Seronegative arthritis
(top of page) What factor(s) is responsible for inducing metalloprotease synthesis? One candidate is interleukin-1 (IL-1). seronegative arthritis Evaluation-of-psoriatic-arthritis. IL-1 is a potent pro-inflammatory cytokine that, in vitro, is capable of inducing chondrocytes and synovial cells to synthesize MMPs (slide). Furthermore, IL-1 suppresses the synthesis of type II collagen and proteoglycans, and inhibits transforming growth factor-? stimulated chondrocyte proliferation. The presence of IL-1 RNA and protein have been confirmed in OA joints. seronegative arthritis Information pictures of rheumatoid arthritis. Thus, IL-1 may not only actively promote cartilage degradation, but may also suppress attempts at repair, in OA. In addition to these effects, IL-1 induces nitric oxide production, chondrocyte apoptosis, and prostaglandin synthesis, which further contribute to cartilage deterioration. Under normal conditions, an endogenous IL-1 receptor antagonist regulates IL-1 activity. seronegative arthritis Causing abdominal pain. A relative excess of IL-1 and/or deficiency of the IL-1 receptor antagonist could conceivably result in the cartilage destruction that is characteristic of OA. It is likely that other cytokines or particulate material from damaged cartilage may also contribute to this inflammatory, degradative process. (top of page) Can cartilage repair itself? Growth factors are produced locally in cartilage and synovium and are likely to contribute to local cartilage remodeling by stimulating the de novo synthesis of collagen and proteoglycans (slide). Transforming growth factor ? (TGF?) is the best characterized and most potent of the chondrocyte growth factors. Not only does TGF? stimulate de novo matrix synthesis, but it also counteracts cartilage degradation by down regulating IL-1 receptor expression and by increasing IL-1 receptor antagonist release and TIMP expression. Insulin-like growth factor (IGF-1) and basic fibroblast growth factor (b-FGF) are also present in OA cartilage and likely to contribute to reparative attempts, although, as noted, degradation ultimately outstrips repair in OA cartilage. (top of page) Summary In summary, MMPs and pro-inflammatory cytokines (e. g. , IL-1) appear to be important mediators of cartilage destruction in OA. Synthesis and secretion of growth factors and of inhibitors of MMPs and cytokines are apparently inadequate to counteract these degradative forces.
Seronegative arthritis
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