Effects of long-term cigarette smoke exposure on bone metabolism, structure, and quality in a mouse model of emphysema.
Mamoru SasakiShotaro ChubachiNaofumi KameyamaMinako SatoMizuha HaraguchiMasaki MiyazakiSaeko TakahashiTakayoshi NakanoYukiko KurodaTomoko BetsuyakuKoichi MatsuoPublished in: PloS one (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.
Keyphrases
- bone mineral density
- chronic obstructive pulmonary disease
- bone loss
- postmenopausal women
- mouse model
- lung function
- soft tissue
- bone regeneration
- body composition
- healthcare
- type diabetes
- mental health
- pulmonary hypertension
- quality improvement
- risk assessment
- skeletal muscle
- early onset
- adipose tissue
- preterm birth
- insulin resistance
- drug induced
- high fat diet induced
- tissue engineering