Osteoarthritis: A cellular differentiation defect?

Thorsten Kirsch

    Research output: Contribution to journalReview articlepeer-review


    Purpose of review: Osteoarthritis is the most common form of arthritis, affecting a large population of mostly elderly people. No cure for osteoarthritis currently exists. Ultimate treatment is joint replacement. Understanding the mechanisms causing onset and progression is critical. This review describes recent findings that provide new insights into changes of cellular phenotype in osteoarthritis as a possible reason for tissue failure. Recent findings: Recent findings suggest that articular chondrocytes, when stimulated, can undergo hypertrophic and terminal differentiation events similar to those occurring during endochondral bone formation. Interestingly, collagenase-3 (matrix metalloproteinase-13), a main matrix-degrading enzyme in osteoarthritis, is expressed only in terminally differentiated chondrocytes during normal development. Summary: Although terminal differentiation events are required for endochondral bone formation, they lead to cartilage destruction when occurring in articular chondrocytes. Maintaining the articular chondrocyte phenotype and preventing these cells from undergoing hypertrophic and terminal differentiation might provide novel therapeutic targets to prevent onset or progression of osteoarthritis.

    Original languageEnglish (US)
    Pages (from-to)356-361
    Number of pages6
    JournalCurrent Opinion in Orthopaedics
    Issue number5
    StatePublished - Oct 2003


    • Articular cartilage
    • Growth plate
    • Hypertrophy
    • Osteoarthritis
    • Terminal differentiation

    ASJC Scopus subject areas

    • Surgery


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