The earliest known documentation of nasopharyngeal angiofibroma (NA) dates to Hippocrates in the fifth century B.C. Commonly referred to as juvenile nasopharyngeal angiofibroma (JNA), it is also known as juvenile angiofibroma (JAF), or fibromatous or angiofibromatous hamartoma of the nasal cavity. Nasopharyngeal may not be entirely accurate, as some sources state that it arises from the sphenopalatine foramen and the posterior nasal cavity, while others proffer that it has more of a choanal and nasopharyngeal origin. What research does agree upon is that JNA is a benign, highly vascular lesion that comprises approximately 0.05 to 0.5% of all head and neck masses. Though histologically benign, it often demonstrates aggressive features with local invasion into the nasal turbinates, nasal septum, and medial pterygoid lamina. It commonly extends into the nasal cavity, nasopharynx, and pterygopalatine fossa, with larger lesions extending into the sphenoid, maxillary, and ethmoid sinuses. They can also demonstrate extension through the inferior orbital fissure, and into the masticator space through the infratemporal fossa. Severe disease is likened to have orbital and intracranial involvement, seen in approximately 10 to 37% of cases.
As previously mentioned, JNA is a highly vascular lesion, with one or more arterial vascular pedicles. The most common primary arterial supply is the internal maxillary artery, a branch of the external carotid artery. Larger lesions may invoke multiple feeding arteries, with even bilateral involvement. The ascending pharyngeal artery is the second most common sizeable supplying branch of the external carotid artery, with additional accessory arteries including the middle meningeal, accessory meningeal, and facial artery branches. Research has also described the recruitment of internal carotid artery branches, most commonly the vidian artery, and to a slightly lesser extent the ophthalmic artery.
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