The effects of subcutaneous injection of nicotine on osseointegration of machined and anodized implants in rabbits

Abstract Purpose: To evaluate the influence of subcutaneous injection nicotine in osseointegration process on different implant surfaces. Methods: Twenty-two male rabbits were distributed into two groups according to the subcutaneous injections: (1) nicotine 3 mg/day/kg and (2) 0.9 % NaCI 3 mL/day/kg, three times a day; subgroups were then designated-machined and anodized implants were placed in the right and left tibia bones, respectively. The animals were submitted euthanasia after periods of eight weeks to determine nicotine and cotinine levels, alkaline phosphatase and biomechanical analysis. Results: The plasmatic levels of nicotine and cotinine were 0.5 ± 0.28 ng/mL and 9.5 ± 6.51 ng/mL, respectively. The alkaline phosphatase analyses in blood levels in control group were observed 40.8 ± 11.88 UI/L and 40.75 ± 12.46 UI/L, for the surfaces machined and anodized, respectively. In the test group was observed levels 37.9 ± 4.84 UI/L, for both implant surfaces. No significant differences were observed between control and test groups and between the implant surfaces regarding alkaline phosphatase blood levels. For biomechanics, no significant differences were observed in control group between the machined (25±8.46 Ncm) or anodized (31.2 ± 6.76 Ncm) implants. However, the treatment with nicotine induced higher torque than control in both machined (38.3 ± 13.52 Ncm) and anodized (35.5 ± 14.17 Ncm) implants, with p = 0.0024 and p = 0.0121, respectively. Conclusion: Subcutaneous injection of nicotine following implant insertion didn't have effect on osseointegration, independently from the implant surface.

Second hand tobacco smoke adversely affects the bone of immature rats

OBJECTIVES: To evaluate the influence of secondhand cigarette smoke exposure on longitudinal growth of the tibia of growing rats and some parameters of bone quality. METHODS: Forty female rats were randomly divided into four groups: control: rats were sham exposed; 30 days: rats were exposed to tobacco smoke for 30 days; 45 days: rats were exposed to tobacco smoke for 45 days; and 60 days: rats were exposed to tobacco smoke for 60 days. Blood samples were collected to evaluate the levels of cotinine and alkaline phosphatase. Both tibias were dissected and weighed; the lengths were measured, and the bones were then stored in a freezer for analysis of bone mineral content and mechanical resistance (maximal load and stiffness). RESULTS: Exposure of rats to tobacco smoke significantly compromised bone health, suggesting that the harmful effects may be time dependent. Harmful effects on bone growth were detected and were more pronounced at 60-day follow-ups with a 41.8% reduction in alkaline phosphatase levels (p<0.01) and a decrease of 11.25% in tibia length (p<0.001). Furthermore, a 41.5% decrease in bone mineral density was observed (p<0.001), leading to a 42.8% reduction in maximum strength (p<0.001) and a 56.7% reduction in stiffness (p<0.001). CONCLUSION: Second hand cigarette smoke exposure in rats affected bones that were weaker, deforming them and making them osteopenic. Additionally, the long bone was shorter, suggesting interference with growth. Such events seem to be related to time of exposure.

Evaluation of Serum Cotinine Cut-Off to Distinguish Smokers From Nonsmokers in the Korean Population

BACKGROUND: Cotinine has been widely used as an objective marker to identify current smokers. We conducted this study to address the absence of Korean studies investigating the efficacy of immunoassays and liquid chromatography-tandem mass spectrometry (LC-MS/MS) for the detection of serum cotinine and to determine the optimal serum cotinine cut-off level for differentiating current smokers from nonsmokers. METHODS: Serum specimens were obtained from 120 subjects. They were randomly chosen to represent a broad distribution of urine cotinine levels based on a retrospective review of questionnaires and results of urine cotinine levels. We determined serum cotinine levels using the IMMULITE 2000 XPi Immunoassay System (Siemens Healthcare Diagnostics Inc., USA) and LC-MS/MS (API-4000, Applied Biosystems, USA). Correlation was analyzed between IMMULITE serum cotinine, urine cotinine, and LC-MS/MS serum cotinine levels. ROC curve was analyzed to identify the optimal IMMULITE serum cotinine cut-off level for differentiating current smokers from nonsmokers. RESULTS: IMMULITE serum cotinine levels correlated with both urine cotinine and LC-MS/MS serum cotinine levels, with correlation coefficients of 0.958 and 0.986, respectively. The optimal serum cotinine cut-off level for distinguishing current smokers from nonsmokers was 13.2 ng/mL (95.7% sensitivity, 94.1% specificity) using IMMULITE. CONCLUSIONS: This is the first study to investigate the use of LC-MS/MS for the measurement of serum cotinine and to determine the optimal serum cotinine cut-off level for the IMMULITE immunoassay. Our results could provide guidelines for differentiating current smokers from nonsmokers in the Korean population.

