Neural lesion involving entire length and

fusiform shaped
Fusiform expansion indicating neural lesion
Vascular lesion showing widening of inferior canal in serpiginous form
20. What is mineralization? Name the Odontogenic lesions with mineralization—

lesions with and without mineraliza- odontoma, odontogenic myxoma.
tion. Odontogenic lesions without mineralization—
Mineralization refers to the elaboration ameloblastoma, keratocystic odontogenic
of mineralized products by the lesion tumor and radicular cyst (this may show
itself; such products include enamel, mineralization in chronic cases).
dentin, and cementum or cementum like 21. What is radiolucent rim around lesion?
calcified tissue. Mineralization produces Give the differential diagnosis of lesions
lesions with varying degrees of opacity and having radiolucent rims.
are classically described as radiopaque or A radiolucent rim or soft tissue capsule is a
lesions of mixed opacity. Nonmineralized kind of well-defined border at the periphery
odontogenic lesions are classically radio- of radiopaque jaw lesions that presents as
lucent and fail to demonstrate internal a radiolucent line. It can be observed in
mineralization. association with a corticated border.
Entity Age/sex Common Distinguishing Diagrammatic

location features representation
Periapical >30 yrs Anterior Vital teeth, <1 cm

cemento-osseous F>M mandible often multiple,
dysplasia circular size
Focal Mean age Posterior Local jaw expansion

cemento-osseous 37 yrs mandible and mild discomfort
dysplasia F>M
Florid Middle to Premolar Bilateral,

cemento-osseous elderly molar area symmetrical
dysplasia F>M both jaws extensive
Cemento- 10–40 yrs Molar Round, expansive,

ossifying F>M mandible painless, slow
fibroma growth. Displacement,
root resorption
Osteoid Mean 19 yrs Long bones Nocturnal

osteoma F>M jaws 1% pain
Osteoblastoma Mean 23 yrs Body of Slight pain, swelling,

F>M mandible expansion
Compound Children and Anterior Denticles, pericoronal

odontoma adolescent maxilla lesion
F>M
Complex F>M Posterior Slow now

odontoma mandible aggressive
Cementoblastoma 10–30 yrs First molar Asymptomatic,

M>F mandible nodular, expansive
22. Enumerate the multilocular radio- 25. Enumerate the conditions causing
lucencies. ground glass appearance.
Ameloblastoma Fibrous dysplasia, hyperparathyrodism,
Central giant cell granuloma Paget’s disease of bone.
Giant cell lesion of hyperparathyroidism
26. Name the conditions causing generali-
Cherubism sed loss of lamina dura.
Odontogenic myxoma
Hyperparathyroidism and Paget’s disease,
Odontogenic keratocyst fibrous dysplasia, osteomalacia, rickets, multi-
Aneurysmal bone cyst ple myeloma, osteoporosis, Pyle’s disease,
Metastatic tumors to the jaws hypophosphatasia, renal osteodystrophy and
Vascular malformations and central heman- leukemia. While thinning is seen in osteo-
gioma of bone. porosis and Cushing’s syndrome.
Rarities 27. Name the conditions in which thicken-
Ameloblastic variants, arteriovenous malfor- ing of lamina dura is seen.
mations, Burkitt’s lymphoma, calcifying epi- Local trauma from occlusion. Marked malposi-
thelial odontogenic tumor, cemento-ossifying tion or served as abutments for fixed bridges.
fibroma, central calcifying odontogenic cyst, Systemic hypoparathyroidism and bisphos-
central giant cell tumor, central salivary gland phonate related osteonecrosis of jaw.
tumors, central odontogenic and nonodonto-
genic fibromas, chondroma, chondrosarcoma, 28. Enumerate the radiographic signs of
fibromatosis, fibrous dysplasia, fibro-odonto- trauma from occlusion.
genic dysplasia, hemangiopericytoma, imma- Widening of periodontal membrane space,
ture odontoma Langerhans’ cell disease thickening of lamina dura, hypertrophy of
(eosinophilic granuloma), leiomyoma lingual cementum and root resorption.
mandibular bone defect, neurilemoma, neuro-
ectodermal tumor of infancy, osteomyelitis 29. What are various radiographic appea-
pseudotumor of hemophilia, squamous rances of hyperparathyroidism?
odontogenic tumor. Only one in five patients has got noticeable
23. Enumerate the multilocular lesions radiographic changes:
associated with mandibular expansion. 1. Earliest and reliable manifestation is subtle
Three entities well-known to cause mandibular erosions of bone from the subperiosteal
expansion with a multilocular presence are the surfaces of phalanges of hands.
ameloblastoma, the odontogenic myxoma,
and the central giant cell tumor. Less common,
but well-known to be multilocular, is a central
arteriovenous hemangioma of the jaws. In
addition, if the lesion is a small, multilocular
lesion between premolar or canine teeth,
a botryoid odontogenic cyst is a strong
consideration.
24. What is Garrington’s sign?
It is a widening of periodontal ligament
space symmetrically on radiograph is an
early sign of osteosarcoma. It is also seen in
chondrosarcoma.
2. Unusual radiolucent appearance from

demineralization of bone.
3. Osteitis fibrosa cystic-localized loss of all

bone/replaced by fibrous tissue.
4. Punctate/nodular appearances of patho-
logic calcifications in the joints and
kidneys.
5. Demineralization of skull shows radio-
lucent appearance. Entire calvarium has a
granular appearance (in prominent hyper-
parathyroidism) due to loss of central
(diploic) trabeculae and thinning of cortical
tables.
6. Radiograph of skull shows ‘pepper-pot’ 9. Demineralization and thinning of cortical
appearance as medullary/inner and outer boundaries often occur in the jaws in
cortices lose their differential pattern. cortical boundaries such as the inferior
7. Brown tumor in late of disease (about border, mandibular canal, and the cortical
10% of cases). These peripheral or central outlines of the maxillary sinuses.
tumors of bone are radiolucent. The gross
specimen has a brown or reddish-brown
colour.
8. Loss of lamina dura complete or partial,
may involve one or several teeth (10%
cases) may give the tooth a tapered
appearance.
10. The density of the jaws is decreased,

resulting in a radiolucent appearance
that contrasts with the density of the teeth.
The teeth standout in contrast to the
radiolucent jaws.
11. A change in the normal trabecular pattern

may occur, resulting in a ground glass
appearance of numerous, small, randomly
oriented trabeculae.
30. What are radiological appearances

