Association between involuntary smoking and salivary markers related to periodontitis: a 2-year longitudinal study.

BACKGROUND: Insufficient data exist regarding the longitudinal influence of involuntary smoking on periodontitis progression. This study examined the relationship between involuntary smoking and periodontitis progression and the effects of involuntary smoking on salivary inflammatory and microbiologic markers related to periodontitis. METHODS: Participants were recruited during annual health checkups in 2003 and 2005. In 2005, 200 of 273 (73%) Japanese employees examined at baseline underwent periodontal measurements, including clinical attachment level (CAL) and probing depth (PD). Periodontitis progression was identified when a subject displayed one or more teeth with an increase > or = 2.0 mm in CAL and PD during the 2 years. Salivary marker levels, including cotinine, were determined by enzyme assay, including enzyme-linked immunosorbent assay. The proportions of six periodontal pathogens in saliva were assessed using real-time polymerase chain reaction methodology. Based on receiver-operating characteristic analysis, non-, involuntary, and active smokers were defined as subjects exhibiting salivary cotinine levels of 0, 1 to 7, and > or = 8 ng/ml, respectively. RESULTS: By simple logistic regression analysis, age, alcohol consumption, smoking, breakfast habits, and working hours were related to the risk for significant periodontitis progression. Multiple logistic regression analysis revealed significantly higher periodontitis odds ratios (OR) in involuntary (OR = 2.23; 95% confidence interval [CI]: 1.03 to 4.83) and active (OR = 2.27; 95% CI: 1.02 to 5.04) smokers relative to non-smokers following adjustment for covariates. Levels of salivary markers, including albumin, aspartate aminotransferase, and lactoferrin, were significantly elevated in involuntary smokers relative to non-smokers. In contrast, the percentages of periodontal pathogens did not differ between the smoking groups, with the exception of Prevotella nigrescens, which displayed significantly lower levels in involuntary smokers compared to non-smokers. CONCLUSION: Involuntary smoking increased the inflammatory response and was associated with a greater risk for periodontitis progression.

Effect of eucalyptus extract chewing gum on periodontal health: a double-masked, randomized trial.

BACKGROUND: Studies in vitro showed that eucalyptus extracts possess antibacterial activity against cariogenic and periodontopathic bacteria; however, the clinical effects with respect to periodontal health in humans remain unproven. The objective of this study was to evaluate the effect of chewing gum containing eucalyptus extract on periodontal health in a double-masked, randomized, controlled trial. METHODS: Healthy humans with gingivitis but not deep periodontal pockets were randomly assigned to the following groups: high-concentration group (n=32): use of 0.6% eucalyptus extract chewing gum for 12 weeks (90 mg/day); low-concentration group (n=32): use of 0.4% eucalyptus extract chewing gum for 12 weeks (60 mg/day); and placebo group (n=33): use of chewing gum without eucalyptus extract for 12 weeks. Plaque accumulation (PLA), gingival index (GI), bleeding on probing (BOP), periodontal probing depth (PD), and clinical attachment level (CAL) were measured at weeks 0, 4, 8, 12, and 14. Significance was analyzed with repeated-measures two-way analysis of variance followed by the Games-Howell pairwise comparison test. RESULTS: The interaction between the effects of eucalyptus extract chewing gum and the intake period was statistically significant for PLA, GI, BOP, and PD but not for CAL. The low- and high-concentration groups exhibited statistically significant (P <0.05) improvements compared to the placebo group for PLA, GI, BOP, and PD. CONCLUSIONS: Eucalyptus extract chewing gum had a significant effect on PLA, GI, BOP, and PD. The use of eucalyptus extract chewing gum may promote periodontal health.

Longitudinal study of the association between smoking as a periodontitis risk and salivary biomarkers related to periodontitis.

