Diabetes mellitus significantly affects skeletal health, increasing the risk of osteoporosis and fractures in both type 1 and type 2 diabetes. In type 2 diabetes, this risk persists despite normal or elevated bone mineral density, indicating deficits in bone quality and microarchitecture. The pathophysiology involves chronic hyperglycemia, which promotes the accumulation of advanced glycation end-products that impair collagen structure, suppress osteoblast activity, and enhance bone resorption. Other contributing factors include insulin resistance, low-grade inflammation, altered adipokines, and diabetic complications, all of which disrupt normal bone remodeling. Standard diagnostic tools such as dual energy X-ray absorptiometry can underestimate fracture risk in diabetic patients, as they fail to capture qualitative changes in bone. Pharmacologic choices also influence skeletal outcomes. Thiazolidinediones are known to impair bone formation and increase fracture risk, while glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors show more neutral or favorable profiles. In conclusion, diabetes contributes to skeletal fragility through multifactorial mechanisms. Comprehensive management including individualized fracture risk assessment and selection of bone-friendly antidiabetic therapies is important to reduce osteoporosis and fracture risk in this vulnerable population.