Guided bone regeneration may be negatively influenced by nicotine administration: a histologic study in dogs.

BACKGROUND: A series of animal and in vitro data confirms that nicotine impairs bone healing, diminishes osteoblast function, and causes autogenous bone graft morbidity. Therefore, this study aimed to investigate the impact of nicotine on the healing of bone defects treated by the guided bone regeneration (GBR) principle. METHODS: Sixteen mongrel dogs were used. One defect was surgically created bilaterally and randomly assigned as an expanded polytetrafluoroethylene (ePTFE) membrane site or a non-membrane control site. The animals were randomly assigned to one of the following groups: group 1, placebo (n = 8) and group 2, subcutaneous administration of nicotine (2 mg/kg) twice daily (n = 8). After 4 months, the animals were sacrificed and the specimens routinely processed for semi-serial decalcified sections. The evaluated parameters were bone height, bone width, bone density, and bone area of newly formed bone. RESULTS: Intergroup analysis (Kruskal-Wallis) showed that membrane-protected defects in the placebo group demonstrated an increased bone area when compared to membrane-protected defects in the nicotine group and non-membrane sites, regardless of nicotine administration (P < 0.05). In addition, nicotine administration significantly affected bone density in membrane- and non-membrane-protected sites (P < 0.05). CONCLUSIONS: Within the limits of the present study, nicotine might affect, but not prevent, bone healing in defects treated by guided bone regeneration. The mechanisms of this effect should be investigated further.

Matrix metalloproteinase-2 may be involved with increased bone loss associated with experimental periodontitis and smoking: a study in rats.

BACKGROUND: Smoking has been associated with periodontitis severity and is considered a risk factor for its development. It has been reported that matrix metalloproteinase (MMP) produced by host cells plays a major role in periodontal tissue destruction. Thus, the present study tested, in rats, the hypothesis that local increased levels of MMP-2 would be associated with the enhanced periodontitis-related bone loss after intermittent cigarette smoke inhalation (CSI). METHODS: Twenty-seven adult male Wistar rats were used. A ligature was placed around one of the mandibular first molars of each animal and they were randomly assigned to the following control (N = 13) or CSI (N = 14) group. Sixty days later, the animals were sacrificed, the gingival tissues harvested, and the specimens processed for decalcified sections. Extracts from the gingival tissues were prepared and assayed for MMP-2 expression. RESULTS: Intergroup comparisons (unligated sites) showed that CSI might directly affect alveolar bone (0.16 +/- 0.03 mm2 versus 0.24 +/- 0.09 mm2 for non-smokers and smokers, respectively; P = 0.001). Moreover, CSI significantly enhanced bone loss resulting from experimental periodontitis (0.64 +/- 0.36 mm2 versus 1.50 +/- 0.50 mm2 for non-smokers and smokers, respectively; P<0.05). In addition, zymography demonstrated that CSI also enhanced both MMP-2 levels and activity in the gingival tissues around ligated teeth. CONCLUSION: Within the limits of the present investigation, it can be assumed that the effect of CSI on MMP-2 levels and activity may account for the increased periodontitis progression rate observed in smokers.

A comparative study on the effect of nicotine administration and cigarette smoke inhalation on bone healing around titanium implants.

BACKGROUND: A series of isolated studies has focused on the influence of smoking on bone around titanium implants. This study proposes to investigate the impact of two conditions, i.e., nicotine administration and cigarette smoke inhalation, on the healing around implants. METHODS: Forty-five Wistar rats were used. After anesthesia, the tibiae surface was exposed and a screw-shaped titanium implant was placed bilaterally. The animals were randomly assigned to one of the following groups: Group 1: control, n = 19; Group 2: intermittent cigarette smoke inhalation, n = 15; and Group 3: subcutaneous administration of nicotine (3 mg/kg) twice daily, n = 11. After 60 days, the animals were sacrificed. The degree of bone-to-implant contact (BIC) and the bone area (BA) within the limits of the threads of the implant were measured in the cortical (zone A) and cancellous bone (zone B) areas. RESULTS: In zone A, cigarette smoke presented a significant negative influence on BIC and BA (Kruskal-Wallis test, P < 0.05). In contrast, the administration of nicotine did not influence either parameter (P > 0.05). In zone B, cigarette smoke inhalation also resulted in a decreased percentage of BIC compared to the control group (P < 0.05). In addition, the BA was significantly decreased in groups 2 and 3 when compared to controls (P > 0.05). CONCLUSION: The negative impact of smoking on implant outcomes may be related to more than one molecule present in the cigarette smoke and nicotine seems to partially contribute, especially in the cancellous bone.

Ascorbic acid improves impaired venous and arterial endothelium-dependent dilation in smokers.

AIM: To compare the acute effects of ascorbic acid on vasodilation of veins and arteries in vivo. METHODS: Twenty-six healthy non-smokers and 23 healthy moderate smokers were recruited in this study. The dorsal hand vein compliance technique and flow-mediated dilation were used. Dose-response curves to bradykinin and sodium nitroprusside were constructed to test the endothelium-dependent and -independent relaxation before and after acute infusion of ascorbic acid. RESULTS: Smokers had an impaired venodilation with bradykinin compared with non-smokers (68.3%+/-13.2% vs 93.7%+/-20.1%, respectively; P<0.05). Ascorbic acid administration in the dorsal hand vein significantly increased the venodilation with bradykinin in smokers (68.3%+/-13.2% vs 89.5%+/-6.3% before and after infusion, respectively; P<0.05) but not in non-smokers (93.7%+/-20.1% vs 86.4%+/-12.4% before and after infusion, respectively). Similarly, the arterial response in smokers had an impaired endothelium-dependent dilation compared with that in non-smokers (8.8%+/-2.7% vs 15.2%+/-2.3%, respectively; P<0.05) and ascorbic acid restored this response in smokers (8.8%+/-2.7% vs 18.7%+/-6.5% before and after infusion, respectively; P<0.05), but no difference was seen in non-smokers (15.2%+/-2.3% vs 14.0%+/-4.4% before and after infusion, respectively). The endothelium-independent dilation did not differ in both the groups studied. No important hemodynamic change was detected using the Portapress device. CONCLUSION: Smokers had impaired endothelium-dependent vasodilation responsiveness in both arterial and venous systems. Ascorbic acid restores this responsiveness in smokers.