BACKGROUND: Insufficient data exist regarding the long-term influence of lifestyle factors including smoking on periodontal health. The objective of this study was to examine the prospective association between smoking and periodontal disease progression and the effects of smoking on salivary biomarkers related to periodontitis. METHODS: Probing depth (PD) was measured at health checkups of workers in 1999 and 2003; additionally, lifestyle information was obtained through a questionnaire. In 2003, 219 of 256 (86%) workers examined at baseline completed PD measurements; saliva samples were also collected. Change in PD was used for assessment of periodontitis progression when three or more sites displayed an increase of >or=2 mm over 4 years. Salivary biomarker levels were determined by real-time polymerase chain reaction and enzyme assay. Statistical methods included bivariate and multivariate regression analyses. RESULTS: In the multiple logistic model, in which lifestyle-related factors served as independent variables, significant variables were current smoking and hours of sleep; respective odds ratios were 2.3 and 2.1. Additionally, 38.5% of periodontal disease progression was attributable to current smoking. Moreover, pack-years of smoking showed a dose-response relationship with disease progression. Levels of salivary markers including prostaglandin E(2), lactoferrin, albumin, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase were significantly lower in current smokers than in non-current smokers. However, no meaningful differences in the proportions of six periodontal pathogens were observed between current and non-current smokers. CONCLUSIONS: Smoking exerted the greatest influence on periodontitis risk among lifestyle factors. Smoking may suppress the host-defense system, which may promote periodontal disease progression.

Association between passive smoking and salivary markers related to periodontitis.

OBJECTIVES: The mechanism of passive smoking in terms of development of periodontitis has not been investigated. This study examined the effect of passive smoking on salivary markers related to periodontitis. METHODS: Periodontal status was evaluated on the basis of probing pocket depth and clinical attachment level in 273 workers. Salivary marker levels were determined by enzyme assay including enzyme-linked immunosorbent assay. Six periodontal pathogens in saliva were assessed using real-time PCR methodology. Non-, passive and active smokers were defined as subjects exhibiting salivary cotinine levels of 0 (53 subjects), 1-7 (118) and > or = 8 ng/ml (102). RESULTS: Levels of salivary markers, including IL-1beta, lactoferrin, albumin and aspartate aminotransferase (AST), were elevated significantly in passive smokers relative to non-smokers. Additionally, these marker levels, with the exception of IL-1beta, decreased significantly in active smokers in comparison with passive smokers. However, no meaningful differences in percentages of periodontal pathogens were observed between non- and passive smokers. Multiple linear regression analyses were performed for each marker utilizing age, gender, cotinine level and periodontal status as independent variables. IL-1beta, albumin and AST were independently associated with cotinine level. CONCLUSION: Passive smoke exposure leads to elevation of IL-1beta, albumin and AST levels in saliva.

Association between passive and active smoking evaluated by salivary cotinine and periodontitis.

AIM: This study attempted to determine the relationship between passive and active smoking on the basis of salivary cotinine levels and periodontitis severity. METHODS: Japanese workers (n=273) were surveyed via an oral examination, a self-administered questionnaire and collection of whole saliva. Probing pocket depth (PPD) and clinical attachment level (CAL) served as periodontal parameters. Periodontitis was defined as the presence of two or more teeth with PPD > or =3.5 mm and CAL > or =3.5 mm. Salivary cotinine was determined using ELISA. Statistical methods included Wilcoxon's rank-sum test and multiple logistic regression analysis. RESULTS: Based on the results of receiver-operating characteristic plots for cotinine-level classification derived from self-reported smoking status, non-, passive and active smokers were defined as those subjects exhibiting cotinine levels of 0, 1-7 and > or =8 ng/ml, respectively. Numbers of teeth displaying CAL > or =3.5 mm in passive and active smokers were significantly higher than those in non-smokers. Multiple logistic regression analysis revealed significantly higher periodontitis odds ratios in passive and active smokers relative to non-smokers following adjustment for other lifestyle factors; odds ratios were 2.87 [95% confidence interval (CI); 1.05-7.82] and 4.91 (95% CI; 1.80-13.35), respectively. CONCLUSION: These findings suggest that passive smoking classified in terms of salivary cotinine level may be an independent periodontitis risk indicator.

