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Updated: Jun 13, 2026

Osteoclast Derivation from Mouse Bone Marrow
Published on: November 6, 2014
Regulation of adult bone turnover by sex steroids
Baruch Frenkel1, Albert Hong, Sanjeev K Baniwal
1Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA. frenkel@usc.edu
Abstract:
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.
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