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Cartilage damage in osteoarthritis and rheumatoid arthritis—two unequal siblings
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Cartilage damage in osteoarthritis and rheumatoid arthritis—two unequal siblings
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Journal Article
Cartilage damage in osteoarthritis and rheumatoid arthritis—two unequal siblings
2015
Overview
Key Points
The molecular mechanisms of cartilage breakdown in rheumatoid arthritis (RA) and osteoarthritis (OA) show considerable overlap, particularly with respect to matrix-degrading enzymes, but also with respect to some inflammatory mediators
The loss of phenotypic stability of articular chondrocytes, and initiation of a programme resembling aspects of embryonic endochondral ossification, could explain important features of OA
In contrast to OA, RA is associated with a stable, tumour-like activation of fibroblast-like synoviocytes that mediate the destruction of articular cartilage through directed invasion
Cartilage has active roles in OA and RA as a signalling scaffold harbouring bioactive matrix components and soluble factors, which interact with embedded chondrocytes and are released upon cartilage degradation
Osteoarthritis (OA) and rheumatoid arthritis (RA) are disorders of the joints that involve degradation of the extracellular matrix of cartilage, and proteases and inflammatory mediators are common to both conditions. However, different cells are affected in OA (chondrocytes) and RA (synoviocytes), and treating these diseases requires an understanding of their differences as well as their similarities.
Cartilage damage is a key feature of degenerative joint disorders—primarily osteoarthritis (OA)—and chronic inflammatory joint diseases, such as rheumatoid arthritis (RA). Substantial progress has been made towards understanding the mechanisms that lead to degradation of the cartilage matrix in either condition, which ultimately results in the progressive remodelling of affected joints. The available data have shown that the molecular steps in cartilage matrix breakdown overlap in OA and RA. However, they have also, to a great extent, changed our view of the roles of cartilage in the pathogenesis of these disorders. In OA, cartilage loss occurs as part of a complex programme that resembles aspects of embryonic bone formation through endochondral ossification. In RA, early cartilage damage is a key trigger of cellular reactions in the synovium. In a proposed model of RA as a site-specific manifestation of a systemic autoimmune disorder, early cartilage damage in the context of immune activation leads to a specific cellular response within articular joints that could explain not only the organ specificity of RA, but also the chronic nature and perpetuation of the disease.
Publisher
Nature Publishing Group UK,Nature Publishing Group