suggestive of cancers?
12. Pulp stones and root resorption. • Radiolucency with ragged and vague
borders.
• Band-like widening of the periodontal
ligament.
• Combined radiolucent-radiopaque lesion
with a vague pattern.
• Radiopacity with vague borders.
• Sunburst appearance from the border of the
bone. Possibly combined with changes in
the first three appearances.
• Hanging tooth or naked tooth.
• Onion skin appearance from the border of
the bone.
• Possibly combined with changes in the first
three appearances.
31. What are the radiographic appearances
of osteogenic sarcoma?
Generally, one of the radiographic features of
osteogenic sarcoma is apparent: Sunburst
appearance; cumulus cloud appearance;
Codman’s triangle; asymmetric, band-like
widening of the periodontal ligament; or
onion skin appearance of redundancy of the
cortical plate.
32. Describe variable radiographic appea-
rances of fibrous dysplasia.
Fibrous dysplasia is defined as a benign
osseous disease characterised by a process of
normal bone resorption, followed by an
abnormal proliferation of a disorganised
fibro-osseous tissue. It ranges from a radio-

lucent lesion to radiopaque mass. The borders
are poorly defined and blending:
1. The classic lesion is ground glass (peau
d’orange effect). This effect is more common
on I/O radiographs. This is also called
frosted glass appearance, it appears on CT
also. There is homogeneous radiopacity by
myriad dispersed minute spicules of bone
within bone.
4. Fingerprint appearance.
2. The plain radiographic features are 5. Superior displacement of mandibular canal

classified into: (1) Pagetoid (56%) it appears is classic feature.
radiographically similar to Paget’s disease
having radiolucency with patchy, irregular
opacities resulting in mottled radiographic
appearance, (2) Sclerotic (23%), (3) Cystic
(21%).
3. Unilocular/multilocular appearances in
long bones. Long-standing disease may
show mottled radiolucent and radiopaque
appearance.
Radiographic appearance may vary Acute Osteomyelitis

according to age and history of tumor. 1. Ragged, patchy, moth-eaten area of radio-
In very young patients with rapidly lucency. The outline of the area of destruc-
expanding fibrous dysplasia multilocular tion is poorly defined.
radiolucent lesion with cortical thinning is 2. Evidence of small radiopaque sequestrate
seen. The teeth may spread apart and evidence of dead bone occasionally within the radio-
of dental eruption. In older patients with lucency.
clinically quiescent lesions it may show mixed 3. Evidence of subperiosteally bone for-
radiolucent/radiopaque or that of simply mation, usually beyond the area of necrosis,
radiopaque mass. particularly along the lower border of
The radiographic appearance in FD varies mandible.
greatly depending upon the stage into 3 types:
Type 1: A small unilocular or multilocular Chronic Osteomyelitis
radiolucency with a well-circumscribed border 1. Localized or moth-eaten areas of bone
containing a network of fine bone trabeculae. destruction.
Type 2: Similar but with increased trabecula- 2. Sclerosis of the surrounding bone.
tion rendering a more opaque and mottled 3. Evidence of small radiopaque sequestra of
appearance. dead bone sometimes within the area of
Type 3: The lesion is quite opaque with many bone destruction.
delicate trabeculae giving a ground glass or 4. Evidence of an involucrum surrounding the
peau d’orange appearance to the lesion. This area of destruction following extensive sub-
type is not well-circumscribed but blends with periosteal bone formation.
the normal bone. The main finding is progressive radiopacity
Fibrous dysplasia and maxillary sinus: It with effacement of cortico-cancellous junction
may expand into antrum by displacing its histologically correlate to bone sclerosis
cortical boundary and subsequently occupying this may be associated with radiolucency
most of maxillary sinus. Extension occurs from corresponding to small resorptive defects
lateral wall and last section is posterorsuperior which are vascularised.
portion. Radiolucent lines that intersect of radio-
The lamina dura disappears and abnormal paque cortical bone are indicative of seques-
bone pattern is laid down. tration.
Superior displacement of inferior nerve Chronic focal sclerosing osteomyelitis
canal is characteristic of fibrous dysplasia. (condensing ostetitis) radiodensity localized to
apex of tooth.
33. What are the radiographic appearances Diffuse sclerosing osteomyelitis seen in
of chronic osteomyelitis? older patients may be showing diffuse
Chronic osteomyelitis may demonstrate four radiopacity in edentulous region. The diffuse
distinct radiographic pictures—completely patchy sclerosis is often described as cotton
radiolucent, mixed radiolucent and radiopaque, wool appearace similar to Paget’s disease of
completely radiopaque, and proliferative bone. It may be extensive and sometimes
periostitis. The last can be recognized as a bilateral and may involve maxilla and
somewhat opaque layering of the periosteum, mandible.
with bone proliferating peripherally. Proliferative periostitis incease mandibular
It varies according to underlying inflam- thickening common in children, the thickening
matory response and age of patient. relates to multilamellar periosteal deposition.
Primary osteomyelitis (course is insidious, Secondary osteomyelitis (more than 4 wk).

lacking an acute stage)
Areas of increased radiopacity with loss of bony Areas of increased radiopacity with loss of
trabeculae, effacement of cortico-cancellous bone bone trabeculae
junction affecting hemimandible.
Minor part of radiolucency Sequestra formation
Rarely periosteal reaction Calcified periosteal reaction
Temporomandibular joint involvement Pathological fractures
Stable radiographic changes may undergo mild Normal bone structures expected after
changes in case of relapse. healing.
Histologically sclerotic bone deposition and 34. Enumerate the sign suggestive of close
trabecular spaces filled with cellular connective relation of inferior alveolar canal and
tissue component. mandibular roots.
Chronic recurrent multifocal osteomyelitis Howe and Payton (1960) suggested the signs.
(CRMO) shows diffuse bony radiopacity. These are seen on:
Garré’s osteomyelitis (chronic osteomyelitis 1. Teeth roots
with proliferative periostitis) young patients a. Darkening of the root: When there was
with onion skin appearance. impingment of canal on tooth root there
was loss of density of tooth root and the
root appears dark (dark band pheno-
menon).
b. Deflected roots: Deflected roots or root
hooks were seen as an abrupt deviation
when the root approaches the canal.
c. Narrowing of root: It is seen when inferior
alveolar canal crossed the apex and
identified by double periodontal mem-
brane space at the apex.
d. Bull’s eye: Overlapping of buccal and
lingual root tips.
e. Illustration of discontinuous image of the
mandibular canal (canal discontinuous
phenomenon).
2. Inferior alveolar canal
a. Interruption of white lines (danger sign
showing true relationship with inferior
alveolar canal and tooth): The corticated
border (superior and inferior) of inferior
alveolar canal is observed. It is consi-
dered to be interrupted if it disappeared
immediately before it reaches apex. It
indicates:
1. Deep grooving if it occurs along the root.
2. Perforation of the root if it is seen with
narrowing of root canal.
b. Diversion of the inferior alveolar canal: It is the radiograph of an impacted mandibular

