Non-Enzymatic Glycation is Associated with Markers of Bone Quality in Human Cortical and Cancellous Bone

Factors other than low bone mass, such as changes in bone quality, may contribute to fracture risk. Non-enzymatic glycation alters bone’s organic matrix [1] and creates collagen crosslinks, collectively termed advanced glycation end products (AGEs) [2]. AGEs accumulation with age stiffens bone's organic matrix, ultimately leading to fracture [3]. Cell culture work in animal models shows increased AGEs decrease osteoclastic activity and reduce bone turnover [4]. Through such alterations in resorption and turnover, non-enzymatic glycation can influence the bone microstructure as well as the matrix and influence bone fragility in both cortical and cancellous bone. Our goal was to investigate the influence of non-enzymatic glycation on bone’s microarchitecture, which in turn affects bone’s fracture resistance through the formation of specific morphologies of microdamage (linear microcracks versus diffuse damage). We hypothesized that trabecular rods will be more glycated than plates and that highly glycated regions of bone will produce more linear microcracks.