Abstract
Although type 2 diabetes is often characterized by normal or high bone mineral density (BMD), diabetes is associated with increased risk of fracture. This paradoxical phenomenon in type 2 diabetes may be explained by poorer "bone quality" by detrimental collagen cross-links in bone. Recently, we showed that the alteration of enzymatic and nonenzymatic crosslinking in bone could be important for explaining the variation of fracture susceptibility in diabetes (Osteoporos Int, 2006. Epub ahead of print). In this review, we describe that low turnover bone, hyperglycemia, mildly hyperhomocysteinemia, and vitamin B(6) insufficiency are crucial determinants of detrimental crosslinking of bone collagen in diabetes.
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