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Updated: May 31, 2026

Osteoclast Derivation from Mouse Bone Marrow
06:17

Osteoclast Derivation from Mouse Bone Marrow

Published on: November 6, 2014

Corticosterone selectively targets endo-cortical surfaces by an osteoblast-dependent mechanism

Holger Henneicke1, Markus Herrmann, Robert Kalak

  • 1Bone Research Program, ANZAC Research Institute, The University of Sydney, Sydney, Australia.

Bone
|July 5, 2011
PubMed
Abstract

Insights

Glucocorticoids negatively impact bone by affecting osteoblasts, particularly at the endosteal surface. However, a protective effect was observed at the pericortical surface, suggesting complex bone remodeling responses to these steroids.

Area of Science:

  • Endocrinology
  • Bone Biology
  • Osteoporosis Research

Background:

  • Glucocorticoid-induced osteoporosis pathogenesis is not fully understood.
  • Osteoblasts play a key role in mediating glucocorticoid effects on bone.
  • A transgenic mouse model with targeted disruption of glucocorticoid signaling in osteoblasts was utilized.

Purpose of the Study:

  • To investigate the role of osteoblasts in glucocorticoid-induced bone changes.
  • To analyze the effects of exogenous glucocorticoids on cortical and trabecular bone.
  • To evaluate the protective capacity of osteoblast-targeted glucocorticoid signaling disruption.

Main Methods:

  • Treatment of wild-type (WT) and transgenic (tg) mice with corticosterone (CS) or placebo.
  • Measurement of serum bone turnover markers (TRAP5b, OCN).
  • Analysis of bone structure using micro-CT and histomorphometry.

Main Results:

  • CS suppressed osteocalcin in both WT and tg mice, with higher levels in tg mice.
  • Corticosterone increased bone resorption and decreased formation at the endosteal surface but decreased resorption at the pericortical surface.
  • Transgenic mice showed partial protection against CS effects, while trabecular bone remained largely unaffected.

Conclusions:

  • Endocortical osteoblasts are highly sensitive to glucocorticoid-induced bone loss.
  • Pericortical bone exhibits an anabolic response to glucocorticoids.
  • Osteoblasts mediate both the catabolic and anabolic actions of glucocorticoids.

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