Effects of long-term cigarette smoke exposure on bone metabolism, structure, and quality in a mouse model of emphysema

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.Effects of long-term cigarette smoke exposure on bone metabolism, structure, and quality in a mouse model of emphysema. Mamoru Sasaki et al. PLOS ONE. 2018. 1(30) doi.org/10.1371/journal.pone.019161

Interaction of BMI and respiratory status in obstructive sleep apnea, a cross-sectional COPD study

Abstract This cross-sectional study of 136 patients with chronic obstructive pulmonary disease (COPD) investigated the mechanism underlying overlap syndrome, defined as coexisting COPD and obstructive sleep apnea (OSA). OSA was defined as a respiratory event index (REI) ≥ 5 events/h, determined using type-3 portable monitors. The mean REI was 12.8 events/h. Most participants (60.1%) had mild OSA (REI: 5–15 events/h). The REI was positively correlated with forced expiratory volume in one second (%FEV1) (r = 0.33, p < 0.001), body mass index (BMI) (r = 0.24, p = 0.005), and fat-free mass index (r = 0.31, p = 0.005), and negatively correlated with residual volume divided by total lung capacity (r = −0.27, p = 0.003). Receiver-operating characteristic curve analysis revealed an optimal BMI cutoff of 21.96 kg/m2 for predicting moderate/severe OSA. A BMI ≥ 21.96 kg/m2 was associated with OSA among participants with %FEV1 ≥ 50%, but not those with %FEV1 < 50%. This study revealed an interaction between airflow limitation and hyperinflation, nutritional status, and OSA

MOESM2 of Determinants of chronic obstructive pulmonary disease severity in the late-elderly differ from those in younger patients

Additional file: Fig. S2. Comparisons of SF-36 components between COPD patients aged < 75 and ≥ 75 years in different stages of COPD. Data are presented as mean ± standard deviation (SD). *p < 0.05. a: Physical role functioning, b: Emotional role functioning, c: Social role functioning, d: Mental health

Effects of long-term cigarette smoke exposure on bone metabolism, structure, and quality in a mouse model of emphysema

<div><p>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.</p></div

Effects of long-term CS exposure on collagen orientation and biological apatite c-axis alignment of vertebral bodies.

<p>(A) Schematic presentation of bone histological indices (H&E staining, polarization, collagen orientation and biological apatite <i>c</i>-axis alignment). (B) Representative polarizing microscope images in the fourth vertebral bodies (longitudinal section) of B6-female mice after 20 and 40 weeks of air- or CS exposure. Scale bars = 100 μm. (C) Intensity ratio of (002/310) as biological apatite c-axis alignment. The data are shown as means ± SDs. *P<0.05 between air-exposed controls (open bars: <i>n</i> = 10 at 20 weeks, <i>n</i> = 5 at 40 weeks) and CS-exposed B6-female mice (closed bars: <i>n</i> = 5 at 20 weeks, <i>n</i> = 12 at 40 weeks). Statistical analysis was performed with Student’s <i>t</i>-test.</p