INFLAMMATION AND BONE METABOLISM IN RHEUM ATOID-ARTHRITIS - PATHOGENETIC ASPECTS AND THERAPEUTIC OPTIONS

Background: Systemic osteoporosis is a common and pathogenetically het erogenous complication in rheumatoid arthritis. Various factors such a s disease activity, dosage and duration of glucocorticoid treatment an d immobilization are involved in pathogenesis of osteoporosis in rheum atoid arthritis. Inflammation and Bone Metabolism: Proinflammatory cyt okines secreted by immunocompetent cells have a role in the regulation of the activity of osteoblasts and osteoclasts. The effects of these proinflammatory cytokines include the inhibition of bone formation and an increase in bone resorption. Interleukin-6 and nitric oxide induce d osteoblasts by proinflammatory cytokines are likely to be important mediators between these cytokines and the function of osteoblasts and osteoclasts. Furthermore, disease activitydependent changes in the sec retion of glucocorticoids and in vitamin D metabolism may be involved in the pathogenesis of osteoporosis in this disease. Alteration of bon e remodeling associated with immobilization is an important factor of systemic bone loss in rheumatoid arthritis. Conclusion: The inflammato ry process in rheumatoid arthritis may cause periarticular and systemi c bone loss by various cytokine and hormone mediated mechanisms. Concl uding from these pathogenetic mechanisms, bisphosphonates and active v itamin D metabolites are likely to be effective therapeutic options in osteoporosis associated with rheumatoid arthritis.