Inflammation in Fibrodysplasia Ossificans Progressiva and Other Forms of Heterotopic Ossification

Koji Matsuo; Robert Dalton Chavez; Emilie Barruet; Edward C Hsiao

doi:10.1007/s11914-019-00541-x

Inflammation in Fibrodysplasia Ossificans Progressiva and Other Forms of Heterotopic Ossification

Curr Osteoporos Rep. 2019 Dec;17(6):387-394. doi: 10.1007/s11914-019-00541-x.

Authors

Koji Matsuo^{1

2

3}, Robert Dalton Chavez^{1

2

3}, Emilie Barruet^{1

2

3}, Edward C Hsiao^{4

5

6}

Affiliations

¹ Division of Endocrinology and Metabolism, University of California, 513 Parnassus Ave., HSE901, San Francisco, CA, 94143-0794, USA.
² Department of Medicine, The Institute for Human Genetics, University of California, CA, San Francisco, USA.
³ The Program in Craniofacial Biology, University of California, CA, San Francisco, USA.
⁴ Division of Endocrinology and Metabolism, University of California, 513 Parnassus Ave., HSE901, San Francisco, CA, 94143-0794, USA. [email protected].
⁵ Department of Medicine, The Institute for Human Genetics, University of California, CA, San Francisco, USA. [email protected].
⁶ The Program in Craniofacial Biology, University of California, CA, San Francisco, USA. [email protected].

Abstract

Purpose of review: Heterotopic ossification (HO) is associated with inflammation. The goal of this review is to examine recent findings on the roles of inflammation and the immune system in HO. We examine how inflammation changes in fibrodysplasia ossificans progressiva, in traumatic HO, and in other clinical conditions of HO. We also discuss how inflammation may be a target for treating HO.

Recent findings: Both genetic and acquired forms of HO show similarities in their inflammatory cell types and signaling pathways. These include macrophages, mast cells, and adaptive immune cells, along with hypoxia signaling pathways, mesenchymal stem cell differentiation signaling pathways, vascular signaling pathways, and inflammatory cytokines. Because there are common inflammatory mediators across various types of HO, these mediators may serve as common targets for blocking HO. Future research may focus on identifying new inflammatory targets and testing combinatorial therapies based on these results.

Keywords: Cytokines; Heterotopic ossification; Immune activation; Inflammation; Macrophages.

Publication types

Research Support, N.I.H., Extramural
Review

MeSH terms

Adaptive Immunity / immunology
Animals
Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
Arthroplasty, Replacement, Hip
Blast Injuries / immunology
Brain Injuries, Traumatic / immunology
Burns / immunology
Cell Differentiation / immunology
Cytokines / immunology
Humans
Hypoxia / immunology
Immunosuppressive Agents / therapeutic use
Inflammation / drug therapy
Inflammation / immunology*
Janus Kinase Inhibitors / therapeutic use
Macrophages / immunology
Mast Cells / immunology
Mesenchymal Stem Cells
Myositis Ossificans / drug therapy
Myositis Ossificans / immunology*
Ossification, Heterotopic / drug therapy
Ossification, Heterotopic / immunology*
Postoperative Complications / immunology
Pyrazoles / therapeutic use
Receptors, Retinoic Acid / agonists
Retinoic Acid Receptor gamma
Signal Transduction
Sirolimus / therapeutic use
Spinal Cord Injuries / immunology
Stilbenes / therapeutic use
Wounds and Injuries / immunology*

Substances

Anti-Inflammatory Agents, Non-Steroidal
Cytokines
Immunosuppressive Agents
Janus Kinase Inhibitors
Pyrazoles
Receptors, Retinoic Acid
Stilbenes
Palovarotene
Sirolimus

Abstract

Publication types

MeSH terms

Substances

Grants and funding