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Related Experiment Video

Updated: Jun 17, 2026

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats

Published on: September 27, 2024

Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice.

Robert S Weinstein¹, Chao Wan, Qinglan Liu

¹Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, USA. weinsteinroberts@uams.edu

|January 6, 2010

Summary

Aging increases glucocorticoids, reducing bone strength by impairing bone vasculature and fluid transport. Protecting bone cells from glucocorticoids prevents age-related bone fragility.

Keywords:

11β-hydroxysteroid dehydrogenase Aging angiogenesis apoptosis bone histomorphometry glucocorticoids hydraulic support osteoporosis

Related Experiment Videos

Last Updated: Jun 17, 2026

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats

Published on: September 27, 2024

Area of Science:

Bone Biology
Endocrinology
Gerontology

Background:

Aging and excess glucocorticoids weaken bone more than they reduce bone mass.
The underlying mechanisms for this bone strength deficit remain unclear.

Purpose of the Study:

To investigate the role of endogenous glucocorticoids in age-related bone fragility.
To elucidate the cellular and molecular mechanisms linking glucocorticoids to decreased bone strength.

Main Methods:

Utilized aging C57BL/6 mice and pharmacologic hyperglucocorticoidism models.
Employed cell-specific transgenic mice expressing 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 2 to inactivate glucocorticoids in osteoblasts and osteocytes.
Assessed bone vasculature, solute transport, osteoblast/osteocyte apoptosis, bone formation, microarchitecture, and fluid content.

Main Results:

Aging increased adrenal glucocorticoid production and bone 11beta-HSD type 1 expression, while decreasing bone vasculature and fluid transport.
Pharmacologic hyperglucocorticoidism mimicked these age-related changes.
Mice protected from glucocorticoids via 11beta-HSD type 2 expression were resistant to age-related bone deficits.
Glucocorticoids suppressed angiogenesis and key factors (HIF-1α, VEGF) in osteoblasts and osteocytes.

Conclusions:

Endogenous glucocorticoids contribute to age-related skeletal fragility.
These effects stem from cell-autonomous actions on osteoblasts and osteocytes, leading to reduced bone angiogenesis, vasculature, and fluid transport.
Targeting glucocorticoid action may offer therapeutic strategies for age-related bone loss.