LOX and diabetes mellitus: Previous studies have reported that in mouse models of diabetes, there is an abnormal arrangement of collagen fibrils that results in a significant reduction in bone material properties without affecting the mineral component of bone.7, 8 Results from these studies suggest that these collagen defects are caused by either accumulation of non‐enzymatic advanced glycation end products or the observed abnormally low levels of lysyl oxidase (LOX)‐mediated enzymatic crosslinks.7, 9