considered to be diverted, if while third molar, the radiolucent shadow of
crossing the inferior canal there was a mandibular canal appears as a dark band
change of its direction. crossing the roots of third molar indicates that
c. Narrowing of inferior canal: It is considered the canal is probably in close proximity of roots.
to be narrowed when the root of The constriction of canal while crossing the
mandibular third molar was crossed by roots of impacted mandibular third molar
it, showing reduction in diameter. indicates that the canal is in close proximity
d. The hourglass form: It indicates the with roots. The darkening of roots is sometimes
displacement of upper/lower border indicative of notching of roots.
toward each other. It indicates a partial
or complete encirclement of canal.
35. What is canal discontinuous pheno-
menon?
The radiograph shows discontinuation of
image of mandibular canal as it crosses the
roots of mandibular third molars. This also
shows close proximity of roots.
37. Enumerate different types of periosteal

reactions and give examples of each.
Periosteal reaction (periostitis/periosteitis) is
a nonspecific radiographic finding that occurs
36. What is dark band phenomenon? What with the periosteal irritation. The periosteal
are the other factors considered for proxi- reactions result when cortical bone reacts to
mity of root surface? one of many possible insults (tumor, infection,
The proximity of impacted mandibular third trauma, certain drugs, and arthritic changes, etc.).
molars roots to inferior alveolar canal has been The appearance depends upon the intensity.
In children the reactions are aggressive and

appear more earlier as the periosteum is more
active and less adherent to underlying cortex.
In jaws these are rare and probably the imaging
is not sufficient to visualize them. It has been
thought to arise after the periosteum is stripped
from the cortex. The frequency of periosteal
group is highest in osteomyelitis group
followed by malignant conditions. The intra-
articular lesions show no periosteal reaction
because there is no periosteum intra-articularly.
Classification
These are classified as benign and aggressive
reactions. 2. The onion skin pattern (lamellated): It is
a multilayered periosteal reaction and
Benign Periosteal Reaction
demonstrates multiple concentric parallel
Low-grade chronic irritation allows time for layers of new bone adjacent to cortex,
the formation of normal or near-normal cortex. reminiscent of layers on an onion. The
The cortex will be thick and dense and have a layers are thought to be result of variable
wavy or uniform appearance. Benign periosteal growth. It indicates more aggressive
reactions can be seen in callus formation in a process, as the periosteum cannot produce
fracture or with slowly growing tumours. the bone as fast as the lesion is growing so
Aggressive Periosteal Reaction intermittent bouts are seen and not as solid
Rapid irritative processes do not allow the
periosteum time to lay down and consolidate
new bone to form normal cortex. The cortex
may appear lamellated, amorphous, or
sunburst-like. Aggressive periosteal reactions
cannot only be seen with malignant tumors,
but also with more benign processes like
infection, eosinophilic granuloma (Langerhans’
cell histiocytosis), aneurysmal bone cyst,
osteoid osteoma, and trauma.
Uniqueness for Specific Reaction Process
Although no specific reaction is unique for any
process:
1. The uninterrupted lamellar: An uninter-
rupted indicates a benign process, which
is slow growing, indolent and long-
standing. It is seen in osteomyelitis and
may be only radiologic manifestation. As
the process is slow growing the periosteum
has ample time to respond and can produce
new bone as fast as the lesion is growing
and may produce uninterrupted new bone
along the margins of the affected bone.
thick compact mass. Garré’s osteomyelitis

(other conditions are Ewing’s sarcoma,
chondrosarcoma, osteosarcoma) as many
as 12 laminations are seen. The affected
areas show increased radiodensity which
may be attributed to osteosclerosis. It is
seen in panoramic radiographs, reverse
Townes view, PA views. The occlusal view
is best to see these reactions.
3. The thick compact type is most commonly 5. Interrupted lamellar: It is seen in osteosar-
noted with resolving Garré’s osteomyelitis coma and its distinction is important. The
(individual lamenations become indistinct), subperiosteal layer is disturbed and not
osteoid osteoma, odontogenic fibroma. continuous.
The periosteum here has got ample time
to produce the bone.
6. The solid irregular mass: Diffused masses

are of radiopacity and seen in osteosarcoma.
4. Buttress formation: It is seen with slow
growing process especially tumors. It
produces triangular bone and invisible
expanded cortical margins. These slow
growing tumor produce focal thickening.
The cortex beneath the buttress is
frequently intact, e.g. ameloblastomas and
ameloblastic fibromas. CT may be correct
modality to visualize.
7. The sunburst appearance is seen in

osteosarcoma and chondrosarcoma: This
is an aggressive form of periosteal reaction.
Perforation and expansion of the cortical
margin by stretching periosteum this
appearance is produced. In the sunburst
subtype of periosteal reaction, the spicules
of new bone radiate in a divergent pattern
instead of perpendicular to the cortex.
The spicules are not straight but forms
irregular, wavy lines. Some authors
claim that this is not a true periosteal
reaction but outgrowth of tumor matrix, 8. Codman’s triangle: This is present in bone
e.g. odontomas, odontogenic myxomas, sarcomas and consists of entirely periosteal
occasionally in intrabony vascular malfor- bone and should be avoided in taking
mations and intraosseous hemangioma. biopsy. This is a bit misnomer as there is
no complete triangle. In fast growing
process the periosteum is raised and edges
will ossify, as the lesion is aggressive and
has no time to ossify. Periosteal newborn
formation with tent like lifting of the cortex
(due to tumor, pus and hemorrhage) leads
to the appearance of a Codman’s triangle.
It forms an angle when a little bit of
ossification is seen tangentially. Taking of
biopsy from this region should be avoided.
spicules perpendicular to bone surface that

look like hair standing on end. It is
classically seen in children/adolescents
with hemolytic anemias, in particular,
thalassemia major. Hair-on-end appea-
rance refers to the skull abnormalities seen
predominantly in patients with hemolytic
anemias, that is, thalassemia major, sickle
cell anemia, pyruvate kinase deficiency—
hereditary elliptocytosis and sphero-
cytosis. It is due to periosteal reaction with
neo-osteogenesis of the outer cranial table
which results in marked calvarial thick-
ening, external displacement and thinning
of the inner table. The changes are due
to marrow hyperplasia. Hair-on-end
appearance is also seen in congenital
syphilis-syphilitic periostitis of tibia,
metastatic neuroblastoma, iron-deficiency
9. Irregular spicules: These form pattern of
interlacing and relatively coarse spicules.
It is seen in osteosarcoma. The spicules are
much more disorganized manner and
bizzare pattern.
10. Hair-on: It is appearance of long, thin