Validation of self-reported smoking status by measuring serum cotinine levels: An Indian perspective.

Background. Serum cotinine levels are a reliable marker of tobacco use. Few studies have validated questionnaires assessing smoking and exposure to environmental tobacco smoke (ETS) against serum levels. We undertook such a study in industrial workers in India. Methods. We chose 426 individuals by stratified random sampling from a database of 3397 individuals surveyed at New Delhi for the cardiovascular disease surveillance programme in a large industrial setting. Questionnaires assessing details of smoking practices and duration of exposure to ETS (if any) were administered. Cotinine levels were measured in the blood samples of these individuals. Results. The study population comprised 142 nonsmokers not exposed to ETS, 142 non-smokers exposed to ETS and 142 active smokers. Cotinine levels among nonsmokers not exposed to ETS were non-detectable; and for non-smokers exposed to ETS and active smokers, the median (interquartile range) levels were non-detectable (non-detectable to 46.1 ng/ml) and 336 ng/ml (204–500 ng/ml), respectively. The best combined sensitivity (91%) and specificity (87.2%) yielded a cotinine cut-off level of 40.35 ng/ml to differentiate active smokers from non-smokers not exposed to ETS and those exposed to ETS (area under the curve 0.902). The cut-off cotinine level was estimated at 10.95 ng/ml using a similar analysis (sensitivity 43%, specificity 82%; area under the curve 0.64) to distinguish non-smokers not exposed to ETS from those exposed to ETS. The misclassification rate was estimated at 19% and 57.1% among self-reported non-smokers not exposed to ETS and those exposed to ETS, respectively. Conclusions. Obtaining a history of tobacco use is an accurate method of detecting smokers in epidemiological studies whereas serum cotinine levels accurately differentiate smokers from non-smokers. However, a brief questionnaire assessing passive exposure to smoke has poor sensitivity in distinguishing non-smokers exposed to ETS from those not exposed to ETS.

Training parents or children? Which is more successful in controlling passive smoking?

Environmental tobacco smoke [ETS] has been shown to have adverse health hazards for children. The objective of this study was to assess the effects of two intervention programs for controlling passive smoking in children based on their serum cotinine level. In this trial, 40 children, aged 8-12 years, who were exposed to ETS were randomly assigned to two groups of equal number. In the first the parents [group P], and in the second group the children [group C] were educated about the harmful effects of passive smoking. Children's blood sample was taken for serum cotinine measurement before and after intervention in both groups. Data were analyzed by SPSSv13/win using paired t-test. Smoking allowed inside home decreased in both groups; however, this decrease in group C was significantly higher than in group P. Serum cotinine concentration decreased in both groups with a more prominent decrease in group C. Education of children can be an effective method for controlling passive smoking. This type of education can be effective for lifestyle change in the entire family

Cigarette smoking as an acute threat for the cardiovascular system

Cigarette smoking is one of the major risk factors for cardiovascular disease as well as hyperlipidemia. Lecithin: Cholesterol acyl transferase [LCAT] activity represented a key factor in the esterification of serum cholesterol and reverse cholesterol transport. Leptin, the protein product of the ob gene, seems to regulate body fat stores. The present study was carried out to evaluate changes in the circulating levels of leptin, LCAT activity, insulin, glucose, cotinine and lipid profile [total cholesterol TC, triglycerides TG, HDLC, LDL-C], free fatty acids [FFA5] and apolipoprotiens [Apo Al and Apo B] in healthy smokers [n=48] and non smokers [n=32] group. The results showed remarkable increase in the levels of LDL-C, FFAs, cotinine, leptin [p<.000], TC[P<0.01] and glucose [p<0.05] in healthy smokers than non smokers group. However, the activity of LCAT and levels of HDL-C and Apo Al, were significantly reduced [p<.000] in smokers subjects than non smokers group. Present results showed, the significant increase in levels of leptin, FFAs, LDL-C and the significant decrease in HDL-C and LCAT activity during cigarette smoking which may implicate high risk for further vascular complications

Serum surfactant protein-A levels in chronic bronchitis and its relation to smoking.

