Periodontal disease has been associated with cardiovascular disease (CVD), and inflammation may represent a common pathophysiology. Oral health screening in the context of CVD risk assessment represents a potential opportunity to identify individuals at risk for CVD. The purposes of this study were to determine if self-reported oral health status is independently associated with inflammatory markers and if oral health assessment as part of CVD risk screening can identify at-risk individuals without traditional CVD risk factors. A baseline analysis was conducted among participants in the National Heart, Lung, and Blood Institute's Family Intervention Trial for Heart Health (FIT Heart; n = 421, mean age 48 ± 13.5 years, 36% nonwhite) without CVD or diabetes who underwent standardized assessment of oral health, lifestyle, CVD risk factors, and the inflammatory markers high-sensitivity C-reactive protein and lipoprotein-associated phospholipase A2. Statistical associations between oral health, risk factors, and inflammatory markers were assessed, and logistic regression was used to adjust for effects of lifestyle and potential confounders. Periodontal disease was independently associated with being in the top quartile of lipoprotein-associated phospholipase A2 compared with the lower 3 quartiles (odds ratio 1.9, 95% confidence interval 1.1 to 3.2) after adjustment for lifestyle and risk factors. Histories of periodontal disease were reported by 24% of nonoverweight, nonhypertensive, nonhypercholesterolemic participants, and of these participants, 37% had elevated high-sensitivity C-reactive protein (≥3 mg/L) or lipoprotein-associated phospholipase A2 (≥215 ng/ml) levels. In conclusion, self-reported periodontal disease is independently associated with inflammation and common in individuals without traditional CVD risk factors.

BACKGROUNDThe role of periodontal disease as a predictor of incident tooth loss in postmenopausal women has not been determined. The aim of this cohort study was to determine the extent of the association between baseline periodontal status and incident tooth loss in a population of postmenopausal women.METHODSThe study population included 106 dentate white postmenopausal women who participated in a cross-sectional study between 1989 and 1991 who were willing and eligible to have a repeat examination after 10 to 13 years. At baseline, full-mouth assessment of periodontal status was performed clinically and radiographically. Assessment of tooth loss during follow- up was assessed clinically by a periodontist. Odds ratio (OR) and its 95% confidence interval (CI) for each periodontal variable was obtained from separate multiple logistic regression analyses adjusting for the effect of age, household income, smoking, hormone therapy, snack consumption, and number of decayed teeth.RESULTSSixty-one (57.5%) subjects lost at least one tooth during follow-up. Mean tooth loss per person was 1.81 +/- 2.77. After adjusting for confounders, each millimeter of alveolar bone loss at baseline increased the risk of tooth loss 3-fold (OR = 3.26; 95% CI: 1.60 to 6.64). The risk of tooth loss also increased 2.5 times for each millimeter of clinical attachment loss (OR = 2.50; 95% CI: 1.24 to 5.07). Probing depth (OR = 2.53; 95% CI: 0.98 to 6.53), gingival bleeding (OR = 1.99; 95% CI: 0.21 to 18.94), calculus (OR = 2.05; 95% CI: 0.91 to 4.61), and plaque (OR = 0.70; 95% CI: 0.13 to 3.34) were not significantly associated with incident tooth loss.CONCLUSIONPeriodontal disease, especially measured by alveolar bone loss, is a strong and independent predictor for incident tooth loss in postmenopausal women.

BACKGROUND:Obesity is an important risk factor for diabetes, cardiovascular disease, and periodontal disease. Adipocytes appear to secrete proinflammatory cytokines which may be the molecules linking the pathogenesis of these diseases. We evaluated the relationship between obesity, periodontal disease, and diabetes mellitus insulin resistance as well as the plasma levels of tumor necrosis factor alpha (TNFα) and its soluble receptors (sTNFα) to assess the relationship of inflammation to obesity, diabetes, and periodontal infections.METHODS:The relationship between periodontal disease, obesity, and insulin resistance was examined in the Third National Health and Nutrition Examination Survey (NHANES III). In a population of 12,367 non-diabetic subjects, the variable body mass index (BMI) was used as an assessment of obesity and periodontal disease was assessed by mean clinical attachment loss. The plasma levels of TNFα and sTNFα were assessed in subsets of 1,221 adults from Erie County, New York, who represented the highest and lowest quartile of BMI. These subjects had extensive periodontal and medical evaluations.RESULTS:In the NHANES III portion of the study, BMI was positively related to severity of periodontal attachment loss (P <0.001). Weighted multiple logistic regressions showed that this relationship is likely mediated by insulin resistance, since overweight individuals (with BMI ≥27 kg/m2 ) with high levels of insulin resistance (IR) exhibited an odds ratio of 1.48 (95% confidence interval 1.13 - 1.93) for severe periodontal disease as compared to overweight subjects with low IR. In the Erie County adult population, the highest levels of TNFα and sTNFα receptors were found in those individuals in the highest quartile of BMI. A positive correlation of TNFα levels with periodontal disease was found only in those in the lowest quartile of BMI.CONCLUSIONS:Obesity is a significant predictor of periodontal disease and insulin resistance appears to mediate this relationship. Furthermore, obesity is associated with high plasma levels of TNFα and its soluble receptors, which in turn may lead to a hyperinflammatory state increasing the risk for periodontal disease and also accounting in part for insulin resistance. Further studies of the molecular basis of insulin resistance and its relationship to diabetes, periodontal disease, and obesity are necessary to fully test the hypothesis that adipocyte production of proinflammatory cytokines is a pathogenic factor linking obesity to diabetes and periodontal infections.