vertical striations of calcified spicules
perpendicular to bone surface that look
like hair on end. The end appearance rare
in jaws may be seen in Ewing’s sarcoma.
The spicules are fine and short sometimes
in odontogenic myxoma. On skull it is
classically seen in thalassemia and sickle
cell anemia. The hair-on-end sign is a
finding seen in the diploic space on skull
radiographs and has the appearance of
long, thin vertical striations of calcified
2. Point destruction where there is a small

defect in the cortex with or without a defect
in the trabecular bone.
3. Gross destruction which is continuous with

a large defect in the trabecular bone; and
anemia, cyanotic-right-to-left shunt-

4. Permeative destruction in which numerous
congenital heart disease, osteomyelitis,
small defects are present in the cortex with
polycythemia vera, thyroid acropachy and
a large defect or rarefaction of the trabecular
hemangiomas. Similar appearance in facial
bone.
bones is rare and suggests an extreme
degree of medullary erythropoiesis.
38. Enumerate the periosteal bone reactions
seen in osteomyelitis.
Uninterrupted lamellar, interrupted lamellar,
onion skin, thick compact type of cortical 41. Enumerate what are the patterns of perio-
thickening. steal reactions odontogenic myxoma may
39. Enumerate what are the patterns of peri- show.
osteal reaction sarcomas can show. The sunburst pattern, irregular spicules and
Onion skin appearance, interrupted lamellar, hair on end.
solid irregular mass, Codman’s triangle, 42. What is brush-fire sign?
sunburst appearance, irregular spicules, hair
Subperiosteal erosion of the radial surface of
on end.
middle phalanges of the second and third
40. How is the pattern of destruction of
cortex present in the vicinity of periosteal
reaction?
The pattern of the destruction of the cortical
bone around the site of the periosteal reaction
is depicted on CT. This pattern is categorized
into the following four types:
1. No destruction
digits may be the sensitive indicator of 3. Sialodochitis: Segmental strictures of duct

secondary hyperparathyroidism. This is called sausage-link appearance.
as ‘brush fire sign’.
43. What is tail sign?
It is an extension of ranula from sublingual
gland in the sublingual space, commonly seen
on CT and MRI. It is core of CT diagnosis of
plunging ranula. It provides an important clue
to differentiate plunging ranulas from other
cystic lesions arising in or near submandibular
space such as cystic hygroma, thyroglossal
duct cyst, second brachial cleft cyst, abscess
and dermoid/epidermoid cyst. A dividing
ranula has a distinct tail sign within sublingual
space with bulk of cyst seen in submandibular
space. 4. Sialolith: Filling defect with retention of
44. Describe various sialographic appea- dye.
rances.
1. Normal parotid: “Leafless tree” or “tree in
winter”.
5. Benign tumors of parotid gland: A

mass within the gland is inferred by the
2. Normal submandibular gland: “Bush in

winter”
appearance of the ducts displaced around 1. Geographic patterns: Implies a large area
the lesion. It is called ‘ball in hand appea- of lysis, absence of expansion and is not
rance’. It is suggestive of space occupying associated with specific type of margins. It
mass. indicates monolocular or nonseparated
45. What are shovel-shaped incisors? What benign/malignant lesion. These are charac-
is shovel-shaped incisor syndrome? terized by a large solitary hole in bone
with sharply demarcated edge. These are
Shovel-shaped incisors show normal crowns
suggestive of less aggressive and slow
except for prominent marginal ridges sur-
growing lesion.
rounding deep lingual fossa in maxillary
central and lateral incisors. It is considered as
an anatomical variant rather than a morpho-
logical defect because of its high prevalence.
Double shovel is shovel-shape associated
with accentuated marginal ridges, which is
seen occasionally. Shovel-shaped incisors may
be seen in Apert’s syndrome. In Klinefelter’s
syndrome correlation between taurodontism
and shovel-shaped incisors is present. Shovel-
shaped incisors with prominent cingula are
associated with dens invaginatus.
When shovel-shaped incisors are seen
clinically following abnormalities should be
looked for interproximal caries, lingual pit
caries, periapical lesions of pulpal origin, the
presence of shortened or tapered roots. The
combination is called shovel-shaped incisor It is seen in:
syndrome. • Unilocular ameloblastoma: Early aggressive
lesion benign in nature.
46. What are the different types of char-
• Residul cyst/traumatic cyst: Slow growing,
acteristics of lesional tissues?
nonaggressive condition.
1. Bone destruction
• Ossifying fibroma: Early stage of lesion
a. Geographic pattern: Moth-eaten patterns that may have calcified tumor matrix.
and permeative patten.
• Suspected malignant disorder: Geographic
b. Multilocular lesions: Honeycomb, soap patterns suggest slower, less aggressive
bubble, tennis racket and scalloping. growth, e.g. solitary or multiple mye-
2. Mineralisation of tumor matrix: Osseous loma, mucoepidermoid carcinoma, and
foci, calcific foci, calcific spherules and metastatic disease.
calcific massules, odantomatous and 2. Moth-eaten pattern: Implies several small
dentinomatous calcification. areas of lytic bone destruction. It also
3. Internal margins: A narrow zone of implies an absence of expansion, but it
transition, a wide zone of transition. indicates a more rapid, aggressive process
Radiolucent lesions are caused by bone than geographic pattern. It is seen with
destruction. The medullary destruction may benign/malignant conditions. (Here radio-
remain inapparent but as the lesion destroys graphically separation from benign/
the endosteal surface, it may appear on malignant is not possible as margins are
radiograph especially on panoramic. same.)
• Lytic malignant diseases in jaws manifest

