Pathophysiology of drug-induced osteoporosis and osteoporosis in inflammatory systemic rheumatic diseases

Secondary osteoporosis is mainly caused by long-term glucocorticoid treatment. Glukokortikoids diminish the proliferative and metabolic activity of osteoblasts which results in changes in the balance between boneforming and bone-resorbing cells. Indirect glucocorticoid-mediated effects on bone metabolism occur probably from a decrease in intestinal calcium absorption and an increase in renal calcium elimination. Besides glucocorticoids, also methotrexate, cyclosporine A, some anticonvulsants and anticoagulants are discussed as diminishing bone mass. However, the exact molecular mechanisms involved are not known in detail. Furthermore, some rheumatic diseases per se seems to lead to osteoporosis. Especially patients with rheumatoid arthritis and ankylosing spondylitis often develop secondary bone loss. It is known of patients suffering from rheumatoid arthritis that the risk for osteoporosis increases with higher disease activity. Of particular importance in this regard are proinflammatory cytokines, which play a significant role in the pathogenesis of various inflammatory diseases. Besides the already mentioned effects of treatment, the reduction in the patient's physical activity must also be taken into account.