Pathogenetic aspects of bone metabolism in diabetes mellitus.

Abstract

Metabolic disorders caused by diabetes affect bone remodeling, alter the structure and reduce the strength of bone tissue, leading to the development of diabetic osteopathy. However, between diabetes mellitus (DM) type 1 and 2 there are noticeable differences in the effect on the bone structure, which is obviously due to the different cellular and molecular mechanisms of these processes. The density of bone tissue with DM typel decreases, which leads to an increase in the risk of fractures by 7 times. With DM type 2, bone mineral density is moderately elevated, which is expected to lead to a decrease in the incidence of osteoporotic fractures, but in fact, this index is approximately doubled. Pathophysiological mechanisms underlying osteoporotic changes in diabetes mellitus are complex and included hyperglycemia, oxidative stress and accumulation of advanced glycation endproducts that alter the properties of collagen, increase fatty infiltration of the bone marrow, release inflammatory factors and adipokines from visceral adipose tissue and potentially change the function osteoblasts. Additional factors are, some antidiabetic drugs that directly affect the metabolism of bones and minerals (such as thiazolidinediones), as well as an increased tendency to fall due to micro- and macroangiopathies, all contribute to an increased risk of low-fracture fractures in patients with diabetes mellitus.