November 05, 2020
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Bone homeostasis is disturbed in smokers, though cessation seems to have a rescuing effect, a recent study has found.
Researchers conducted two human studies. The first included 471 pre- and post-menopausal women, of whom 54 were current smokers and 417 were nonsmokers. The second included 139 current smokers who were determined to quit. Osteocalcin and uncarboxylated osteocalcin (ucOC) were used as markers of bone homeostasis.
In the first study, the basic demographic characteristics were comparable between smokers and nonsmokers, but the latter group showed significantly greater bone mineral density (BMD).
Levels of osteocalcin and ucOC, both markers of bone formation, were comparable between smokers and nonsmokers. However, among pre-menopausal women, serum concentrations of tartrate resistant acid phosphatase 5b (TRACP5b), an indicator of osteoclastic bone resorption, were higher in smokers. On the other hand, serum N-terminal telopeptide of type 1 collagen (NTX), a different marker of resorption, was lowered in smokers.
The second study uncovered a recovery effect due to cessation. Of the 139 participants, 54 men and 22 women reported that they had stopped smoking. Subsequent lab analyses found 47 participants saw statistical suppression of blood cotinine levels. These 47 patients were deemed to have successfully quit smoking.
While levels of urinary NTX and serum TRACP5b were unchanged after cessation, the researchers documented a significant spike in serum osteocalcin and ucOC, suggesting that quitting could potentially reverse the adverse effects of smoking on bone homeostasis.
“We conclude that based on our findings, deleterious changes in bone homeostasis associated with smoking can be rescued by smoking cessation. Such changes in smoking behaviours should be encouraged as a potential means to improve bone metabolism and reduce risk of osteoporosis development,” they said.
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