Cartilage destruction and bone erosion in arthritis: the role of
tumour necrosis factor 
Richard O Williams, Marc Feldmann, Ravinder N Maini
Kennedy Institute of
Rheumatology, 1 Aspenlea Road, London W6 8LH
Correspondence to: Dr Williams (r.williams@cxwms.ac.uk)
| The first 150 words of the full text of this article appear below. |
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Introduction |
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Rheumatoid arthritis (RA) is a chronic disabling disease characterised by synovitis, destruction of cartilage and bone and, ultimately, loss of joint function. A great deal of research in rheumatology over the past two decades has focused on identifying cytokines and other mediators responsible for the inflammatory and degenerative processes in RA, with the aim of developing specific inhibitors or antagonists of therapeutic value. A key question in this research has been whether there is a degree of hierarchy in proinflammatory cytokine expression in RA, such that inhibiting the activity of a cytokine high up in the inflammatory cascade has an impact on the expression of downstream mediators of inflammation and joint damage.
Of the many cytokines thought to contribute to the inflammatory and
degenerative changes that occur in RA, tumour necrosis factor 
(TNF) has emerged as being of major pathological significance. For
example, TNF was identified in the synovial
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