[Drugs influencing bone metabolism in diabetic patients]

A significant improvement in the knowledge of physiology, pathophysiology and pathobiochemistry of bone metabolism has enhanced the understanding not only of regulatory mechanisms of bone remodelation in adulthood but also of the dysfunction of such regulatory processes with other diseases. In the pathophysiology of metabolic bone disease in diabetic patients, attention is currently being focused on the method in which the differentiation of mesenchymal stem cells in osteoblasts, or adipocytes is regulated. The key role of PPAR-gamma, its activation or activity inhibition and thus also the directing of the differentiation in fat cells or osteoblasts is especially important in diabetic patients. Thiazolidinediones, in particular of the rosiglitazone type, have a positive impact on increased tissue sensitivity to insulin built on the activation of PPAR-gamma. Therefore, they can provoke the image of an aging bone in case of prolonged administration. Nevertheless, many factors contribute to the causes of increased fragility of bones in diabetic patients, both directly and indirectly--AGE, changes in insulin and IGF-I concentrations, renal dysfunctions, chronic inflammatory processes and impaired immunity. The treatment of osteoporosis in diabetic patients does not principally differ from the treatment of postmenopausal osteoporosis.