BACKGROUND Infections have been suggested in the etiology of oral cancer. This study was carried out to evaluate the effect of periodontal disease on oral soft tissue lesions. METHODS A total of 13,798 subjects aged 20 years and older with at least six natural teeth and who participated in the Third National Health and Nutrition Examination Survey (NHANES III) constituted the study population. Severity of periodontal disease was represented by clinical attachment loss (CAL) and was dichotomized as < or =1.5 mm versus >1.5 mm according to its distributions in the NHANES III population. Three separate dependent variables were employed: 1) tumor (non-specific); 2) precancerous lesions; and 3) any oral soft tissue lesion. The independent effect of CAL on those three dependent variables was assessed by weighted multiple logistic regression analyses adjusting for the effects of number of filled teeth, number of decayed teeth, presence of prosthesis, age, gender, race/ethnicity, education, tobacco, alcohol, occupational hazard, and interaction term "tobacco*occupational hazard." Odds ratios (OR) and their 95% confidence intervals (CI) were calculated. RESULTS CAL was not related to the presence of any soft tissue lesion (OR = 1.09, 95% CI: 0.91 to 1.31), but was specifically related to the presence of tumor (OR = 4.57, 95% CI: 2.25 to 9.30) and precancerous lesions (OR = 1.55, 95% CI: 1.06 to 2.27). CONCLUSION This study suggests associations between periodontal disease and the risk for precancerous lesions and tumors generating a hypothesis about a possible relationship between periodontal disease and oral neoplasms. Prospective or well-designed case-control studies with histologically confirmed incident oral cancer cases are necessary to confirm this relationship.

Objective: This study was carried out to evaluate the effect of alcohol consumption on the severity of periodontal disease.Material and Methods: This cross-sectional study employed 13,198 subjects of the Third National Health and Nutrition Examination Survey (NHANES III) aged 20 and older who have at least six natural teeth. Alcohol intake was represented both as a continuous variable and dichotomized using 5, 10, 15, and 20 drinks/week as cut-points. Periodontal disease was represented by clinical attachment loss (CAL) and was assessed both as a continuous variable and dichotomized as < 1.5 mm and >= 1.5 mm. Independent effect of alcohol on CAL was assessed by weighted multiple linear and logistic regression analyses adjusting simultaneously for the effects of age, gender, race, education, income, smoking, diet, diabetes, gingival bleeding, number of remaining teeth.Results: There was a significant linear relationship between number of drinks per week and log CAL (p = 0.0001). Odds ratios for the risk of attachment loss using 5, 10, 15, and 20 drinks/week as cut-points were 1.22 [1.02-1.47], 1.39 [1.13-1.71], 1.54 [1.22-1.93], and 1.67 [1.25-2.23], respectively.Conclusion: Alcohol consumption may be associated with increased severity of CAL in a dose-dependent fashion. Prospective studies and studies of mechanism are needed to confirm the role of alcohol as a risk factor for periodontal disease.

Background: Probing depth (PD) is a commonly used method to determine periodontal disease severity in both treating and evaluating disease progression. Agreement among examiners collecting data in scientific investigations is necessary to establish reliable criteria for determining levels of periodontal attachment loss. The objective of our study was to evaluate inter- and intraexaminer variability of PD measurements among study examiners using a constant force periodontal probe, and to compare the variability of tooth-mean and quadrant-mean.Methods: Three examiners, who had been previously trained and calibrated, performed measurements on 20 volunteers. Intra- and interexaminer variability of sites was determined by means of standard error of measurement (SE). Data analysis included determination of error for both quadrant mean and tooth mean.Results: PD measurements for the quadrant-mean were used to calculate the intraexaminer variability, resulting in a mean (SD) value for an SE of 0.40 mm (+/-0.02). Interexaminer variability for quadrant mean was 0.16 mm (+/-0.02). For tooth-mean SE, the intraexaminer variability values were equal to 0.38 mm (+/-0.07), and interexaminer variability equal to 0.24 mm (+/-0.05).Conclusions: All three examiners participating in our study were able to obtain reliable measurements for PD, using the constant force electronic probe. Reproducibility did not vary appreciably when using the whole quadrant mean compared to the tooth mean. These trained examiners were able to provide reproducible measures under 0.5 mm.

