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Related Concept Videos

Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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Direct Mouse Trauma/Burn Model of Heterotopic Ossification
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Published on: August 6, 2015

Fibrodysplasia ossificans progressiva.

Frederick S Kaplan1, Martine Le Merrer, David L Glaser

  • 1Departments of Orthopedic Surgery & Medicine, The University of Pennsylvania School of Medicine, c/o Hospital of The University of Pennsylvania, Philadelphia, PA, USA. frederick.kaplan@uphs.upenn.edu

Best Practice & Research. Clinical Rheumatology
|March 11, 2008
PubMed
Summary

Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disorder causing bone malformations and progressive heterotopic ossification. A specific ACVR1/ALK2 mutation drives FOP, offering a target for new drug development.

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Area of Science:

  • Genetics
  • Biochemistry
  • Medical Research

Background:

  • Fibrodysplasia ossificans progressiva (FOP) is a rare, disabling genetic disorder characterized by congenital skeletal malformations and progressive heterotopic ossification (HO).
  • FOP is the most catastrophic known disorder of HO in humans, with episodic flare-ups triggered by soft tissue injury leading to cumulative immobility.

Purpose of the Study:

  • To highlight the significance of the recently identified recurrent mutation in ACVR1/ALK2 as a highly specific disease-causing mutation in FOP.
  • To underscore the potential for developing targeted therapies based on the discovery of the FOP gene and its role in the TGF-beta/BMP signaling pathway.

Main Methods:

  • Genetic analysis to identify mutations in sporadic and familial cases of classic FOP.
  • Review of current understanding of FOP pathogenesis and its relation to BMP signaling.

Main Results:

  • A recurrent mutation in activin receptor IA/activin-like kinase 2 (ACVR1/ALK2) was identified in all classic FOP cases.
  • This mutation represents one of the most specific disease-causing mutations discovered in the human genome.

Conclusions:

  • The discovery of the ACVR1/ALK2 mutation is a milestone in understanding FOP.
  • This finding provides a conserved target for drug development, specifically small molecule inhibitors of ACVR1/ALK2 signaling, for FOP and potentially other HO conditions.
  • Current management focuses on early diagnosis, injury avoidance, and symptomatic relief, but future therapies may involve blocking ACVR1/ALK2 signaling.