Bone is a dynamic tissue that is constantly being remodelled. Resolution of bone and formation of new bone are closely linked, so that bone mass remains constant. With age, this process becomes unlinked with an imbalance in bore resorption and formation that results in a net loss of bone. Especially, osteoporosis is a disease characterized by low bone mass with age. One form of aging-related primary osteoporosis is postulated with the reduction of circulating estrogen, rapid bone loss occurs as a result of enhanced bore remodelling with an excess of resorption over bore formation. The oxidative stress is also involved in the pathogenesis of osteoporosis. Oxidative stress by cytokines, such as IL-a and TNF-${alpha}$, inhibits osteoblast function in vitro and stimulates osteoblast apoptosis resulting in an imbalance in bore remodelling. The present article reviews the current perspectives on the interaction between bone remodelling and factors such as estrogen and oxidative stress, providing an interpretation of bone diseases in a view of molecular mechanisms