BACKGROUND: Surfactant protein-A (SP-A), which is an important constituent of natural surfactant, occurs physiologically in small amounts in blood. Tobacco smoke induces increased alveolo-capillary leakage of surfactant proteins into blood and its level in blood may help in the assessment of lung injury caused by smoke. Little is known on the SP-A levels in patients with chronic obstructive pulmonary disease (COPD). METHODS: Prospective analytical study of 30 patients with clinical diagnosis of chronic bronchitis, which was made on the basis of symptoms, signs and chest radiographic findings. Serum SP-A and serum cotinine levels were measured. RESULTS: Out of 30 patients, 21 were smokers and nine were non-smokers. The serum SP-A level in smokers with chronic bronchitis is significantly higher than the non-smokers. The plasma cotinine levels are also high in smokers. However, there was no correlation between the serum SP-A level and plasma cotinine level (r=0.044). Serum SP-A levels were related to age in smokers (r=0.566, p<0.01) but not in non-smokers with chronic bronchitis (r=0.017, p>0.05). CONCLUSION: The increase in SP-A level in smokers with chronic bronchitis suggests that tobacco smoking causes a chronic increase in permeability of the lung parenchyma. The SP-A, a lung-specific secretory protein, is a potential marker for non-invasive assessment of the integrity of the lung epithelium. Further studies are required to find out whether SP-A can be used as a marker for early identification of smokers who are at risk of COPD.

Marcadores de exposição tabágica em ratas lactantes utilizando um modelo de exposição passiva desde o início da gestação / Tobacco exposure markers in lactating rats, using a passive exposure model from the beginning of pregnancy

Marcadores de exposição tabágica permitem avaliar a intensidade da exposição à fumaça do tabaco, quantificando a absorção da fumaça pelo fumante. O objetivo deste estudo é avaliar a intensidade da exposição tabágica em ratas lactantes, utilizando um modelo simplificado de exposição passiva, desde o início da gestação, por meio da medida de cotinina e carboxiemoglobina em sangue animal. Metodologia: ratas foram expostas, do segundo dia de gestação ao 17º dia de lactação, ao ar comprimido (n=18), à fumaça de 5 cigarros (n=15) e comparadas a grupo não exposto (n=18), segundo o sistema de exposição descrito por Le Mesurier et al, e modificado por Silva et al, variando a quantidade de cigarros e o número de dias de exposição. A cotinina plasmática e a carboxiemoglobina foram determinadas pela técnica adaptada de Feyerabend et al e pela técnica de Beutler e West, respectivamente. Resultados: a detecção de cotinina ocorreu somente nos animais expostos à fumaça do tabaco (mediana 78,8 ng/mL; min 25,4 nd/mL – max 223,3 ng/mL) e a mediana de carboxiemoglobina foi significantemente mais elevada nos animais fumantes (mediana 11,4%; min 5,7% – max 11,8%) do que nos animais dos grupos de controle (mediana 0,1%; min 0,1% – max 1,22%) e expostos ao ar comprimido (mediana 0,1%; min 0,1% – max 1,1%). Conclusão: para o modelo de exposição animal estudado e com animais em fase de reprodução, foi possível detectar cotinina e elevação do percentual sanguíneo de carboxiemoglobina, nos animais expostos à fumaça do tabaco.

Histologic evaluation of the effect of nicotine administration on bone regeneration: a study in dogs

O objetivo do presente estudo foi avaliar histometricamente a influência da nicotina sobre a regeneração óssea de defeitos criados cirurgicamente em rebordos alveolares edêntulos de cães. Defeitos ósseos foram criados cirurgicamente em um dos lados da mandíbula de dezesseis cães e foram deixados para que curassem espontanea-mente. Os animais foram aleatoriamente designados para um dos seguintes grupos: Grupo 1 - controle (n = 8) e Grupo 2 - administração subcutânea de nicotina (2 mg/kg) duas vezes ao dia durante 4 meses (n = 8). Os animais foram sacrificados, e secções semi-seriadas descalcificadas, obtidas. Os parâmetros histométricos avaliados foram altura, largura, área e densidade do tecido ósseo neoformado. A análise intergrupos (Mann-Whitney "rank sum test") demonstrou que a administração de nicotina não influenciou altura, largura e área de tecido ósseo neoformado (p > 0,05). Entretanto, a administração de nicotina influenciou significativamente a densidade do tecido ósseo neoformado (p < 0,001). Dentro dos limites do presente estudo, pode-se concluir que a nicotina pode afetar, mas não impedir a regeneração de defeitos ósseos criados cirurgicamente em mandíbulas edêntulas de cães.