mainly as moth-eaten and permeative
patterns, although geographic changes
are seen.
47. What are the patterns of multilocular
patterns of bone destruction?
Multilocular lesions indicate internal septation.
The Septation Rules Out
• Some benign lesions and all cysts (except
traumatic bone cyst).
• It also rules out different pattern of
calcification in tumor matrix.
It is seen in:
• With a few exceptions (e.g. central mucoepi-
• Inflammatory conditions: Chronic osteo- dermoid carcinoma), these are indicative of
myelitis chiefly and osteoradionecrosis. benign, aggressive lesions.
• Malignant conditions: Metastatic disease. • These indicate cortical expansion and
3. A permeative pattern: Implies an absence cortical expansion indicates aggressiveness
of expansion but is almost seen in in benign lesion. The recurrence rate is
aggressive, rapidly destructive malignant higher in multilocular lesions. Honeycomb,
disease. These may be seen in medullary soap bubble, tennis racket and scalloped are
areas or seen in adjacent cortex also. It is variants. Honeycomb is an earlier change
characterized by numerous tiny radio- than soap bubble, probably honeycomb
lucencies in between the residual bone may turn into soap bubble.
trabeculae. Due to the minute size of 1. Honeycomb pattern: Circles are little
radiolucencies the lesion may be difficult smaller and probably of the same size and
to see and to delineate on the plain film. meeting each other. Ameloblastoma central
Generally, the more rapidly growing a giant cell granuloma.
lesion, the more difficult it is to see on
plain film. It indicates destruction of both
medullary and cortical bone.
It is seen in:
• Metastatic diseases and malignant
disorders.
2. Soap bubble: Larger circles. Unequal size circles, coalesing sometimes or overlapping
somewhat. Examples are ameloblastoma, central giant cell granuloma.
2a. Spider is a variant in which the septae radiate from central body.
3. Tennis racket: Irregularly shaped septae meeting at right angle. Exclusively odontogenic
myxoma.
4. Scalloped variant: Keratocystic odontogenic tumor. Sometimes in central giant cell

granuloma.
snowflake like patterns. Large tumors show

nodules, flocculent or popcorn like rings and
arc of calcific density. Still it is not more dense
than surrounding bone.
Multilocular patterns appear earlier, while

scalloped/crenated margin is later change. A
scalloped margin may or may not be associated
with expansion.
48. What are mineralization of tumor
matrix?
The lesions may develop radiolucency and
some may show radiodense appearance. The
patterns are osseous foci, calcific foci, calcific Calcific spherules and calcific massules:
spherules and massules, odontomatous These are mineralized flecks seen in cemental
calcifications, dentinomatous calcifications. lesions. Calcific spherules are tiny circular
Osseous foci (flecks): These indicate bone (0.2–0.5 mm in diameter) structures with
or osseous trabeculae histologically. These foci radiolucent structures, faintly radiopaque.
may join together and form clumps. Trabeculae Outline. These are commonly seen in ossifying
may project from foci. fibromas and benign cementoblastomas.
These spherules join together and form
massules (0.5–1.0 mm in diameter).
Calcific foci: These denote mineralization

of chondroid matrix. The density is less than Odontomous calcification: These consi-
surrounding bone. They are round, tiny and dered to be pathognomonic. They present three
sometimes invisible. Use of magnifying lens is forms:
necessary. The tendency of foci to clump • The density is similar to teeth and tend to
together is almost diagnostic. Small tumors be denser than surrounding bone and is
show small/punctate forms and may form most common.
Pindborg flecks Gorlin flecks AOT flecks
• Washer like radiodensity with a radiolucent be seen in benign and malignant lesions.
centre. The benign lesions which are aggressively
• Hodgepodge dental structures with little to growing are having rapid growth. Examples—
identify them as odontomous calcification. eosinophillic granuloma, central giant cell
These calcifications can be associated with granuloma and aneurysmal bone cyst. A
dentigerous cyst, Gorlin cyst, ameloblastic wide zone of transition in the absence of
odontoma, and ameloblastic fibro-odontoma. expansion suggests a malignancy such as
metastatic disease.
Dentinomatous calcification—rarely seen. It
is present in dentinoma and ameloblastic
fibrodentinoma.
49. What is zone of transition?
Zone of Transition
In order to classify osteolytic lesions as well-
defined or ill-defined, we need to look at the
zone of transition between the lesion and the
adjacent normal bone.
The zone of transition is the most reliable
indicator in determining whether an osteolytic
lesion is benign or malignant.
The zone of transition only applies to osteolytic
lesions since sclerotic lesions usually have a
narrow transition zone. Wide zone of transition
• A narrow zone of transition: Sclerotic bone
is deposited by host. Indolent or slow 50. What are the different types of internal
growing lesions are usually marginated by margins?
sclerotic bone. Rapid growth shows no Internal margin relates to the interface between
sclerotic bone or may be seen in some area. the lesion and host bone within which it occurs.
In aggressive bone growth the sclerotic It provides the information regarding
margins may be thinned out, discontinuous aggressiveness and growth rate.
and even break out (discussed below). • Thick condensed sclerotic rim, thick diffuse
• A wide zone of transition: It indicates that sclerotic rim, thin condensed sclerotic rim,
the lesion is aggressive, margin between punched out lesions with no sclerosis at the
healthy and abnormal bone is wider. It may margin.
Benign tumors/cysts have a condensed

type of sclerosis while reactive process
usually have a diffuse type of marginal
sclerosis. Examples—diffuse and thick
sclerotic rims at margins of cementomas
which indicates slow growing lesions.
Odontogenic myxoma have highest rate
and probably will be marked by condensed
sclerotic bone reactions.
Myeloma may show punched out margins
sharply defined but lack sclerotic margins,
this may indicate that periosteum may be
injured by disease.
Thin condensed sclerotic rim
Thick condensed sclerotic rim
Punched out lesion
51. How the relationship of the teeth and

of resorption at root apex helps in
diagnosis?
Teeth Conditions
1. The conditions associated with the crown
of unerupted teeth are almost odontogenic
in nature (cysts/benign tumors). The
presence of radiopaque foci further enhance
the diagnosis.
2. Some lesions may displace the teeth while
others cause unerupted teeth to become
impacted. Benign process displace tooth
(ossifying fibroma may displace, cemento-
Thick diffuse sclerotic rim blastoma does not) displacement of
unerupted teeth may be seen in dentigerous Resorption of Root

cyst, Gorlin’s cyst, inflammatory paradental 1. Resorption of one/several teeth root apex
cyst and in keratocystic odontogenic tumor. suggest benign process with aggressive
It is also seen in odontogenic mysoma, nature.
ameloblastoma and brown tumor. Amelo- 2. Rarely resorption may be associated with
blastic fibro-odontoma and ameloblastic malignant disease which may suggest a
odontoma are associated with displaced slower malignant growth pattern.
tooth and are more aggressive. 3. Knife edge resorption may be seen in
3. No displacement and causing unerupted ameloblastoma.
teeth to become impacted, then the lesion 4. Multiple root planes resorption is common
is less aggressive. Odontoma is associated in central giant cell granuloma and some-
with nondisplaced impacted tooth. times in ameloblastoma.
5. Spiking root resorption may suggest malignant disorder. The malignant disorders are too
rapidly destructive.
52. What are the other factors in root are

