The collagen network in bone provides resistance against fracture and may be susceptible to changes with aging and disease. This review identifies the changes in quality of collagen matrix as contributors to bone fragility. With aging and in diabetes, cross-links accumulate in bone collagen as a result of nonenzymatic glycation and consequently impair matrix properties, increasing bone fragility. Cell-culture and animal studies suggest that the accumulation of cross-links induced by nonenzymatic glycation may be related to a reduction in bone turnover resulting from the altered responses of osteoblasts and osteoclasts to advanced glycation end products.
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