Nicotine induced proliferation and cytokine release in osteoblastic cells

Abstract

Abstract. Smoking has deleterious effects on osteoporosis and periodontitis both characterized by bone loss. Smoking also interferes with the protective effect that hormone replacement therapy (HRT) has on bone loss. Our study investigated two mechanisms by which smoking may affect bone metabolism: nicotine-induced proliferation and nicotine-induced cytokine secretion in osteoblasts. Two osteoblastic cell models were used: mouse osteoblasts derived from mouse calvaria and human osteoblasts. Thymidine incorporation and immunoassays were used to evaluate proliferation, interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-·) secretion. Parametric and nonparametric statistical analyses were used for comparisons. The results showed that nicotine induced stimulation and inhibition of proliferation in both osteoblastic cell models. In human osteoblasts, the proliferative and inhibitory effects were also donor dependent. IL-6 secretion showed different patterns in mouse and human osteoblasts. In mouse osteoblasts, nicotine significantly increased IL-6 secretion and estradiol significantly inhibited the nicotine-induced IL-6 release. In human osteoblasts, cells derived from one subject did not respond to nicotine. However, in the second sample, nicotine increased secretion of IL-6 but estradiol did not oppose this effect. In human osteoblasts, nicotine also induced an increase in the TNF-· secretion and estradiol opposed this increase. These results suggest that nicotine affects bone metabolism by modulating proliferation, and IL-6 and TNF-· secretion. These studies provide a possible explanation for differences in bone loss among subjects who smoke and offer a possible mechanism for the oppositional effect of smoking on HRT in subjects with bone loss.

Skeletal microstructural abnormalities in postmenopausal women with chronic obstructive pulmonary disease

“…Another study demonstrated that nicotine increases Values are expressed as mean AE SD. secretion of the cytokines interleukin 6 (IL-6) and tumor necrosis factor a (TNF-a) (45) that could have their own effects on skeletal integrity. One could use this information to suggest a twophased effect of smoking on bone: an initial increase in remodeling activity followed by a long period of suppressed bone formation.…”

Short-term effects of nicotine on orthodontically induced root resorption in rats

“…In a human in vitro study, nicotine was found to upregulate the expression of IL-6 and tumor necrosis factor (TNF)-alpha. 23 Those factors can stimulate RANKL expression and are important for the induction and the further process of root resorption in the rat. 24,25 These findings suggest that the effect of nicotine on root resorption may act via various cytokines and signal pathways and further verify our hypothesis that the aggravated root resorption caused by nicotine is related to the elevated expression of RANKL.…”

Orthodontic forces add to nicotine-induced loss of periodontal bone

“…Furthermore, nicotine apparently adds to preexisting periodontal inflammation [30,38]. Chemical evaluations have revealed that smoking results in accumulation of nicotine in periodontal fibroblasts [16] and at dental roots [10] and that nicotine promotes synthesis of inflammatory factors and osteoclastogenesis [17,19,52]. Also, nicotine promotes changes in the subgingival environment which has been suggested to facilitate the growth of periodontal pathogens [33].…”