Abstract
Osteoporosis, which patients are estimated as more than 13 million in Japan, is mainly caused by postmenopausal osteoporosis. Estrogen deficiency induced by menopause can disturb endocrine feedback and homeostasis, followed by bone loss by increased bone resorption with high bone turnover. Recent studies using systemic or conditional Estrogen Receptor α(ERα)gene knockout mice have unveiled molecular mechanisms underlying bone metabolism. In this review, it will be discussed that direct and indirect effects of estrogen and its metabolites for bone metabolism.
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