The effects of advanced glycation endproducts (ages) on bone biomechanics and remodeling

Accumulation of advanced glycation end products (AGEs) in bone matrix induced by aging and diabetes mellitus is one of the major causes of increased bone fracture risk and deteriorated bone remodeling process. AGEs, a posttranslational non-enzymatic glycation modification in longlived matrix proteins such as collagen, are spontaneously formed between amino groups and reducing sugars via Millard reaction. Currently, it is believed that AGEs modifications to bone matrix may have impacts to bone in two ways. One is to modify the ultrastructure of collagen and bone matrix via glycation-induced non-enzymatic crosslinks, thus directly imposing adverse effects on the bone toughness and other biomechanical properties. The other is to affect bone remodeling by impairing the osteoblast proliferation/differentiation in bone formation and osteoclast function/activities in bone resorption process, thus leading to a delayed process of bone healing in both orthopaedic and dental patients. This chapter will provide a review of current understanding on the role and impact of AGEs to bone tissue biomechanics and bone remodeling.