Abstract
Diabetes mellitus (DM) is a well known risk factor for osteoporosis and an increased risk of fractures. A lot of data has been published about the relationship between diabetes and bone health. DM type 1 and DM type 2 have different effects on bone mineral density (BMD). The central link in pathogenesis of bone fragility in patients with DM type 1 is a violation of the activity and gifferentiation of osteoblasts. On the contrary, hyperinsulinemia in DM type 2 activates the division and gifferentiation of osteoblasts and contributes to an increase in BMD. However, Higher BMD values in patients with DM type 2 are combined with slowdown in bone metabolism. As the result, high-quality bone remodeling does not occur. And bone strength decreases despite the high BMD. Despite the differences, DM type 1 and DM type 2 have common pathogenic pathways, that lead to increased bone fragility. For example, non-enzymatic glycation of bone matrix collagen and increase in concentration of sclerostin, which blocks the Wnt signaling pathway. In this review, we will analyze current data about epidemiology and pathogenesis of osteoporosis in DM and discuss the practical issues of the clinic, diagnosis, stratification of fracture risk and treatment. Special attention will be paid to the effects of glucose-lowering and anti-osteoporotic drugs on bone tissue.
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