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Osteocyte Apoptosis Contributes to Cold Exposure-induced Bone Loss
Jingke Du1, Zihao He2, Junqi Cui3
1Shanghai Key Laboratory of Orthopedic Implants, Department of Orthopedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Cold exposure initially reduces bone mass in mice by increasing osteocyte apoptosis. Bone density recovers after prolonged cold exposure, suggesting a time-dependent effect on bone remodeling.
Area of Science:
- Bone Biology
- Metabolic Regulation
- Environmental Physiology
Background:
- Systemic energy balance influences bone mass.
- Temperature variations affect energy metabolism and bone remodeling.
- The precise mechanisms linking cold exposure to bone changes are not fully understood.
Purpose of the Study:
- To investigate the effects of cold exposure on bone mass and remodeling in mice.
- To elucidate the cellular and molecular mechanisms underlying cold-induced bone changes.
Main Methods:
- Male C57BL/6J mice exposed to cold (4°C) or normal (23°C) temperatures for 28 days.
- Micro-computed tomography (micro-CT) for bone structure analysis.
- Histological staining (Ploton silver) and immunohistochemistry for osteocyte markers (E11, MMP13) and apoptosis (Caspase-3).
- In vitro studies with brown adipocytes and osteocytes.
Main Results:
- Cold exposure significantly reduced bone volume fraction after 14 days, with recovery by 28 days.
- Cold decreased osteocyte canalicular length and E11/MMP13 expression at 14 days, returning to baseline by 28 days.
- Cold exposure increased osteocyte apoptosis (Caspase-3 positive cells) and brown adipocytes positively influenced osteocyte dendrites and E11 expression in vitro.
Conclusions:
- Cold exposure influences bone mass in a time-dependent manner, causing initial reduction followed by recovery.
- Osteocyte apoptosis appears to be a key mechanism mediating cold-induced bone mass changes.
- Brown adipose tissue may play a role in modulating bone remodeling in response to cold.
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