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High extracellular calcium concentrations directly stimulate osteoclast apoptosis
F Lorget1, S Kamel, R Mentaverri
1Laboratoires de Pharmacie Clinique et de Physiologie, Faculté de Pharmacie, 1 rue des Louvels, Amiens, F-80037, France. florence.lorget@sa.u-picardie.fr
Biochemical and Biophysical Research Communications
|February 19, 2000
Summary
High extracellular calcium concentrations directly induce osteoclast apoptosis, a key mechanism for regulating bone resorption. This finding reveals a negative-feedback loop involving calcium and osteoclast cell death.
Area of Science:
- Cell Biology
- Bone Biology
- Physiology
Background:
- High extracellular calcium concentrations ([Ca](e)) are known to inhibit osteoclastic bone resorption.
- The precise mechanism underlying this inhibition remains largely unelucidated.
Purpose of the Study:
- To investigate the potential role of extracellular calcium in inducing osteoclast apoptosis.
- To elucidate the mechanism by which calcium influences osteoclast survival and function.
Main Methods:
- Primary rabbit osteoclasts were purified and cultured under varying calcium concentrations.
- Apoptotic changes were assessed using time-course experiments and morphological analysis.
- The involvement of calcium channels and receptors was evaluated using specific blockers and agonists.
Main Results:
- Extracellular calcium directly promoted osteoclast apoptosis in a dose-dependent manner.
- Significant apoptotic changes were observed as early as 8 hours, with 80% of cells showing apoptosis after 72 hours at 20 mM calcium compared to 20% at 1.8 mM calcium.
- Calcium channel blockers and ryanodine inhibited calcium-induced apoptosis, suggesting calcium influx is critical.
Conclusions:
- High extracellular calcium concentrations induce osteoclast apoptosis, likely through calcium influx.
- This apoptosis serves as a negative-feedback mechanism, regulating bone resorption during periods of high calcium availability, such as bone demineralization.