Rheumatoid arthritis is a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks synovial joints. About 1% of the world's population is afflicted by rheumatoid arthritis, women three times more often than men. The exact causes of rheumatoid arthritis are unknown. Rheumatoid arthritis is most likely triggered by a combination of factors, including an abnormal autoimmune response, genetic susceptibility, and some environmental or biologic trigger, such as a viral infection or hormonal changes. The process produces an inflammatory response of the synovium (synovitis) secondary to hyperplasia of synovial cells, is excess synovial fluid, and the development of pannus in the synovium. The pathology of the disease process often leads to the destruction of articular cartilage and ankylosis of the joints. Cytokines like TNF-a and IL-1 are found to be present in the rheumatoid joint fluids and synovial membranes of patients with rheumatoid arthritis (RA). TNF-a is important in inflammation and tissue destruction, upregulates the production of IL-1 through autocrine and paracrine mechanisms and hepatic synthesis of IL-6. Both IL-1 and TNF-a trigger activation and proliferation of synovial cells, induce collagen synthesis, inhibit proteoglycan synthesis, and stimulate bone resorption, induce production of other cytokines, and upregulate the expression of adhesion molecules on endothelial cells. Thus, cytokines play a crucial role in the pathogenesis of the Rheumatoid arthritis.
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