Diabetes, a chronic hyperglycemic condition, is caused by insufficient insulin secretion or functional impairment. Long-term inadequate regulation of blood glucose levels or hyperglycemia can lead to various complications, such as retinopathy, nephropathy, and cardiovascular disease. Recent studies have explored the molecular mechanisms linking diabetes to bone loss and an increased susceptibility to fractures. This study reviews the characteristics and molecular mechanisms of diabetes-induced bone disease. Depending on the type of diabetes, changes in bone tissue vary. The molecular mechanisms responsible for bone loss in diabetes include the accumulation of advanced glycation end products (AGEs), upregulation of inflammatory cytokines, induction of oxidative stress, and deficiencies in insulin/IGF-1. In diabetes, alveolar bone loss results from complex interactions involving oral bacterial infections, host responses, and hyperglycemic stress in periodontal tissues. Therapeutic strategies for diabetes-induced bone loss may include blocking the AGEs signaling pathway, decreasing inflammatory cytokine activity, inhibiting reactive oxygen species generation and activity, and controlling glucose levels; however, further research is warranted.