P33 Epidemiological studies have demonstrated a significant link between periodontal disease (PD) and increased risk of cardiovascular disease (CVD). This study was conducted to evaluate if lipid metabolism and peroxidation may represent potential pathways linking PD to CVD. The study sample included 747 randomly selected residents of Erie and Niagara counties of New York who had 6 or more teeth and no history of heart attack. Periodontal assessments included pocket depth (POD) and attachment loss (ATL). Periodontitis was defined by 2+ teeth with ATL≥6mm and 1+ teeth with POD≥5mm. Subgingival plaque was sampled and tested using immunofluorescence microscopic technique for the presence of four putative periodontal pathogens: Bacteriodes forsythus (BF), Porphyromouas gingivilis (PG), Prevotella intermedia (PI), and Campyglobacter recta (CR). Fasting blood sample was obtained and determinations of total and LDL cholesterol, triglycerides, and plasma thiobarbituric acid reacting substance (TBARS) were performed. In the sample as a whole, prevalence of specific bacteria in the subgingival plaque were 29.6% for BF, 8.3% for PG, 31.6% for PI, and 4.4% for CR. As expected, prevalence was much higher in participants with periodontitis. Presence of BF and CR (but not PI and PG) was associated significantly with higher levels of LDL cholesterol (Mean LDL cholesterol (mg/dl), 151.3 for BF + and 142.8 for BF -, p<0.05; and 158.4 for CR + and 144.7 for CR -, p<0.05). Presence of PG and CR (but not BF and PI) was significantly associated with higher TBARS (Mean TBARS (nmol/ml), 1.51 for PG + and 1.38 for PG -, p<0.05; and 1.57 for CR + and 1.38 for CR -, p<0.05). These associations remained statistically significant after adjustment by sex, age, education, body mass index, diabetes status, smoking and alcohol use. No significant association with bacteria was found for total cholesterol and triglycerides. In conclusion, subgingival presence of specific periodontal bacteria (bf, pg, and cr) was associated with higher serum LDL cholesterol and/or plasma TBARS. This suggests that lipid alteration and peroxidation may represent potential pathways in the link between PD and CVD.

BACKGROUND:Alcohol consumption, like smoking, may be related to periodontal disease independently of oral hygiene status. This study assessed the relationship between alcohol consumption and severity of periodontal disease. METHODS:A cross-sectional study of 1,371 subjects ages 25 to 74 in the Erie County, NY population was performed. Alcohol intake was assessed by means of previously validated self-reported questionnaires. Outcome variables were gingival bleeding, clinical attachment loss, alveolar bone loss, and presence of subgingival microorganisms. RESULTS:Logistic regression analyses adjusting for age, gender, race, education, income, smoking, diabetes mellitus, dental plaque, and presence of any of 8 subgingival microorganisms showed that those consuming > or =5 drinks/week had an odds ratio (OR) of 1.65 (95% CI: 1.22 to 2.23) of having higher gingival bleeding, and OR of 1.36 (95% CI: 1.02 to 1.80) of having more severe clinical attachment loss compared to those consuming <5 drinks/week. Those consuming > or =10 drinks/week had an odds ratio (OR) of 1.62 (95% CI: 1.12 to 2.33) of having higher gingival bleeding and OR of 1.44 (95% CI: 1.04 to 2.00) of having more severe clinical attachment loss compared to those consuming <10 drinks/week. Alcohol consumption was not significantly related to alveolar bone loss nor to any of the subgingival microorganisms. CONCLUSIONS:The results suggest that alcohol consumption is associated with moderately increased severity of periodontal disease. Longitudinal studies are needed to determine whether alcohol is a true risk factor for periodontal disease.

