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  Discussion on Research Summary: Inflammation and Arthritis
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DrO

Posted on Monday, Oct 8, 2007 - 9:04 am:

This is really just a review but emphasises some poorly understood concepts of arthritis. The synovial membrane (joint capsule) is an important source of inflammatory chemicals that cause the ongoing inflammation. Some of the newer parts of this inflammatory cascade that we are starting to look at are the cytokines and MMP's.

From a practical standpoint it postulates that by modulating inflammation we may slow down the progress of the disease. Currently the most practical modulators are controlled exercise, oral NSAID's, and oral nutraceuticals and the most powerful are intra-articular injections of inflammatory mediating drugs. Our article on arthritis discusses how to balance these factors together to decrease pain and rate of progress of the disease. However this summary illustrates there are many other places we might attack the inflammatory cascade to slow down the rate of degeneration. Currently some of our IA injections appear to work by diluting or "using up" the reactive parts of this inflammatory cascade. I look forward to reporting on more effective therapies as they are discovered.
DrO

Vet J. 2007 Sep 30;
The contribution of the synovium, synovial derived inflammatory cytokines and neuropeptides to the pathogenesis of osteoarthritis.

Sutton S, Clutterbuck A, Harris P, Gent T, Freeman S, Foster N, Barrett-Jolley R, Mobasheri A.
Department of Veterinary Preclinical Sciences, University of Liverpool, Liverpool L69 7ZJ, UK.

Osteoarthritis (OA) is one of the most common and disabling chronic joint disorders affecting horses, dogs and humans. Synovial inflammation or synovitis is a frequently observed phenomenon in osteoarthritic joints and contributes to the pathogenesis of OA through formation of various catabolic and pro-inflammatory mediators altering the balance of cartilage matrix degradation and repair. Catabolic mediators produced by the inflamed synovium include pro-inflammatory cytokines, nitric oxide, prostaglandin E(2) and several neuropeptides, which further contribute to the pathogenesis of OA by increasing cartilage degradation. Recent studies suggest that substance P, corticotropin-releasing factor, urocortin and vasoactive intestinal peptide may also be involved in OA development, but the precise role of these neuropeptides in the pathogenesis of OA is not known. Since increased production of matrix metalloproteinases by the synovium is stimulated by pro-inflammatory cytokines, future anti-inflammatory therapies should focus on the synovium as a means of controlling subsequent inflammatory damage.
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