Cigratte smoking effects on Bones

Effect of Cigarette Smoking on Bone and Calcium Homeostasis:

Proposed Mechanisms

Cigarette smoking is a frequently cited risk factor for osteoporosis and has been implicated as such in several retrospective and prospective studies. The mechanism by which smoking exerts its debilitating effect on bone is unclear. The adverse effect of smoking could be attributable to the tendency of smokers to have poorer health and eating habits compared with nonsmokers. Some researchers have suggested that the effect of smoking on bone mass is influenced by the low body weight so common among smokers. It has also been speculated that smoking reduces the peak bone mass attained in early adulthood. Perhaps the most convincing evidence is that smoking alters estrogen metabolism and hence may modify estrogen effects on bone mass. Smoking is associated with early natural menopause, greater risk of oligomenorrhea, and infertility. It is not, however, known whether this anti-estrogenic effect of smoking is due to a decrease in estrogen production or an increase in estrogen degradation. Evidence for a decrease in production is suggested by direct inhibition of human granulosa cell aromatase activity and the consequent reduction in androgen to estrogen conversion. Alternatively, there is evidence for an increase in deactivation of estrogens via enhanced 2-hydroxylation of estradiolMore recently, evidence indicates that smoking accelerates bone loss by lowering intestinal calcium absorption. Studies in the elderly and postmenopausal women report a 1.7–13% difference in mean fractional calcium absorption between smokers and nonsmokers, after adjustment for various confounding factors. Need and colleagues proposed that the smoking-mediated impairment in calcium absorption might be caused by the suppression of the parathyroid hormone (PTH)–1,25 dihydroxyvitamin D (1,25[OH]2D)–endocrine axis. Although there was no significant difference in calcium absorption between postmenopausal female smokers and nonsmokers who had similar serum 1,25(OH) 2D concentrations, they observed significantly lower concentrations of circulating PTH and 1,25(OH) 2D in smokers. Likewise, Brot et al. reported that serum concentrations of 25 hydroxyvitamin D (25[OH]D) and 1,25[OH]2D were approx 10% lower, and PTH 20% lower in Danish perimenopausal female smokers than nonsmokers, with serum ionized calcium concentrations being similar in the two groups. In contrast, Rapuri et al. did not find significant differences in 1,25(OH) 2D, intact PTH, serum calcium, or ionized calcium concentrations between elderly female smokers and nonsmokers.  However, they reported a significant 12% decrease in circulating 25(OH)D in the smoking group.

Cigratte smoking effects on Bones

Cigarette Smoking and Risk of Bone Fracture

The impact of cigarette smoking on bone, vitamin D status, and calcium homeostasis appears to be more pronounced in postmenopausal women and the elderly, particularly in heavy smokers (at least one pack per day) or long-term smokers (at least 2 yr), whereas it is less apparent in younger individuals.  Although studies that have examined the association between cigarette smoking and BMD differ somewhat in their reports of bone sites most susceptible to the deleterious effect of smoking, there is general agreement that smoking accelerates the rate of bone loss. A significant, smoking-mediated decrease in BMD has been noted at the total proximal femur, femoral neck, total body, lumbar spine, and the radius. Some earlier studies, however, did not show that smoking had an independent effect on bone mass.  The magnitude of the difference in BMD between postmenopausal or elderly nonsmokers and heavy smokers depends on age and bone site, and ranges from 4 to 6% .  Pocock and colleagues  compared twin pairs discordant for tobacco use (subject age was not reported). They found that twins who were heavy smokers had a 2.4% lower BMD in the lumbar spine than their siblings who were light smokers.

Effect of Smoking Cessation on Fracture Risk

Evidence suggests that the adverse effect of smoking on bone is at least partially reversible when smoking is discontinued. As the duration of smoking cessation increases, the risk of a bone fracture decreases and, after 14–15 yr, may approach the risk of never-smokers. The age-adjusted risk of hip fracture is increased 35% for current and 15% for past (quit within past 14 yr) elderly smokers compared with never-smokers, after correcting for body mass index and HT. Duration of smoking appears to be a stronger predictor of hip fracture risk than the number of cigarettes smoked, and may account for an incremental increase of 6% in fracture risk for every 5 yr of smoking.

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