Kaumudi Joshipura

Poor Oral Health and Coronary Heart Disease

A few recent studies have shown associations between poor oral health and coronary heart disease (CHD). The objective of this study was to examine the incidence of CHD in relation to number of teeth present and periodontal disease, and to explore potential mediators of this association, in a prospective cohort study. This study is a part of the ongoing Health Professionals Follow-Up Study (HPFS). Participants included a US national sample of 44,119 male health professionals (58% of whom were dentists), from 40 to 75 years of age, who reported no diagnosed CHD, cancer, or diabetes at baseline. We recorded 757 incident cases of CHD, including fatal and non-fatal mvocardial infarction and sudden death, in six years of follow-up. Among men who reported pre-existing periodontal disease, those with 10 or fewer teeth were at increased risk of CHD compared with men with 25 or more teeth (relative risk = 1.67; 95% confidence interval, 1.03 to 2.71), after adjustment for standard CHD risk factors. Among men without pre-existing periodontal disease, no relationship was found (relative risk = 1.11; 95% confidence interval, 0.74 to 1.68). The associations were only slightly attenuated after we controlled for dietary factors. No overall associations were found between periodontal disease and coronary heart disease. Tooth loss may be associated with increased risk of CHD, primarily among those with a positive periodontal disease history; diet was only a small mediator of this association.

Periodontal Disease, Tooth Loss, and Incidence of Ischemic Stroke

Background and Purpose— Periodontal and other infections have been suggested as potential risk factors for stroke. This study evaluates periodontal disease and tooth loss as risk factors for ischemic stroke. Methods— The study population consisted of 41 380 men who were free of cardiovascular disease and diabetes at baseline. Periodontal disease history was assessed by mailed validated questionnaires. During 12 years of follow-up, stroke incidence was assessed and subclassified by use of medical history, medical records, and imaging reports. Hazard ratios (HRs) were adjusted for age, amount smoked, obesity, alcohol, exercise, family history of cardiovascular disease, multivitamin use, vitamin E use, profession, baseline reported hypertension, and hypercholesterolemia. Sex and socioeconomic status were inherently controlled for by restriction. Confounding variables were updated in the analyses for each 2-year follow-up interval. Results— We documented 349 ischemic stroke cases during the follow-up period. Men who had ≤24 teeth at baseline were at a higher risk of stroke compared to men with ≥25 teeth (HR=1.57; 95% CI, 1.24 to 1.98). There was little evidence of an increased risk with recent tooth loss during follow-up. A modest association was seen between baseline periodontal disease history and ischemic stroke (HR=1.33; 95% CI, 1.03 to 1.70). Addition of dietary factors to the model changed the HR only slightly. Conclusions— Our results suggest that periodontal disease and fewer teeth may be associated with increased risk of ischemic stroke.

Periodontal Disease and Biomarkers Related to Cardiovascular Disease

Periodontal disease is a chronic infection of the gums characterized by a loss of attachment between the tooth and bone, and by bone loss. We evaluated cross-sectionally the association between periodontal disease and C-reactive protein (CRP), fibrinogen, factor VII, tissue plasminogen activator (t-PA), LDL-C, von Willebrand factor, and soluble tumor necrosis factor receptors 1 and 2. The final sample consisted of 468 men (ages 47–80 yrs), participating in the Health Professional Follow-up Study, who provided blood and were free of CVD, diabetes, and cancer. In multivariate regression models controlling for age, cigarette smoking, alcohol intake, physical activity, and aspirin intake, self-reported periodontal disease was associated with significantly higher levels of CRP (30% higher among periodontal cases compared with non-cases), t-PA (11% higher), and LDL-C (11% higher). Based on our data, periodontal disease showed significant associations with biomarkers of endothelial dysfunction and dyslipidemia, which may potentially mediate the association between periodontal and cardiovascular disease.

Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study.

