Premium
Regulation of adult bone turnover by sex steroids
Author(s) -
Frenkel Baruch,
Hong Albert,
Baniwal Sanjeev K.,
Coetzee Gerhard A.,
Ohlsson Claes,
Khalid Omar,
Gabet Yankel
Publication year - 2010
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22159
Subject(s) - bone remodeling , rankl , estrogen , osteoporosis , endocrinology , medicine , osteoclast , bone resorption , skeleton (computer programming) , runx2 , osteoprotegerin , osteoblast , biology , receptor , anatomy , biochemistry , activator (genetics) , in vitro
Recent reports reveal increasing complexity of mechanisms underlying the bone sparing effects of sex steroids. This review focuses on mechanisms by which sex steroids attenuate endocortical and trabecular adult bone turnover, perhaps their most important property as bone mass regulators. Clearly, estrogen withdrawal increases osteoclast number and bone resorption; however, important open questions are the extent to which osteoblasts and their precursors are involved, and the relative contributions of the RANK/RANKL/OPG system, Fas ligand and Runx2. In addition to reviewing these aspects of estrogen action, we also discuss proskeletal effects of androgens on the adult male skeleton, including aromatization to estrogens and male‐specific mechanisms. Detailed understanding of skeletal site‐ and gender‐dependent mechanisms by which sex steroids protect the adult skeleton will provide the foundation for improved risk assessment, prevention and management of osteoporosis. J. Cell. Physiol. 224: 305–310, 2010. © 2010 Wiley‐Liss, Inc.