considered for radiological diagnosis?
1. The deposition of material on root apex is
indicative of benign process, e.g. hyper-
cementosis and cementoblastoma (the
dentinal outline is lost in benign cemento-
blastoma, whereas it can be seen in hyper-
cementosis).
Paget’s disease and Gardener’s syndrome
are said to be associated with generalized
hypercementosis.
2. Relationship of root apex with radiolucent
lesion. If apex of one or more root tip
protrude in the lesion indicates neoplasia, 3. Traumatic bone lesion is only one lesion
(as tumors go around the tooth) while in that characteristically straddles the roots.
cystic lesion the apices do not protrude and The superior portion projects up between
are in close proximity of root (cysts either teeth with or without destruction of lamina
cut off the teeth or cyst margins stop at dura.
apices of teeth). Resorption may or may not 53. How the cortical changes are useful for
be a feature of cyst or tumor. radiological diagnosis?
The expanded cortex is suggestive of locally
aggressive benign lesion:
• The absence of septation within the expan-
ded cortex is suggestive of less aggressive
lesion and is hallmark of slow growing
benign lesion.
• The expanded cortex on radiograph may
be intact and visible, intact and invisible or
perforated. The perforated cortex is a sign
of most aggressive benign lesions, with
propensity to recur and even few low-grade
malignant conditions also show this feature.
CT may show perforations exactly.
– The characteristics – Cystic exapansion – Neoplastic expansion.

