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Sex steroids and bone.

S C Manolagas1, S Kousteni, R L Jilka

  • 1Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock 72205, USA. manolagasstavros@uams.edu

Recent Progress in Hormone Research
|May 23, 2002
PubMed
Summary

Sex steroid loss accelerates bone remodeling by increasing osteoclast and osteoblast production. It also promotes osteoclast death while protecting osteoblasts, leading to bone loss. Novel therapies may target these dual receptor actions.

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Area of Science:

  • Endocrinology
  • Bone Biology
  • Cellular Signaling

Background:

  • The adult skeleton undergoes continuous remodeling, a process regulated by sex steroids like estrogens and androgens.
  • Loss of sex steroids increases bone remodeling rates and shifts the balance towards bone resorption, leading to bone loss.
  • Sex steroid receptors play a dual role in bone metabolism, influencing both bone cell proliferation and survival.

Purpose of the Study:

  • To elucidate the mechanisms by which sex steroids regulate bone remodeling and influence bone cell lifespan.
  • To investigate the dual functions of sex steroid receptors, including their nuclear and non-nuclear actions.
  • To explore the potential of novel therapeutic strategies targeting sex steroid receptor signaling for bone health.

Main Methods:

Related Experiment Videos

  • Studies involved examining the effects of estrogens and androgens on osteoclast and osteoblast progenitor proliferation and differentiation.
  • Investigated the impact of sex steroids on the lifespan of mature osteoclasts, osteoblasts, and osteocytes.
  • Utilized classical and non-classical signaling pathways, including Src/Shc/ERK, and ligand-activated transcription factors.

Main Results:

  • Estrogens and androgens attenuate osteoclast and osteoblast production by regulating gene transcription.
  • Sex steroids exert pro-apoptotic effects on osteoclasts and anti-apoptotic effects on osteoblasts and osteocytes via non-genotropic pathways.
  • Non-genotropic signaling, mediated by the receptor's ligand-binding domain, can be dissociated from transcriptional activity.

Conclusions:

  • Sex steroid deficiency leads to increased bone remodeling due to enhanced osteoclastogenesis and osteoblastogenesis.
  • Loss of non-genotropic anti-apoptotic effects on osteoblasts/osteocytes, coupled with increased osteoclast apoptosis, drives bone resorption imbalance and bone loss.
  • Targeting non-genotropic sex steroid receptor actions offers potential for developing bone anabolic agents with fewer side effects than hormone replacement therapy.