Abstract
Smoking is thought to be a risk factor for osteoporosis development; however, the consequences of stopping smoking for bone homeostasis remain unknown. Here we conducted two separate human studies and show that bone mineral density was significantly lower in smokers than in non-smokers. The first was an observational study of pre- and post-menopausal healthy female smokers and non-smokers; the second included 139 current smokers determined to stop smoking. In the second study, levels of bone formation markers such as osteocalcin and uncarboxylated osteocalcin significantly increased after successful smoking cessation, as verified by significantly reduced levels of serum cotinine, a nicotine metabolite. Moreover, nicotine administration to mice reduced bone mineral density and significantly increased the number of osteoclasts in bone. Reduced bone mass phenotypes seen in nicotine-treated mice were significantly increased following nicotine withdrawal, an outcome accompanied by significantly reduced serum levels of tartrate-resistant acid phosphatase, a bone resorption marker. Taken together, our findings suggest that bone homeostasis is perturbed but can be rescued by smoking cessation.
Highlights
Smoking is thought to be a risk factor for osteoporosis development; the consequences of stopping smoking for bone homeostasis remain unknown
We demonstrate that: (1) in post-menopausal women, bone mineral density (BMD) is significantly lower in smokers than non-smokers; (2) serum levels of osteocalcin and uncarboxylated osteocalcin, both markers of bone formation markers, significantly increase after smoking cessation; (3) nicotine administration to wild-type mice reduces bone mass, a phenotype reversible by nicotine withdrawal; and (4) in mice treated as in (3) serum levels of tartrate resistant acid phosphatase 5b (TRAP5b), a marker of osteoclastic bone resorption, significantly decrease following nicotine withdrawal
We evaluated male and female smokers before and after they quit smoking and found that levels of bone formation markers significantly increased within 124 days of smoking cessation
Summary
Smoking is thought to be a risk factor for osteoporosis development; the consequences of stopping smoking for bone homeostasis remain unknown. We showed that α7nAchR-deficient mice exhibit significantly increased bone mass due to inhibition of osteoclastogenesis rather than to stimulation of osteoblastogenesis compared to wild-type mice[18] It is still unclear whether smoking cessation has a positive effects on bones, and whether altered bone homeostasis can be reversed when individuals stop smoking. We demonstrate that: (1) in post-menopausal women, BMD is significantly lower in smokers than non-smokers; (2) serum levels of osteocalcin and uncarboxylated osteocalcin, both markers of bone formation markers, significantly increase after smoking cessation; (3) nicotine administration to wild-type mice reduces bone mass, a phenotype reversible by nicotine withdrawal; and (4) in mice treated as in (3) serum levels of tartrate resistant acid phosphatase 5b (TRAP5b), a marker of osteoclastic bone resorption, significantly decrease following nicotine withdrawal. Our results indicate that disturbance of bone homeostasis by smoking can be recovered by smoking cessation
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