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Classically, inflammatory arthritis was defined in part based on cellular inflammation represented by increased numbers of leukocytes in the affected joint tissues and synovial fluid. Classic cellular inflammation is not prominent in osteoarthritis , where the number of leukocytes in the joint fluid is normally low, and rarely exceeds 1000 to 2000 cells per milliliter. This is in contrast to forms of inflammatory arthritis, such as rheumatoid arthritis , where the number of synovial fluid leukocytes will commonly exceed 2000 and will be accompanied by a more extensive synovial infiltrate of leukocytes with synovial fibroblast proliferation resulting in pannus formation. Synovial inflammation is also present in OA and in some individuals can be indistinguishable from rheumatoid arthritis. An important difference is that macrophages are the predominant leukocyte found in OA synovium, while in RA there are more T cells and B cells. At the molecular level, OA is characterized by the presence of a host of proinflammatory mediators, including cytokines and chemokines, that are part of an innate immune response to joint injury . proinflammatory factors appear to be driving the production of the proteolytic enzymes responsible for the degradation of the extracellular matrix that results in joint tissue destruction. Although destruction and loss of the articular cartilage is a central component of OA, all joint tissues are affected in some way, indicating that OA is a disease of the joint as an organ . Mechanical factors certainly play a key role in OA and there is some debate in the field as to the extent to which OA is mediated by abnormal joint mechanics. However, the balance of evidence suggests that rather than simply causing joint tissue damage by wear and tear, excessive or abnormal joint loading also stimulates joint tissue cells to produce proinflammatory factors and proteases that mediate joint tissue destruction.