Document Type

Article

Publication Date

2-2010

Abstract

Studies on rodent models and rare human disorders of estrogen production or response have revealed an increased complexity of the actions of estrogen on bone. ERalpha disruption in human males results in delayed epiphyseal maturation, tall stature, trabecular thinning, marked cortical thinning, genu valgum and significantly reduced cortical vBMD, but trabecular number is preserved and there is normal to increased periosteal expansion. Aromatase deficiency results overall in a similar phenotype, although less is known about skeletal architecture. Importantly, estrogen replacement in these individuals, even if provided late in the third decade, may normalize aBMD. Less certain is whether there is complete recovery of normal skeletal architecture and strength. Rodent models, in general, are consistent with the human phenotype but are confounded by inherent differences between mouse and human physiology and issues regarding the completeness of the different knock-out lines. Both human and rodent studies suggest that residual effects of estrogen through ERbeta, truncated ERalpha forms or nonclassical estrogen receptors might account for different phenotypes in the hERKO man, aromatase deficient subjects and rodents. Importantly, androgen, particularly by preserving trabecular number and augmenting both periosteal and epiphyseal growth, also has significant actions on bone.

Publication Title

The Journal of Steroid Biochemistry and Molecular Biology

Volume

118

Issue

4-5

First Page

264

Last Page

272

DOI of Published Version

10.1016/j.jsbmb.2009.10.016

PMID

19900547

Publisher

Elsevier

Rights

© 2010 Elsevier

Creative Commons License

Creative Commons Attribution 3.0 License
This work is licensed under a Creative Commons Attribution 3.0 License.

Comments

This is the authors peer-reviewed and accepted manuscript. The version of record was published in (2010) The Journal of Steroid Biochemistry and Molecular Biology, 118 (4–5), DOI:10.1016/j.jsbmb.2009.10.016.

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