Abstract

Among the rheumatological diseases, rheumatoid arthritis (RA) represents an excellent model for gaining insights into the effects of local as well as systemic consequences of inflammatory processes on skeletal tissue remodeling. RA is characterized by three types of bone loss: focal subchondral and joint margin bone erosion, periarticular osteopenia adjacent to inflamed joints, and generalized osteoporosis involving the axial and appendicular skeleton. There is still considerable debate concerning the specific cellular and biochemical mechanisms responsible for the progressive loss of articular cartilage, focal bony erosions, and subchondral osteolysis that characterizes the synovial lesion of RA. Results from studies employing histochemical and immunolocalization techniques support the concept that the production of collagenase and other proteinases at the cartilage-pannus junction play a prominent role in the pathogenesis of the cartilage destruction. Periarticular osteopenia is the radiographic hallmark of early RA; it typically appears in areas of active synovitis and usually precedes the appearance of focal erosions. The generalized osteoporosis observed in patients with RA has in part been ascribed to sedentary lifestyle related to chronic pain and joint inflammation. Patients with active synovitis experience significant stiffness of the joints after immobility, and pain is increased with motion or impact-loading of joints. As a result, the general level of physical activity in patients with RA is reduced.

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