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Skeletal Mechanoresponsiveness: Effects of Sex Hormones

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Skeletal Aging and Osteoporosis

Abstract

Sex hormones regulate bone mass, and their age-associated decline contributes to bone loss seen clinically with menopause and aging. Mechanical loading in surgical models of hormone deficiency has been examined extensively as a therapy to overcome the decreased bone mass associated with sex hormone deficiency. Exercise and controlled loading can overcome cancellous bone loss following ovariectomy and orchidectomy in rodent models. In addition, several signaling pathways associated with skeletal mechanotransduction have recently been shown to be regulated by sex hormones or, more specifically, their receptors. Deletion of hormone cellular receptors (estrogen receptors α and β, and androgen receptor) in mice suggests a critical role for estrogen in the response of bone tissue to mechanical stimuli. In this chapter we review the literature on skeletal adaptation to mechanical loading in surgical and genetic rodent models of sex hormone deficiency.

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Acknowledgments

This work was supported by the National Institutes of Health (R01-AG028664, R01-AR053571) and the National Science Foundation (GRFs to KMM and NHK).

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Correspondence to Marjolein C. H. van der Meulen .

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Melville, K.M., Kelly, N.H., van der Meulen, M.C.H. (2012). Skeletal Mechanoresponsiveness: Effects of Sex Hormones. In: Silva, M. (eds) Skeletal Aging and Osteoporosis. Studies in Mechanobiology, Tissue Engineering and Biomaterials, vol 5. Springer, Berlin, Heidelberg. https://doi.org/10.1007/8415_2012_135

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