Bone Abstracts

Background and Aim: Smoking increases fracture risk and contributes to COPD-associated osteoporosis. However, its impact on bone metabolism is largely unknown. We thus aimed to determine the effect of smoking cessation on bone metabolism.

Subject and Method: In this prospective study, we recruited 29 healthy Japanese male subjects with smoking habit (37.7±8.2 years old, 16.9±11.3 pack years). Pulmonary function test was done before smoking cessation, and various bone and calcium metabolic markers, inflammatory markers and plasma cotinine levels were examined at 0, 1 and 4 weeks.

Result: Mean FEV1.0/FVC, FEV 1.0% predicted was 81.9% and 101.7%, respectively. Cotinine concentration was 149±119 pg/ml. We confirmed that cotinine levels clearly decreased after cessation except for one subject who failed, and the remaining 28 subjects were analyzed. Smoking cessation caused increases in P1NP at 1 and 4 weeks (+8.7±16.7%, P=0.014; +10.5±20.0%, P=0.062), and under-carboxylated osteocalcin (ucOC) at 1 and 4 weeks (21.4±37.9%, P=0.020; 21.9±25.6%, P=0.002). Interestingly, %change of P1NP correlated with %change of intact PTH (r=0.421, P=0.026 at 1 week: r=0.556, P=0.002 at 4 weeks). At baseline PTH showed no correlation with 25-hydroxyvitamin D (25D). When the subjects were divided into two groups by 25D levels, the group with lower 25D levels showed larger increases in PTH (19.8% vs. −4.6%) and P1NP (14.2% vs 5.7%) at 1 week. Moreover, negative correlation between PTH and 25D was partially restored after smoking cessation. IL-6, TNF-α and hsCRP were closely interrelated, but consistent changes could not be observed. TRACP-5b levels tended to increase at 4 weeks without significance.

Conclusion: The results indicate that bone formation is suppressed by smoking at least partially in a reversible manner and is recovered after cessation. The mechanism remains to be determined, but appears to be in part associated with impaired PTH secretion due to a disturbed PTH-vitamin D axis.