Abstract

0 STEOARTHRITIS (OA) is generally thought of as a disease of articular cartilage failure induced by a variety of genetic, metabolic, and biomechanical factors. Coexisting with the cartilage abnormalities, most affected joints exhibit synovial inflammatory responses that may range from minimal lining cell layer hyperplasia to severe acute and chronic synovitis. The synovial response may be responsible for the pain symptomatology associated with early OA. Although it is unlikely that immune processes play an important primary role in initiating synovial inflammation, cellular and humoral immune responses to cartilage macromolecules may constitute important factors in the maintenance and severity of synovitis in OA. This review focuses on the specific immunologic mechanisms that may be operative in OA. The physiopathogenesis of inflammation induced by immunologic mechanisms is not discussed in detail because it is likely that once the antigenspecific interactions occur, the development of the inflammatory process results from the generation of cellular and humoral proinflammatory factors that constitute a final common pathway to most inflammatory processes, regardless of the disease entity under consideration.

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