The pathophysiological mechanisms underlying bone metabolic abnormalities in T2DM patients involve multiple factors (10): (1) Deposition of advanced glycation end products (AGEs) in bone matrix directly impairs bone biomechanical properties; (2) Insulin resistance and hyperglycemia disrupt osteogenic differentiation and accelerate bone resorption through interfering with multiple signaling pathways; (3) Aberrant secretion of bone turnover markers such as osteocalcin (OC) further disturbs the dynamic balance of bone remodeling. This evidence concerns the gene BGLAP and Hyperglycemia.