BACKGROUND Studies suggest that tooth loss and periodontal disease might increase the risk of developing various cancers; however, smoking might have confounded the reported associations. We aimed to assess whether periodontal disease or tooth loss is associated with cancer risk. METHODS The analysis was done in a prospective study (the Health Professionals Follow-Up Study [HPFS]), which was initiated in 1986 when US male health professionals aged 40-75 years responded to questionnaires posted by the Department of Nutrition, Harvard University School of Public Health, Boston, MA, USA. In addition to the baseline questionnaires, follow-up questionnaires were posted to all living participants every 2 years and dietary questionnaires every 4 years. At baseline, participants were asked whether they had a history of periodontal disease with bone loss. Participants also reported number of natural teeth at baseline and any tooth loss during the previous 2 years was reported on the follow-up questionnaires. Smoking status and history of smoking were obtained at baseline and in all subsequent questionnaires. Additionally at baseline, participants reported their mean frequency of food intake over the previous year on a 131-item semiquantitative food-frequency questionnaire. Participants reported any new cancer diagnosis on the follow-up questionnaires. Endpoints for this study were risk of total cancer and individual cancers with more than 100 cases. Multivariate hazard ratios (HRs) and 95% CIs were calculated by use of Cox proportional hazard models according to periodontal disease status and number of teeth at baseline. FINDINGS In the main analyses, 48 375 men with median follow-up of 17.7 years (1986 to Jan 31, 2004) were eligible after excluding participants diagnosed with cancer before 1986 (other than non-melanoma skin cancer, n=2076) and those with missing data on periodontal disease (n=1078). 5720 incident cancer cases were documented (excluding non-melanoma skin cancer and non-aggressive prostate cancer). The five most common cancers were colorectal (n=1043), melanoma of the skin (n=698), lung (n=678), bladder (n=543), and advanced prostate (n=541). After adjusting for known risk factors, including detailed smoking history and dietary factors, participants with a history of periodontal disease had an increased risk of total cancer (HR 1.14 [95% CI 1.07-1.22]) compared with those with no history of periodontal disease. By cancer site, significant associations for those with a history of periodontal disease were noted for lung (1.36 [1.15-1.60]), kidney (1.49 [1.12-1.97]), pancreas (1.54 [1.16-2.04]; findings previously published), and haematological cancers (1.30 [1.11-1.53]). Fewer teeth at baseline (0-16) was associated with an increase in risk of lung cancer (1.70 [1.37-2.11]) for those with 0-16 teeth versus those with 25-32 teeth. In never-smokers, periodontal disease was associated with significant increases in total (1.21 [1.06-1.39]) and haematological cancers (1.35 [1.01-1.81]). By contrast, no association was noted for lung cancer (0.96 [0.46-1.98]). INTERPRETATION Periodontal disease was associated with a small, but significant, increase in overall cancer risk, which persisted in never-smokers. The associations recorded for lung cancer are probably because of residual confounding by smoking. The increased risks noted for haematological, kidney, and pancreatic cancers need confirmation, but suggest that periodontal disease might be a marker of a susceptible immune system or might directly affect cancer risk.

A review of the relationship between tooth loss, periodontal disease, and cancer

Recent studies have investigated the association between periodontal disease, tooth loss, and several systemic diseases including cancer, cardiovascular disease, and preterm birth. Periodontal disease, a chronic inflammatory condition, is highly prevalent in adult populations around the world, and may be preventable. Estimates of prevalence vary between races and geographic regions, with a marked increase in the occurrence of periodontal disease with advancing age. Worldwide estimates for the prevalence of severe periodontal disease generally range from 10 to 15%. The relationship between oral health and cancer has been examined for a number of specific cancer sites. Several studies have reported associations between periodontal disease or tooth loss and risk of oral, upper gastrointestinal, lung, and pancreatic cancer in different populations. In a number of studies, these associations persisted after adjustment for major risk factors, including cigarette smoking and socioeconomic status. This review provides a summary of these findings, discusses possible biological mechanisms involved, and raises methodological issues related to studying these relationships.

NUTRITION AS A MEDIATOR IN THE RELATION BETWEEN ORAL AND SYSTEMIC DISEASE: ASSOCIATIONS BETWEEN SPECIFIC MEASURES OF ADULT ORAL HEALTH AND NUTRITION OUTCOMES

Recent associations between oral health and systemic disease have led to renewed interest in the mouth and its contribution to health outcomes. Many pathways for this relationship have been postulated, among them the potential mediating role of nutrition. The link between various nutrients and systemic disease has been established, but relatively little work has been done in relating oral conditions with nutrition. We searched MEDLINE, from 1966 to July, 2001, to identify articles relating specific oral measures to nutrition outcomes. We included original articles written in English with a sample size greater than 30 that used objective oral health measures. We reviewed a total of 56 articles. Only a small proportion of these studies were methodologically sound. Although many studies were small and cross-sectional, the literature suggests that tooth loss affects dietary quality and nutrient intake in a manner that may increase the risk for several systemic diseases. The impact of tooth loss on diet may be only partially compensated for by prostheses. To date, there is little information relating periodontal disease and oral pain and nutrition. A few studies suggest poorer nutrition among individuals with xerostomia and altered taste. Further, impaired dentition may contribute to weight change, depending on age and other population characteristics. There is a paucity of well-designed studies addressing oral health and nutrition. Before we can acquire a better understanding of how nutrition and oral health interrelate, however, more studies will be required to confirm these associations-preferably longitudinal studies with larger sample sizes and better control of important confounders.

