Sasaki Mamoru, Chubachi Shotaro, Kameyama Naofumi, Sato Minako, Haraguchi Mizuha, Miyazaki Masaki, Takahashi Saeko, Nakano Takayoshi, Kuroda Yukiko, Betsuyaku Tomoko, Matsuo Koichi
Division of Pulmonary Medicine, Keio University School of Medicine, Tokyo, Japan.
Division of Materials and Manufacturing Science, Graduate School of Engineering, Osaka University, Suita, Japan.
PLoS One. 2018 Jan 30;13(1):e0191611. doi: 10.1371/journal.pone.0191611. eCollection 2018.
Smoking is a common risk factor for both chronic obstructive pulmonary disease (COPD) and osteoporosis. In patients with COPD, severe emphysema is a risk factor for vertebral fracture; however, the effects of smoking or emphysema on bone health remain largely unknown. We report bone deterioration in a mouse model of emphysema induced by nose-only cigarette smoke (CS) exposure. Unexpectedly, short-term exposure for 4-weeks decreased bone turnover and increased bone volume in mice. However, prolonged exposure for 20- and 40-weeks reversed the effects from suppression to promotion of bone resorption. This long-term CS exposure increased osteoclast number and impaired bone growth, while it increased bone volume. Strikingly, long-term CS exposure deteriorated bone quality of the lumbar vertebrae as illustrated by disorientation of collagen fibers and the biological apatite c-axis. This animal model may provide a better understanding of the mechanisms underlying the deterioration of bone quality in pulmonary emphysema caused by smoking.
吸烟是慢性阻塞性肺疾病(COPD)和骨质疏松症的常见风险因素。在COPD患者中,严重肺气肿是椎体骨折的风险因素;然而,吸烟或肺气肿对骨骼健康的影响在很大程度上仍不清楚。我们报告了仅通过鼻腔暴露于香烟烟雾(CS)诱导的肺气肿小鼠模型中的骨质恶化情况。出乎意料的是,4周的短期暴露会降低小鼠的骨转换并增加骨量。然而,20周和40周的长期暴露则使效果从抑制骨吸收转变为促进骨吸收。这种长期的CS暴露增加了破骨细胞数量并损害了骨骼生长,同时增加了骨量。引人注目的是,长期CS暴露会使腰椎的骨质恶化,如胶原纤维和生物磷灰石c轴的取向紊乱所示。该动物模型可能有助于更好地理解吸烟引起的肺气肿中骨质恶化的潜在机制。