Determination of smoking and obesity as periodontitis risks using the classification and regression tree method.

BACKGROUND: A model that focuses on personal risk factors associated with poor lifestyle has been proposed for the etiology of generalized periodontitis. Numerous investigations have linked individual lifestyle-related factors to periodontitis risk; however, a definite relationship among lifestyle-related factors remains unclear. The objective of this study was to determine which lifestyle-related factors demonstrated the greater impact on periodontitis risk. METHODS: The association of lifestyle-related factors, such as smoking status and obesity, with periodontitis was assessed in 372 Japanese workers via a self-administered questionnaire. Smoking status and obesity were evaluated in terms of pack-years and body mass index (BMI), respectively. Clinical periodontal examination included probing depth (PD). The effective impact on periodontitis risk was analyzed by the classification and regression tree (CART) method and multiple logistic regression analysis. RESULTS: Simple logistic regression analyses revealed that factors such as age, gender, alcohol consumption, smoking status, BMI, and frequency of toothbrushing were associated with periodontitis. CART results demonstrated a significant correlation between periodontitis and pack-years, BMI, and age; in contrast, alcohol consumption, gender, and toothbrushing frequency were not correlated with periodontitis. The strongest factor for periodontitis risk was pack-years of smoking. Additionally, both pack-years and BMI exhibited clear dose-response relationships with periodontitis. These relationships were maintained despite adjustment for known confounding factors. CONCLUSIONS: Smoking displays the greatest impact on periodontitis among lifestyle-related factors. Both smoking and obesity are independent risk indicators for periodontitis; moreover, these parameters exhibit a dose-response relationship with respect to periodontitis risk.

Contribution of periodontal pathogens on tongue dorsa analyzed with real-time PCR to oral malodor.

Oral malodor is considered to originate primarily from tongue microbiota populations. However, the relationship between oral malodor and tongue microbiota remains unclear. In this study, tongue periodontal pathogens were analyzed via real-time PCR, and the association between oral malodor and tongue periodontal pathogens, including Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia, Prevotella nigrescens and Treponema denticola, was examined. The subject population consisted of 29 individuals with and 10 healthy persons without oral malodor. Oral malodor was assessed by organoleptic test and volatile sulfur compound (VSC) levels as measured by gas chromatography. Real-time PCR was conducted for anaerobes in tongue biofilm samples employing a LightCycler system; furthermore, bacterial proportion served as a quantitative parameter. Among the five anaerobes, only T. forsythia displayed higher proportions in malodor subjects than corresponding values in healthy controls. Proportions of P. intermedia and P. nigrescens correlated strongly with hydrogen sulfide concentration. Proportions of P. gingivalis and P. nigrescens also exhibited strong correlation with methyl mercaptan concentration. The correlation coefficient between the proportion of the total of the five anaerobes and total VSC level (r = 0.88) was greater than that between bacterial proportion and organoleptic score (r = 0.29). When a linear regression analysis was performed utilizing the proportion of each of the five periodontal pathogens as an independent variable, the explanatory power of these independent variables revealed 81% for total VSC level and 16% for organoleptic score. These results suggest that these five periodontal pathogens on tongue dorsa may contribute greatly to VSC production.

Characterization of binding of Streptococcus oralis glyceraldehyde-3-phosphate dehydrogenase to Porphyromonas gingivalis major fimbriae.

Binding of Streptococcus oralis glyceraldehyde-3-phosphate dehydrogenase (GAPDH) to Porphyromonas gingivalis fimbriae was characterized via a biomolecular interaction analysis system. The interaction was specific, and the association constant value was 4.34 x 10(7) M(-1), suggesting that S. oralis GAPDH functions as a dominant receptor for P. gingivalis and contributes to P. gingivalis colonization.