– The nature of pressure – Hydraulic effect is applied – The vector growth is often but not
on cortex. exactly perpendicular to the cortex.
– The direction of pressure – The pressure is equally on – The pressure applied is not uniform.
all margins.
– Nature of expansion of – The cortex is expanded – Not always uniform. It may be paper
cortex evenly and smoothly. thin, may have a slightly wavy,
irregular surface.
– Disappearance of cortex – The cortex may not seem to – It may seem to disappear.
disappear at the greatest bulk.
– The meeting angle with – The expanded cortex meeting – Acute angle on one side and different
normal cortex. the normal cortex at an acute or obtuse angle on other side.
obtuse angle on both sides.
• Once the cortex is perforated the soft tissue 3. Are most primitive in differentiation,
may be herniated through it. This characteri- 4. Cells that do not perform any specialized
stic may seen on MRI (e.g. odontogenic functions.
myxoma, aneurysmal bone cyst). High radiosensitive cells include white
• Jaws give rise to more cystic lesions than blood cells, bone marrow, and eyecells.
any other bones in skeleton. Radiosensitive organs are blood forming
• Scalloping of the cortex appears at endo- organs (bone marrow, lymph nodes, and
steal surface of the cortex (e.g. keratocystic thymus and spleen).
odontogenic tumor/central giant cell Low radiosensitive are red blood cells, muscle
granuloma). cells, bone cells, and cells of nervous system.
• Saucerization may be seen in outer cortex Undernourished cells are generally less
and may seen with lesions arising from radiosensitive than normal cells.
gingival and periosteum (Examples are sub-
These findings are still true except for
mandibular, sublingual and parotid gland
lymphocytes and oocytes, which are very
depressions. Scleroderma, gingival cyst
radiosensitive even though they are highly
of adults, neural sheath tumors and
differentiated and nondividing. Mammalian
traumatic neuroma and peripheral giant
cells may be divided into five categories of
cell granuloma).
radiosensitivity on the basis of histologic
54. Classify side-effects of radiotherapy. observations of early cell death:
What are temporary and permanent side 1. Vegetative intermitotic cells are the most
effects of radiotherapy? radiosensitive. They divide regularly, have
These can be classified as: long mitotic futures, and do not undergo
1. Acute (early, temporary) or chronic (late, differentiation between mitoses. These are
permanent). stem cells that retain their primitive pro-
2. Stochastic/nonstochastic. perties and whose function is to replace
The temporary or acute side-effects are short themselves. Examples include early precur-
term side-effects. These may occur close to the sor cells, such as those in the spermatogenic
time of treatment and usually gone completely or erythroblastic series, and basal cells of
within a few weeks of finishing the treatment. the oral mucous membrane.
Hairloss may be temporary, fatigue, skin 2. Differentiating intermitotic cells are some-
changes and mucosites are the examples. what less radiosensitive than vegetative
Chronic, long-term or permanent may take intermitotic cells because they divide less
months or years to develop and usually are often. They divide regularly, although they
permanent. Hairloss may be permanent. undergo some differentiation between
Hearing loss in children. divisions. Examples of this class include
intermediate dividing and replicating
55. Describe how different cell type affects
cells of the inner enamel epithelium of
radiosensitivity.
developing teeth, cells of the hematopoietic
Different cells from various organs of the same series that are in the intermediate stages of
individual may respond to irradiation quite differentiation, spermatocytes, and oocytes.
differently.
3. Multipotential connective tissue cells
This variation was recognized as early as have intermediate radiosensitivity. They
1906 by the French radiobiologists Bergonie divide irregularly, usually in response to a
and Tribondeau. They observed that the most demand for more cells, and are also capable
radiosensitive cells are those that: of limited differentiation. Examples are
1. Have a high mitotic rate, vascular endothelial cells, fibroblasts, and
2. Undergo many future mitoses, and mesenchymal cells.
4. Reverting postmitotic cells are generally Oral carcinoma once it invades jaw bones
radioresistant because they divide infre- surgery is the treatment of choice as it becomes
quently. They also are generally specialized radioresistant once it involves jaw bones.
in function. Examples include the acinar Mandible is four times more radiosensitive
and ductal cells of the salivary glands and than maxilla, radiosensitivity does not
pancreas as well as parenchymal cells of the necessarily indicate curability, nor should
liver, kidney, and thyroid. radioresistance be taken to imply incurability.
5. Fixed postmitotic cells are most resistant to 57. What is radiation caries? What are
the direct action of radiation. They are the different types of radiation caries?
most highly differentiated cells and, once It is rampant form of dental caries that may
mature, are incapable of division. Examples occur in individuals who receive radiotherapy
of these cells include neurons, striated or radiation caries is a term used to describe
muscle cells, squamous epithelial cells that rapidly advancing caries, which characteristi-
have differentiated and are close to the cally occur at incisal or cervical aspects of teeth,
surface of oral mucous membrane, and starting at incisors and canines. The rapid onset
erythrocytes. and widespread attack are characteristics of
56. Enumerate the radiosensitive and radio- radiation caries. The caries often begins at
resistant tumors of jaw bones. cervical area, encircle the tooth aggressively
Those tumours that respond to treatment with causing the entire crown to be lost, with only
radium or X-rays are called radioactive or root fragments remaining. It may occur as early
radiosensitive. Example—lymphoma because as three months and can progress at an
of open lymphatic channels, squamous cell alarming rate, rarely pain is associated. The
carcinoma (especially poorly differentiated). lesion resembles more of demineralization
Basal cell carcinoma and some adenocarcinoma, than caries. It sweeps around the tooth and
Ewing’s sarcoma. Those tumors of other type may cause amputation at tooth neck. Teeth are
resist treatment by radium and X-rays are called brittle and pieces of enamel may fracture.
radioresistant. Examples—ameloblastoma, Clinically there are three types:
salivary gland neoplasms (parotid tumors 1. Widespread superficial lesion attacking
are the least radiosensitive, while tumors buccal, occlusal, incisal, and palatal sur-
in ectopic sites are relatively radiosensitive), faces. This is most common type.
osteogenic sarcomas, fibrosarcomas and 2. Involving cementum and dentin
malignant melanoma, eosinophilic granuloma. 3. Dark pigmentation of entire crown.
Blackish discolored multiple root stumps (shows multiple black discolored root, the posterior maxilla and
right central incisor with stumps in mandible) class V caries in maxillary anteriors
Radiation caries results from changes in in tissue may lead to tumor recurrences at
salivary glands and saliva. These are: low dose.
1. Reduced flow 59. What are radioisotopes?
2. Decrease pH Isotopes are the nuclei which are having same
3. Decrease buffering capacity number of protons and different numbers
4. Altered flora of neutrons, i.e. same atomic number but
5. Low concentration of Ca++. This results in different mass number. These are produced in
greater solubility of tooth structure and a nuclear reactor by exposing the target
greater demineralization. material to the neutrons in a reactor.
Direct effect of radiation on teeth makes Radioisotopes are a version of chemical
them more prone to flaking particularly in element that has an unstable nucleus and emits
areas of occlusal loading or stress. radiation during its decay to stable form.
Apple core appearance: It appears as Radiations given by some of radioisotopes are
punched out radiolucency seen on radiograph, very effective in curing certain diseases, e.g.
60Co radiocobalt is used in treatment of brain
radiographically radiolucent shadows at necks
of teeth most obvious on mesial and distal tumor, 32P radiophosphorus in bone diseases,
131I in thyroid cancer.
aspects.
Use of topical fluoride as remineralizing 60. What are radiopharmaceuticals?
solution and meticulous oral hygiene are These are unique medicinal formulations
helpful. containing radioisotopes. It may be 133Xe, 131I
iodinated proteins and Tc 99m labelled
compounds. These are sterile and non-
pyogenic.
61. What are newer developments in
radiotherapy?
1. Nonsealed injectable radionuclides:
Isotopes I131 I/V administered iodine is
absorbed by thyroid gland. Strontium 29
after systemic administration, they become
concentrated at osteoblastic activity which
58. What is brachy therapy? is used to palliate painful bone metastasis
Brachio is short. It uses selected isotopes or and treatment of osteogenic sarcoma.
specialized instruments to directly administer 2. Radioimmune therapy: One therapeutic
radiation to tumor or its bed. The radiation approach that has demonstrated potential
sources are placed either adjacent to surface of involves the selective targeting of radio-
a tissue mass or bed or inside tumor itself. nuclides to cancer-associated cell surface
The treatment may involve permanent im- antigens using monoclonal antibodies. Such
plantation of radioactive sources (e.g. perma- radioimmunotherapy (RIT) permits the
nent 125I seeds into recurrent nasopharyngeal delivery of a high dose of therapeutic radia-
mass). tion to cancer cells, while minimizing the
It travels only short distance to target lesion exposure of normal cells. Radiation emitting
and its dose intensity falls of rapidly with isotopes conjugated with high affinity
distance according to inverse square law. antibodies to generate radioimmunoglo-
Major advantage spares normal tissue at bulins. Yttrium 90 (90Y) and rituximab two
distant locations while major disadvantage is injections (Zevalin).
heterogenous distribution of dose deposition 3. Gene therapy and radiotherapy
4. Total and subtotal skin electron beam 5. Hyperthermia: Heating tumor cells in
therapy (TSEB): This treatment is directed combination with radiation therapy can
at a large surface, or the entire surface, of help shrink tumors and relieve symptoms
the body. The radiation penetrates the outer for patients who have failed prior con-
layers of the skin without affecting deeper ventional treatment, including radiation,
organs or tissue. Temple is the most surgery or chemotherapy.
experienced centre in the region to offer this 6. Three-dimensional: Conformal radiation
therapy to patients with rare cancers and therapy (3D-CRT)—the radiation beam is
conditions such as cutaneous T-cell and absolutely tailored to the shape and confi-
cutaneous B-cell lymphoma and Kaposi's guration of the tumor to avoid nearby
sarcoma. normal critical structures.
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Index
A Coalesced vesicles 4
ABCDE of melanoma 129 Codman’s triangle 229
Ackerman’s tumor 112 Compound nevus 126
Adamantiades syndrome 29 Condyloma accuminatum 83
Addison’s disease 129 Coronoid impedance 70
AIDS-related complex 105 Cottage cheese appearance 22
Albright’s syndrome 129 Cowden’s syndrome 85
Ameloblastoma 95 Coxsackie virus 104
Anchored disc phenomenon 69 Crepitus 65
Anesthesia dolorosa 51 Cross syndrome 85
Angular cheilitis 89 Cupid’s bow 134
Aneurysmal bone cyst (ABC) 94 Curtain like appearance 13
Apple core appearance 245 Cushing’s disease 130
Ascher’s syndrome 133 Cutright lesion 86
Aunt Minnie phenomenon 210
D
Auspitz sign 107
Darrier’s disease 8
B Desmoplastic ameloblastoma 95
Bannayan-Zonana syndrome 26 Diascopy 43
Behçet’s syndrome 29 Digital imaging 206
Benign lesions of oral cavity 77 Disorders of temporomandibular joints 48
Benign tumors 3, 77 Donovan’s technique 185
Bleb 42 Down’s syndrome 19
Bloom syndrome 106, 110
Blue nevus 126 E
Blue rubber bleb nevus syndrome 26 Edison effect 162
Brachy therapy 245 Elliptical rima oris 13
Brush-fire sign 231 Ellis-van Creveld syndrome 135
Bulla 4 End feel test 60
Burning mouth syndrome 51 Epstein’s pearls 90
Buschke-Löwenstein tumor 112 Epstein-Barr virus 104
Eruption hematoma 91
C
Campbell’s lines 210 F
Capsulitis 59 Factitious cheilitis 153
Cervical ranula 93 Fanconi’s anemia 110
Charge coupled device 207 Forchheimer’s sign 105
Choriostoma 77 Fountain sign 6
Chvostek sign 144 Frey’s syndrome 154
Classification of Tori 80 Furred tongue 20
249
G Leukoplakia 9
Gottron’s sign 106 Lichen planus 6
Graft-versus-host disease 8 Ludwig’s angina 102
Graham Little syndrome 7 M
Granuloma 102
Mach band effect 214
Greenspan lesion 104
Maffucci’s syndrome 26, 27
Grenz rays 161
Magic syndrome 29
Grinspan syndrome 7
Malignant neoplasms 3
H Marshall’s syndrome 29
Hairy leukoplakia 105 Miescher’s granulomatosis 102
Hamartoma 77 Mikulicz’s disease 120
Hand-foot-mouth disease 104 Moeller’s glossitis 143
Heck’s disease 103 Mohr syndrome 135
Heel effect 164 Mural ameloblastoma 95
Herpes barbae 104 Murray-Puretic-Drescher syndrome 85
Herpes gladiatorum 104 N
Herpes simplex virus 4
Nicotinic stomatitits 14
Herpes zoster 4, 104
Nikolsky’s sign 5
HIV/AIDS 29
Numb chin syndrome 154
Hockey stick like appearance 13
Hodgkin’s lymphoma 5 O
Hunter’s glossitis 143
Odontoameloblastoma 96
HVL 171
Oral submucous fibrosis 12
I Orofacial pain 48
IASP 48 Osler-Weber-Rendu syndrome 26
Id reaction 23 P
Intramucosal nevus 126
Inverse square law 167 Palatal petechiae 5
Panoramic errors 202
J Paraneoplastic syndrome 5
Jump sign 73 Patriotic sign 107
Junctional nevus 126 Penny test 189
Peripheral ameloblastoma 95
K President’s tumor 213
Kasabach-Merritt syndrome 26 Pseudocysts 94
Keratocystic odontogenic tumor 97 Psychosomatic diseases 56
Keratosis 15 Ptregyoid sign 145
Kimura’s disease 120 Pup-tent sign 7
Kissing lesion 19
Klippel-Trénaunay syndrome 27 Q
Koebner’s phenomenon 108 Quincke’s disease 144
L R
Laband syndrome 85 Rad 159
Laskin’s criteria 73 Radiology 159, 210
Le master technique 184 Raspberry tongue 103
Lesion 3 Reddened bald appearance 22
primary lesions 3 Reiter’s syndrome 19
secondary lesions 3 Rem 159
Index 251
Robinow’s syndrome 19 T
Roentgen 159 Tail sign 232
Rubinstein-Taybi syndrome 135 Tear drop sign 211
Rutherford syndrome 85 Teratoma 77
Tori 80
S Trousseau’s sign 1
Servelle-Martorell syndrome 27 TVL 171
Sjögren’s syndrome 119, 120 Two-thirds tumor 92
SLOB rule 195
SLOB technique 205 U
Smoker’s Umbra and penumbra 185
palate 14
V
patch 15
melanosis 15 Varicella 4
Soft tissue tumors 3 Varicella-zoster virus 104
Squamous papilloma 83 Verruca vulgaris 83
Vesicle 4
Stafne’s bone cyst 135
Vesiculobullous lesions 4
Stippled leukoplakia 11
von Hippel-Lindau syndrome (vHL syndrome) 27
Strawberry tongue 103
Sturge-Weber syndrome (encephalotrigeminal W
angiomatosis) 26 Wegener’s granulomatosis 120
Sturge-Weber’s syndrome 135 Wickham’s striae 6
Stylohyoid complex 55 Winter lines 215
Styloid process 52 Witkop’s disease 8
Sweet syndrome 29 Wolff's law 215
Synovitis 59
Systemic corticosteroid regimen I 45 Z
Systemic corticosteroid regimen II 45 Zosteriform lesions 105