Validation of Self-reported Periodontal Disease: A Systematic Review

Self-report is an efficient and accepted means of assessing many population characteristics, risk factors, and diseases, but has rarely been used for periodontal disease (chronic periodontitis). The availability of valid self-reported measures of periodontal disease would facilitate epidemiologic studies on a much larger scale, allow for integration of new studies of periodontal disease within large ongoing studies, and facilitate lower-cost population surveillance of periodontitis. Several studies have been conducted to validate self-reported measures for periodontal disease, but results have been inconsistent. In this report, we conducted a systematic review of the validation studies. We reviewed the 16 studies that assessed the validity of self-reported periodontal and gingivitis measures against clinical gold standards. Seven of the studies included self-reported measures specific to gingivitis, four included measures only for periodontitis, and five included both gingivitis and periodontal measures. Three of the studies used a self-assessment method where they provided the patient with a detailed manual for performing a self-exam. The remaining 13 studies asked participants to self-report symptoms, presence of periodontal disease itself, or their recollection of a dental health professional diagnosing them or providing treatment for periodontal disease. The review indicates that some measures showed promise, but results varied across populations and self-reported measures. One example of a good measure is, “Has any dentist/hygienist told you that you have deep pockets?”, which had a sensitivity of 55%, a specificity of 90%, positive predictive value of 77%, and negative predictive value of 75% against clinical pocket depth. Higher validity could be potentially obtained by the use of combinations of several self-reported questions and other predictors of periodontal disease.

Alcohol Consumption Increases Periodontitis Risk

Alcohol consumption impairs neutrophil, macrophage, and T-cell functions, increasing the likelihood of infections. We examined the association between alcohol consumption and periodontitis, prospectively, among 39,461 male health professionals aged 40 to 75 years and free of periodontitis at the start of follow-up. Alcohol intake was assessed at baseline and updated every 4 years by a food-frequency questionnaire. Periodontal disease status was self-reported and validated against radiographs. Multivariate analysis was adjusted for age, smoking, diabetes, body-mass index, physical activity, time period, and caloric intake. During 406,160 person-years of follow-up, there were 2125 cases of periodontitis. Compared with non-drinkers, the relative risk (95% confidence interval) among men reporting usual alcohol intake of 0.1-4.9 g/day was 1.24 (1.09, 1.42); 5.0 to 14.9 g/day, 1.18 (1.04, 1.35); 15 to 29.9 g/day, 1.18 (1.01, 1.38); and > 30 g/day, 1.27 (1.08, 1.49). The results suggest that alcohol consumption is an independent modifiable risk factor for periodontitis.

Tobacco Use and Incidence of Tooth Loss among US Male Health Professionals

Data on the dose-dependent effects of smoking and smoking cessation on tooth loss are scarce. We hypothesized that smoking has both dose- and time-dependent effects on tooth loss incidence. We used longitudinal data on tobacco use and incident tooth loss in 43,112 male health professionals, between 1986 and 2002. In multivariate Cox models, current smokers of 5 to 14 and 45+ cigarettes daily had a two-fold (HR, 1.94; 95% CI, 1.72, 2.18) and three-fold (HR, 3.05; 95% CI, 2.38, 3.90) higher risk of tooth loss, respectively, compared with never-smokers. Risk decreased with increasing time since cessation, but remained elevated by 20% (95% CI, 16%, 25%) for men who had quit 10+ years before. Current pipe/cigar smokers had a 20% (95% CI, 1.11, 1.30) increased risk of tooth loss compared with never- and former smokers of pipes/cigars.

Mutans Streptococci and Non-mutans Streptococci Acidogenic at Low pH, and in vitro Acidogenic Potential of Dental Plaque in Two Different Areas of the Human Dentition

Samples of human dental plaque were obtained from sound tooth surfaces in the lower anterior and upper posterior areas of each of 11 subjects with various degrees of caries experience. Both types of plaque were compared for: (1) their pH-loweringpotential [pH at 10 and 60 min after sugar addition and the pH drop between 0 and 10 min (delta pH)] with an in vitro method involving dispersed plaque suspensions and excess glucose supply; (2) the proportions ofmutans streptococci; and (3) the distribution of the predominant non-mutans streptococci according to their final pH in glucose broth. Compared with plaque from the lower anterior area, plaque from the upper posterior area exhibited a significantly higher pH-lowering potential, i.e., a lower pH at 10 and 60 min and a greater delta pH and significantly higher levels of mutans streptococci. The final pH values for the non-mutans streptococci exhibited a wide range from about 4.4 to over 5.0. The proportions of such organisms designated as capable of acidogenesis at low pH (final pH < 4.6), whether expressed as a percentage of the total non-mutans streptococci or of the total plaque flora, were significantly increased in plaque from the upper posterior area. The proportions of non-mutans streptococci capable of acidogenesis at low pH in plaque from the upper posterior area were also significantly increased, with decreasing pH values at 10 and 60 min. The findings strengthen the link between the capacity of the plaque flora for acidogenesis at a low pH and its pH-loweringpotential as well as the role of bacterial acidogenesis at a low pH as an oral ecological determinant.