Abstract
The main sources of estrogens (E) are ovarian secretion (the major source) and peripheral conversion from androgens (the minor source) in premenopausal women, whereas in postmenopausal women, E derive only from peripheral conversion. E play a central role not only in female reproduction but also in the skeletal homeostasis, in the regulation of bone mass during puberty, adult life, and menopause. E have multiple functions on the bone and other cells related to the bone such as chondrocytes and cells of the immune system. Normally, E suppress osteoclastogenesis in the trabecular bone, increase osteoblastogenesis on endocortical surface and reduce osteoblastogenesis on periosteum of cortical bone, reduce apoptosis of osteocytes, and decrease T- and B-cell activation with consequent inhibition of osteoclastogenesis. Additionally, they possess antioxidant properties, protecting bone cells from oxidative stress, and participate in intestinal calcium absorption and renal conservation. During puberty, E enhance bone formation through direct and indirect mechanism. After reaching the peak of bone mass, E cease growth, maintaining balance between bone formation and resorption. After menopause, E decline leads to rapid bone loss due to increased bone resorption that is followed by slow bone loss associated predominantly with aging processes. In this latter phase, E worsen age-related changes.
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Colao, A., Di Somma, C., Zhukouskaya, V.V. (2018). Skeletal Tissue and Ovarian Function: Puberty and Menopause. In: Lenzi, A., Migliaccio, S. (eds) Multidisciplinary Approach to Osteoporosis. Springer, Cham. https://doi.org/10.1007/978-3-319-75110-8_8
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