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Oral Medicine and

CBS Publishers & Distributors Pvt Ltd

First eBook Edition: 2019

Published by Satish Kumar Jain and produced by Varun Jain for

Section 1 ORAL MEDICINE

2. Orofacial Pain and Disorders of Temporomandibular Joints 48

3. Benign Lesions of Oral Cavity 77

4. Infections and Autoimmune Disorders of Oral Cavity 101

5. Potentially Malignant Disorders of Oral Cavity and Oral Cancers 109

6. Diseases of Salivary Glands, Pigmented Lesions of Oral Cavity 118

7. Developmental Disturbances, Physical and Chemical Injuries to the

8. Systemic Manifestations in Oral Cavity and Traumatic Lesion 141

10. Radiology—Part 2 210

Suggested Reading 247

Since malignant neoplasms invade or • Bulla is elevated blister containing clear

11. State all categories under which lichen

“fountain”. This phenomenon is mostly seen

22. Define leukoplakia. What are the clinical

• Nodular lesion: White lesion with granular

• Reversible and irreversible leukoplakias:

7. Pan (betel quid) stain

it lace-like appearance. Over the time one type

Heavy curtain like appearance

Heavy curtain and shrunken uvula appearance

36. What is heavy curtain like appearance

3. Palatal white patches in reverse smoking:

7. Smoker’s patch: This condition describes

41. What are the palatal changes associated

Excrescences: It is present in severe form in Patches: Same as leukoplakia, but differ

Hyperpigmentation: It presents melanin pig-

42. What are multimorphic lesions in palate

43. What is geographic tongue? What is

epithelium particularly of the filiform papillae

The etiology and pathogenesis remains obs-

Hairy tongue and furred tongue

Systemic causes are medications causing

This is also called cottage cheese appearance

Table 1.1: Characteristic differences between hemangioma and vascular malformation

58. What are the complications of AVH?

Hematoma on right buccal mucosa

hematoma causes thickening or enlargement rubber nipple or rubber skin. Identical

62. What is acquired hemangioma?

Central hemangioma is a great mimicker,

Recurrent intraoral herpes on palate and gingiva

Entropion after epilation

77. How erythema multiforme differs from SJS and TEN?

80. What is angina bullosa hemorrhagica? Strawberry gingivitis: Particularly straw-

81. What are strawberry like lesions in and

Strawberry nevus (strawberry hemangioma):

Treatment and Prognosis • Pemphigus

Presentation in pemphigus and cicatricial pemphigoid

Characteristics peeling of tissues showing desquamation

Reactive osseous and chondromatous 89. Enumerate the various inflammatory

92. Describe differences between gingival polyp and pulp polyp.

93. Why peripheral giant cell granulomas

94. In which conditions central giant cell

95. What is parulis?

101. What is diascopy? State in which condi-

103. Why the prednisone should be taken in

104. Mechanism of action of corticosteroids

Systemic Corticosteroid Regimen I Systemic Corticosteroid Regimen II

Systemic Corticosteroid Regimen IIIB mucosa and as an adjunct in treatment of

Clinically migraine, TMJ dysfunction, atypical facial