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Issue title: 2nd International Symposium on Mechanobiology: Cartilage and Chondrocyte. Paris, France, April 2001
Article type: Research Article
Authors: Colville‐Nash, Paul R. | Willoughby, Derek A.
Affiliations: Department of Experimental Pathology, William Harvey Research Institute, Barts and The London, Queen Mary's School of Medicine and Dentistry, University of London, London, UK
Note: [] Address for correspondence: Department of Experimental Pathology, William Harvey Research Institute, Barts and The London, Queen Mary's School of Medicine and Dentistry, University of London, Charterhouse Square, London EC1M 6BQ, UK. Tel.: +44 20 7882 6160; Fax: +44 20 7882 6095; E‐mail: p.r.colville‐[email protected].
Abstract: It is widely accepted that whilst exhibiting clinically useful anti‐inflammatory and analgesic activity, the application of non‐steroidal anti‐inflammatory drugs (NSAIDs) does not affect the underlying pathogenesis of articular diseases such as rheumatoid arthritis. The demonstration of a role for COX‐2 in the resolution of inflammation may partly underly the lack of disease modifying activity seen with NSAIDs in long term use in these inflammatory joint diseases. This has led to the suggestion that the anti‐arthritic efficacy of these agents may be improved by altering prescribing practice such that they are not given during periods of disease remission, which may be difficult to achieve in the clinic. Alternatively, they may benefit from concomitant administration of chondroprotective agents, such as diacetylrhein, which may protect against the deleterious effects of traditional NSAIDs on cartilage degradation and, further, inhibit additional pathways such as cytokine elaboration which are important in joint destruction.
Journal: Biorheology, vol. 39, no. 1-2, pp. 171-179, 2002
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