Hyperthyroidism is one of the causes of secondary osteoporosis (OP).Thyroid hormone (TH) and thyroid stimulating hormone (TSH) can act on chondrocytes,osteoblasts and osteoclasis to regulate bone metabolism through a variety of signaling pathways and regulatory factors.The effect of immune factors on bone in Graves' disease (GD) has gradually become a research hotspot with the development of bone immunity theory,but its mechanism remains unclear.In hyperthyroidism,calcium and phosphorus metabolism are disturbed,bone resorption and bone formation are increased,and bone resorption is greater than bone formation,and bone mineral density (BMD)is decreased and fracture risk is increased,especially in elderly and postmenopausal women.The degree and duration of hyperthyroidism were correlated with the degree of bone loss.BMD decreased in the whole body,especially in the forearm.Active anti-thyroid therapy or combined anti-osteoporosis therapy can effectively improve BMD and reduce fracture risk,but there is no standardized treatment plan.This article reviews the pathogenesis and clinical characteristics of OP induced by hyperthyroidism,in order to provide scientific diagnosis and treatment basis for this disease.