Evaluation of the Cellular Origins of Heterotopic Ossification

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CME REVIEW ARTICLE 

Evaluation of the Cellular Origins of Heterotopic Ossification

Lixin Kan, MD, PhD; John A. Kessler, MD

• Orthopedics
• May 2014 - Volume 37 · Issue 5: 329-340
• DOI: 10.3928/01477447-20140430-07

Abstract

EDUCATIONAL OBJECTIVES

As a result of reading this article, physicians should be able to:

1. Update the current knowledge about candidate cell populations as heterotopic ossification (HO) contributors.

2. Understand the potential limitations of the experimental designs and techniques underlying the identification of putative HO contributors.

3. Clarify the confusion about the phenotypes of candidate populations in the literature.

4. Contrast the fundamental cellular differences between HO and normal skeletogenesis to identify potential disease-specific targets.

Heterotopic ossification (HO), acquired or hereditary, is featured by the formation of bone outside of the normal skeleton. Typical acquired HO is a common, debilitating condition associated with traumatic events. Cardiovascular calcification, an atypical form of acquired HO, is prevalent and associated with high rates of cardiovascular mortality. Hereditary HO syndromes, such as fibrodysplasia ossificans progressiva and progressive osseous heteroplasia, are rare, progressive, life-threatening disorders. The cellular origins of HO remain elusive. Some bona fide contributing cell populations have been found through genetic lineage tracing and other experiments in vivo, and various other candidate populations have been proposed. Nevertheless, because of the difficulties in establishing cellular phenotypes in vivo and other confounding factors, the true identities of these populations are still uncertain. This review critically evaluates the accumulating data in the field. The major focus is on the candidate populations that may give rise to osteochondrogenic lineage cells directly, not the populations that may contribute to HO indirectly. This issue is important not solely because of the clinical implications, but also because it highlights the basic biological processes that govern bone formation. [Orthopedics. 2014; 37(5):329–340.]

The authors are from the Department of Neurology (LK, JAK), Northwestern University’s Feinberg Medical School, Chicago, Illinois; and the Department of Pathophysiology (LK), School of Basic Medicine, Anhui Medical University, Anhui, China.

The material presented in any Keck School of Medicine of USC continuing education activity does not necessarily reflect the views and opinions ofOrthopedics or Keck School of Medicine of USC. Neither Orthopedics nor Keck School of Medicine of USC nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

Correspondence should be addressed to: Lixin Kan, MD, PhD, Department of Neurology, Northwestern University’s Feinberg School of Medicine, Ward Building 10-233, 303 E Chicago Ave, Chicago, IL 60611 ( l-kan@northwestern.edu).

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Received: April 19, 2013

Accepted: November 22, 2013