TY - JOUR
T1 - Effects of long-term cigarette smoke exposure on bone metabolism, structure, and quality in a mouse model of emphysema
AU - Sasaki, Mamoru
AU - Chubachi, Shotaro
AU - Kameyama, Naofumi
AU - Sato, Minako
AU - Haraguchi, Mizuha
AU - Miyazaki, Masaki
AU - Takahashi, Saeko
AU - Nakano, Takayoshi
AU - Kuroda, Yukiko
AU - Betsuyaku, Tomoko
AU - Matsuo, Koichi
N1 - Publisher Copyright:
Copyright: © 2018 Sasaki et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2018/1
Y1 - 2018/1
N2 - 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.
AB - 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.
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U2 - 10.1371/journal.pone.0191611
DO - 10.1371/journal.pone.0191611
M3 - Article
C2 - 29381718
AN - SCOPUS:85041191938
SN - 1932-6203
VL - 13
JO - PLoS One
JF - PLoS One
IS - 1
M1 - e0191611
ER -