Related Experiment Videos
Effect of cortisone on cells at the bone-marrow interface
D J Simmons1, L Kidder, M Thomas
1University of Texas Medical Branch, Department of Surgery, Galveston 77550.
Calcified Tissue International
|May 1, 1990
Summary
Cortisone acetate treatment reduced bone mineralization and marrow stromal cell proliferation in rats. Recovery was partial, with a relapse in the third week, suggesting fibroblast colony-forming units (FCFU) can indicate osteoblast activity.
Area of Science:
- Bone Biology
- Cell Biology
- Pharmacology
Background:
- Osteopenia is a condition characterized by reduced bone mass.
- Cortisone acetate is a corticosteroid with known effects on bone metabolism.
- Marrow stromal cells play a crucial role in bone formation.
Purpose of the Study:
- To investigate the relationship between marrow fibroblast-like stromal cell proliferation and endosteal bone mineralization.
- To assess the impact of cortisone acetate on these parameters in an osteopenic rat model.
Main Methods:
- Cortisone acetate was administered to male rats.
- Marrow fibroblast colony-forming units (FCFU) were measured in vitro.
- Endosteal bone mineralization rate (EsMR) was assessed using tetracycline labeling in vivo.
- Measurements were taken at the femoral midshaft.
Main Results:
- Cortisone acetate treatment decreased both FCFU and EsMR.
- Following treatment, FCFU and EsMR normalized within the first week of recovery.
- A relapse in FCFU and EsMR was observed in the third week of recovery, indicating incomplete healing.
- Body weight changes did not correlate with these findings.
Conclusions:
- The fibroblast colony-forming unit (FCFU) count can serve as an indicator of endosteal osteoblast activity.
- Cortisone acetate negatively impacts bone mineralization and stromal cell function.
- The recovery process from cortisone-induced bone changes is complex and may not be complete.