Abstract: Reduced bioavailability of estrogen increases osteoporosis and fracture risk in postmenopausal women significantly，but the mechanisms by which estrogen regulates bone mass are incompletely understood. In recent years，mouse models with cell-specific deletion of the estrogen receptor α（ERα） have provided novel insights into the function and signaling of ERα which provide opportunity to develop new drugs for preventing and treating osteoporosis. Illuminating the role of ERα in different bone cells，including chondrocyte，osteoclast，osteoblast progenitor cells，osteoblast and osteocyte to figure out the mechanisms of ERα in the pathogenesis of osteoporosis is of great importance to find new targets for osteoporosis.

Key words: Estrogen receptor alpha, Osteoporosis, Osteoporosis, postmenopausal, Postmenopause, Mice