Rheumatoid arthritis is a chronic inflammatory disease of unknown etiology that is marked by synovial inflammation and destruction of articular extracellular matrix. Several studies of the pathogenesis of tissue destruction have focused on the production of metalloproteinases and their inhibitors in synovium as determinants of joint preservation. Also, the role of cytokines in the perpetuation of synovitis and of superantigens in synovial T-cell activation have led to novel hypotheses that attempt to explain abnormalities of synovial structure and function in rheumatoid arthritis. Recent studies that dealt with these topics are briefly reviewed in the context of current paradigms of inflammatory synovitis.
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