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Increasing evidence indicates that tumour necrosis factor (TNF) has an important role not only in inflammatory arthritis but also in degenerative joint disease.1–3 TNF controls the homoeostasis of matrix synthesis and matrix degeneration in articular cartilage in concert with other cytokines, such as interleukin 1 (IL1), transforming growth factor β, or insulin-like growth factor 1. Overproduction of TNF and IL1 skews the balance towards matrix degradation, at least in part by virtue of induction of nitric oxide synthesis and subsequent metalloproteinase production. In osteoarthritis (OA), increased TNF production by activated synoviocytes and articular chondrocytes together with increased p55 TNF receptor expression on chondrocytes imply the contribution of TNF mediated matrix degradation to disease …
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