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Introduction <p>There are many risk factors for fractures in chronic obstructive pulmonary disease patients, and investigating the effects of any particular factor on bones is extremely difficult. We hypothesized that the presence of pulmonary emphysema would delay the recovery of bone mass by reloading after unloading, and our study aimed to assess changes in bone metabolism dynamics in response to mechanical stress under pulmonary emphysema in model mice.</p> Materials and methods <p>We used C57BL/6J mice, with or without emphysema, via intratracheal administration of elastase or vehicle. Half of these mice underwent 1 week of hindlimb unloading followed by reloading, with bone assessed by μCT and histomorphometry.</p> Results <p>Mice without emphysema exhibited transient bone loss, with bone mass fully recovering by week 3 after unloading, driven by a robust rebound in bone formation. Conversely, mice with emphysema showed a delay in the response of bone metabolism dynamics to mechanical stress; bone loss due to unloading were delayed by week 3 after unloading and bone recovery due to reloading by week 6.</p> Conclusions <p>Slow changes in bone metabolism dynamics were observed during both unloading and reloading in mice with elastase-induced emphysema. The mechanism underlying these phenomena is unclear and requires further investigation.</p>

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Changes in bone metabolism dynamics in response to mechanical stress under pulmonary emphysema

  • 期刊论文

  • 发表日期：

    2025年11月17日

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  • Daisuke Arakawa,
  • Manabu Tsukamoto,
  • Ke-Yong Wang,
  • Takayuki Nabeshima,
  • Yosuke Mano,
  • Yoshiaki Yamanaka,
  • Hitoshi Suzuki,
  • Makoto Kawasaki,
  • Eiichiro Nakamura,
  • Kagaku Azuma,
  • Kazuhiro Yatera,
  • Akinori Sakai

摘要

Introduction

There are many risk factors for fractures in chronic obstructive pulmonary disease patients, and investigating the effects of any particular factor on bones is extremely difficult. We hypothesized that the presence of pulmonary emphysema would delay the recovery of bone mass by reloading after unloading, and our study aimed to assess changes in bone metabolism dynamics in response to mechanical stress under pulmonary emphysema in model mice.

Materials and methods

We used C57BL/6J mice, with or without emphysema, via intratracheal administration of elastase or vehicle. Half of these mice underwent 1 week of hindlimb unloading followed by reloading, with bone assessed by μCT and histomorphometry.

Results

Mice without emphysema exhibited transient bone loss, with bone mass fully recovering by week 3 after unloading, driven by a robust rebound in bone formation. Conversely, mice with emphysema showed a delay in the response of bone metabolism dynamics to mechanical stress; bone loss due to unloading were delayed by week 3 after unloading and bone recovery due to reloading by week 6.

Conclusions

Slow changes in bone metabolism dynamics were observed during both unloading and reloading in mice with elastase-induced emphysema. The mechanism underlying these phenomena is unclear and requires further investigation.