SOST and Hyperglycemia: This may be because hyperglycemia leads to an increase in advanced glycation end products (AGEs) as well as reactive oxygen species (ROS), which inhibit osteoblast and osteoclast function [41]; Also diabetic patients have higher levels of sclerostin, which may also reduce osteoblast differentiation and proliferation by inhibiting the Wnt/β-catenin signaling pathway [35].