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Kanazawa, Ippei; Sugimoto, Toshitsugu

2018

Accumulating evidence has shown that the risk of osteoporotic fracture is increased in patients with diabetes mellitus independently of bone mineral density. Thus, diabetes-related bone disease is now recognized as one of diabetic complications. Collagen cross-links of advanced glycation end products (AGEs), dysfunction of osteoblasts with low bone turnover, as well as abnormal microstructure of trabecular and cortical bone are involved in bone fragility in diabetes mellitus. Circulating levels of AGEs and homocysteine are increased in patients with diabetes, and AGEs and homocysteine directly inhibited the differentiation of osteoblasts. In addition, these induce the apoptosis and regulate expression levels of sclerostin and RANKL in osteocytes, which play important roles of bone remodeling. Moreover, several antidiabetic drugs affect bone metabolism and fracture risk. Therefore, the underlying mechanism of diabetes-related bone fragility is very complex and not still fully understood. In this review, we described effects of diabetes on bone metabolism and the risk of fracture based on the recent evidence.

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