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Title: Oxidative Marker Found In Rheumatoid Arthritis Synovial Tissue

URL: http://ard.bmjjournals.com/cgi/content/abstract/61/6/488

Annals of the Rheumatic Diseases 2002;61:488-492. "Identification of the advanced glycation end products N[epsilon]-carboxymethyllysine in the synovial tissue of patients with rheumatoid arthritis"
06/12/2002 12:56:17 PM
By Anne MacLennan

For the first time, N-[^ecarboxymethyllysine has been detected in both rheumatoid and osteo arthritic synovial tissue. This N-^ecarboxymethyllysine (CML), a marker of oxidative stress, may thus play a role in the pathogenesis of rheumatoid arthritis (RA), report S Drinda and colleagues from the Friedrich Schiller University Jena, Jena, Germany. CML's possible role in RA pathogenesis is suggested by different patterns of immunostaining in RA and osteoarthritis (OA) and the presence of CML on macrophages and T cells found in this study. This may be due to presentation of new epitopes which can maintain or even trigger an autoimmune response, these authors propose. Generation of advanced glycation end products (AGEs), an inevitable process in vivo, can be accelerated under such pathological conditions as oxidative stress. Raised AGE levels have been found in the serum and synovial fluid of patients with RA. To detect the presence of CML in RA synovial tissue by immunohistology was the objective of this study, in which frozen synovial tissue samples from 10 RA patients and eight controls (four patients without joint disease and four patients with OA) were treated with rabbit-anti-CML-IgG and goat-antirabbit-IgG. Immunostaining was visualised by streptavidine-alkaline phosphatase (chromogen fuchsin), and cell differentiation was performed with antibodies against CD68, CD45RO, and CD20. CML was found in the synovial lining, sublining and endothelium in all 10 of the RA and all four of the OA synovial specimens. In RA some macrophages (CD68+) and T cells (CD45RO+) showed positive immunostaining for CML, whereas B cells were negative. Compared with RA, staining in OA synovial sublining was weak.

http://ard.bmjjournals.com/cgi/content/abstract/61/6/488

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