OA includes a component of low-grade inflammation (reviewed in ) and also complement activation has been suggested to take a part in the pathogenesis. OA is a disease of the whole joint associated with mechanical wear of the joint surfaces and involvement of the surrounding tissue, subchondral bone, cartilage, and synovium. The features of excess bone resorption suggest that there are multiple soluble and insoluble signaling molecules that contribute to the excess bone resorption in RA.īesides RA, osteoarthritis (OA) is another even more common joint-decaying disease, which also results in changes in local bone turnover. RA is also associated with secondary osteoporosis, which is thought to be a result of generalized inflammatory stimulus that originates from generalized inflammation of the affected joints. In RA, the bone erosions are located at a special milieu at the sides of the joint where the synovial lining is adjacent to the bone and the bone is not covered by articular cartilage. The local inflammation is believed to increase osteoclast activity and result in local bone loss specific for the disease. The synovial tissue inflammation is a very common feature of the disease and leads to secondary damage in both the cartilage and bone. Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory joint disease that targets mainly the synovial tissue, but the exact disease etiology and pathogenesis are unknown.
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