P34 Epidemiological studies have demonstrated a significant association between periodontal disease and increased risk of cardiovascular disease. Periodontal organisms were hypothesized to be the underlying factor for the association. This study investigated the relation of myocardial infarction (MI) with both periodontal health status and presence of periodontal pathogens in subgingival plaque. The study sample included 171 MI cases and 574 controls who had at least 6 teeth and were residents of Erie and Niagara counties of New York. Periodontal assessments included pocket depth and attachment loss. Subgingival plaque was sampled and tested using immunofluorescence microscopic technique for the presence of Bacteriodes forsythus (BF), Porphyromouas gingivilis (PG), Prevotella intermedia (PI), and Campyglobacter recta (CR). Results: Mean (SD) pocket depth (mm) was 2.2 (0.7) for MI cases and 2.0 (0.5) for controls (p<0.01). Mean (SD) attachment loss (mm) was 2.6 (1.2) and 2.2 (0.7) for cases and controls (p<0.01), respectively. Presence of periodontal pathogens was significantly more frequent among MI cases than controls. For the four bacteria (BF, PG, PI, and CR), the prevalence (%) of subgingival bacterum presence was 45.0, 14.6, 39.8, and 12.3 among MI cases, and 26.8, 8.2, 31.2, and 5.1 among controls. After adjustment for sex, age, education, smoking status, alcohol use, body mass index, diabetes status, and dental plaque index using logistic regression, the odds ratios (95% confidence intervals) of MI were 1.62 (1.17-2.25) for pocket depth (per 1 mm change), 1.36 (1.10-1.69) for attachment loss (per 1 mm change), 1.93 (1.30-2.88) for BF, 1.41 (0.81-2.48) for PG, 1.18 (0.80-1.73) for PI, and 1.83 (0.96-3.52) for CR presence in subgingival plaque. In conclusion, this case-control study demonstrated that poorer periodontal status and presence of specific bacteria such as BF in subgingival plaque were associated with an increased risk of MI.

BACKGROUND:Vitamin C has long been a candidate for modulating periodontal disease. Studies of scorbutic gingivitis and the effects of vitamin C on extracellular matrix and immunologic and inflammatory responses provide a rationale for hypothesizing that vitamin C is a risk factor for periodontal disease.METHODS:We evaluated the role of dietary vitamin C as a contributing risk factor for periodontal disease utilizing the Third National Health and Nutrition Examination Survey (NHANES III) which is representative of the U.S. civilian, non-institutionalized population.RESULTS:A sample of 12,419 adults (20 to 90+ years of age), with dental measurements and assessment of dietary information as well as demographic and medical histories were included in the studies. Dietary vitamin C was estimated by a 24-hour dietary record. Individuals with periodontal disease were arbitrarily defined as those who had mean clinical attachment levels of > or =1.5 mm. Using multiple logistic regression analysis, we found a relationship between reduced dietary vitamin C and increased risk for periodontal disease for the overall population (odds ratio [OR] = 1.19; 95% CI: 1.05 to 1.33). Current and former tobacco users who were taking less dietary vitamin C showed an increased risk of periodontal disease with OR of 1.28, 95% CI: 1.04 to 1.59 for former smokers, and an OR of 1.21, 95% CI: 1.02 to 1.43 for current tobacco users. There was a dose-response relationship between the levels of dietary vitamin C and periodontal disease with an OR of 1.30 for those taking 0 to 29 mg of vitamin C per day, to 1.16 for those taking 100 to 179 mg of vitamin C per day as compared to those taking 180 mg or more of vitamin C per day.CONCLUSION:Dietary intake of vitamin C showed a weak, but statistically significant, relationship to periodontal disease in current and former smokers as measured by clinical attachment. Those taking the lowest levels of vitamin C, and who also smoke, are likely to show the greatest clinical effect on the periodontal tissues.

BACKGROUNDSystemic bone loss has been proposed as a risk factor for periodontal disease; however, the relationship between these two diseases is still not clear. The objective of this study was to assess the relationship between systemic bone mineral density and periodontal disease, controlling for known confounders.METHODSThe study population included 70 postmenopausal Caucasian women aged 51 to 78 (mean +/- SD: 62.10 +/- 7.1 years). Skeletal bone mineral density (BMD) was assessed by dual energy x-ray absorptiometry (DXA) at the neck, trochanter, intertrochanter, Ward's triangle, and total regions of the femur, and from the anterior-posterior view of the lumbar spine. Periodontal disease severity was represented by clinical attachment loss (CAL) and interproximal alveolar bone loss (ABL). Other measures of periodontal status included probing depth (PD), supragingival plaque, gingival bleeding on probing, and calculus. DXA and oral examinations were performed by calibrated examiners. Partial correlation coefficients (r) were obtained from multiple linear regression analysis adjusting for age, age at menopause, estrogen supplementation, cigarette smoking, body mass index, and supragingival plaque.RESULTSMean ABL was significantly correlated with BMD of the trochanter (r =- 0.27), Ward's triangle (r = -0.26), and total regions of the femur (r = -0.25). Mean CAL appeared to be related to BMD consistently at all regions of the skeleton, although the association did not reach statistical significance.CONCLUSIONSWe can conclude that skeletal BMD is related to interproximal alveolar bone loss and, to a lesser extent, to clinical attachment loss, implicating postmenopausal osteopenia as a risk indicator for periodontal disease in postmenopausal Caucasian women.