Effects of low dose aspirin and antioxidant on Haemostatic equilibria in females oral contraceptives

Abnormalities in coagulation equilibria and prooxidant antioxidant status have been observed in consequence to cigarette smoking and oral contraceptive pill use. The study aims to evaluate parameters of hemostatic equilibria and endothelial damage in females with thrombotic tendencies arising from oral contraceptive [OC] pill use for more than three years besides the cumulative impact of cigarette smoke inhalation [CSI]. As well assessment of the influence of cessation of CSI for six months in conjunction with therapeutic regimen involving low dose aspirin and antioxidant supplementation. Selected cases were within age range 27-35 years and included active smokers [GII n = 20] and passive smokers [G11 n=20]. For six months they followed a regimen of daily supplementation of low dose [75 mg] aluminum aspirin tablets and antioxidants [antox tablets and dietary resources] besides cessation or avoidance of cigarette smoke inhalation as well as use of conventional contraception instead of OC. The results illustrated variations in the evaluated parameters of hemostatic equilibria including protein C, protein S and thrombin antithrombin complex as well as of total antioxidant - capacity and lipid peroxidation product malonedialdehyde versus serum cotinine levels. These variations were more bronounced in passive than active smokers when values were compared to those assessed before commencing the six month regimen. The aforementioned therapeutic regimen provided appropriate changes after six months for passive smokers and should be extended for another six months for active smokers who stopped smoking to fulfill the regimen requirements for rebalancing of hemostatic equilibria

effects of passive cigarette smoking on the respiratory system among the healthy wives of active smokers

This study included 50 adult healthy volunteers; 20 currently smokers, 20 wives of active smokers spouse [passive smokers] and the remaining 10 subjects were nonsmokers controls. Ventilatory pulmonary function tests [FVC% predicted, FEV1/FVC ratio, FEV1% predicted and FEF25-7.5% predicted] were made to all subjects. Urinary cotinine, serum cotinine and lipid peroxides levels were assessed using spectrophotometric method. Data demonstrated that passive smokers are at risk to develop subsequent destructive lung disease, which was evident by an increase in the level of lipid peroxides [marker of oxidative stress] and a decline in the spirometric indices [especially a decline in FEV1% predictive which is the most strongly predictive index of chronic obstructive lung diseases in adults]. The decline in FEF25-75% predictive indicated the possibility of small airway diseases. The benefit of the use of urinary and serum cotinine as cheap biomarkers of exposure to cigarette smoke was clarified

Maternal and fetal serum cotinine levels and uteroplacental hemodynamics in pregnant passive smokers

45 pregnant women married to heavy smokers and exposed for at least 2 hours/day were studied at 38-40 weeks of gestational age. Another 20 pregnant women of the same gestational age and not exposed to tobacco smoke, were studied as control. Maternal and fetal serum cotinine levels were assayed. The S/D ratio was determined by uterine and umbilical Doppler velocimetry wave-form analysis. The maternal serum cotinine levels were significantly higher in passive smokers [5.5 +/- 2.7 ng/ml] than nonsmokers [2.4 +/- 1.5 ng/ml] [P <0.001]. The fetal serum cotinine levels were also significantly higher in passive smokers than nonsmokers [2.14 +/- 1.3 and 0.79 +/- 0.3 ng/ml] respectively [P <0.001]. The S/D in passive smokers [2.5 +/- 0.8 and 2.7 +/- 0.9] was significantly higher than in nonsmokers [2.1 +/- 0.2 and 2.2 +/- 0.6] [P <0.01]. The elevated cotinine levels could be significantly correlated with the elevated S/D ratio of the uterine and umbilical arteries. This study strengthens the link between passive smoking and the adverse effects on the utero-placental hemodynamics and elucidates the value of cotinine as a monitor of passive exposure to tobacco smoke