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Updated: Oct 1, 2026
Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
Genetic approaches to determine the role of glucocorticoid signaling in osteoblasts
John R Harrison1, Henning W Woitge, Barbara E Kream
1Department of Orthodontics, School of Dental Medicine, University of Connecticut Health Center, Farmington, USA.
Abstract:
A variety of in vivo and in vitro experimental models have been used to explore the effects of glucococorticoids in bone. Chronically high levels of glucocorticoids typically decrease bone mass in humans and animals and inhibit markers of bone formation in organ and cell cultures. However, under certain experimental conditions, glucocorticoids can stimulate osteoblast differentiation and bone formation in vitro. The relevance of these effects seen in culture models to the role of endogenous glucocorticoids in bone remains unclear. In this article, we briefly review possible pathways for the opposing effects of glucocorticoids on bone formation and propose several genetic loss-of-function mouse models in which disruption of glucocorticoid signaling in cells of the osteoblast lineage would provide a means to determine the role of endogenous glucocorticoids in bone.
Insights
Glucocorticoids can both decrease and increase bone mass. This review explores their opposing effects on bone formation and proposes mouse models to study endogenous glucocorticoid actions.
Area of Science:
- Bone biology
- Endocrinology
- Pharmacology
Background:
- Glucocorticoids influence bone metabolism, with high levels typically reducing bone mass.
- In vitro studies show glucocorticoids can also stimulate osteoblast differentiation, but in vivo relevance is unclear.
Purpose of the Study:
- To review the dual effects of glucocorticoids on bone formation.
- To propose genetic mouse models for investigating endogenous glucocorticoid roles in bone.
Main Methods:
- Review of existing in vivo and in vitro experimental models.
- Proposal of genetic loss-of-function mouse models targeting glucocorticoid signaling in osteoblasts.
Main Results:
- Glucocorticoids exhibit opposing effects on bone formation, depending on experimental conditions.
- Existing models provide insights but do not fully elucidate endogenous glucocorticoid roles.
Conclusions:
- Further research using targeted genetic models is needed to clarify the precise role of endogenous glucocorticoids in bone homeostasis.
- Understanding these pathways is crucial for developing therapeutic strategies for bone diseases.
