Skeletal Mechanoresponsiveness: Effects of Sex Hormones - Skeletal Aging and Osteoporosis: Biomechanics and Mechanobiology - page 214

Skeletal Mechanoresponsiveness:
Effects of Sex Hormones

Katherine M. Melville, Natalie H. Kelly
and Marjolein C. H. van der Meulen

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 a and b, 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 adap-
tation to mechanical loading in surgical and genetic rodent models of sex hormone
deficiency.

1 Introduction

Mechanical loading is a critical regulator of skeletal mass and structure starting
during embryonic development and continuing into senescence. During growth
and development, additional mechanical stimuli can further enhance already-
increasing bone mass whereas reduced loading slows or inhibits growth. In the

K. M. Melville N. H. Kelly M. C. H. van der Meulen
College of Engineering, Cornell University, Ithaca, NY 14853, USA
M. C. H. van der Meulen (

)
Research Division, Hospital for Special Surgery, New York, NY 10021, USA
e-mail: [e-mail]

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