A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as "chronic" or "aggressive" are now grouped under a single category ("periodontitis") and are further characterized based on a multi-dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history-based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient. Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category. Endodontic-periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment. Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination.

It is our central hypothesis that periodontal diseases, which are chronic Gram-negative infections, represent a previously unrecognized risk factor for atherosclerosis and thromboembolic events. Previous studies have demonstrated an association between periodontal disease severity and risk of coronary heart disease and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis. We further suggest that periodontal disease, once established, provides a biological burden of endotoxin (lipopolysaccharide) and inflammatory cytokines (especially TxA2, IL-1 beta, PGE2, and TNF-alpha) which serve to initiate and exacerbate atherogenesis and thromboembolic events. A cohort study was conducted using combined data from the Normative Aging Study and the Dental Longitudinal Study sponsored by the United States Department of Veterans Affairs. Mean bone loss scores and worst probing pocket depth scores per tooth were measured on 1,147 men during 1968 to 1971. Information gathered during follow-up examinations showed that 207 men developed coronary heart disease (CHD), 59 died of CHD, and 40 had strokes. Incidence odds ratios adjusted for established cardiovascular risk factors were 1.5, 1.9, and 2.8 for bone loss and total CHD, fatal CHD, and stroke, respectively. Levels of bone loss and cumulative incidence of total CHD and fatal CHD indicated a biologic gradient between severity of exposure and occurrence of disease.

A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as "chronic" or "aggressive" are now grouped under a single category ("periodontitis") and are further characterized based on a multi-dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history-based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient. Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category. Endodontic-periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment. Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination.

It is our central hypothesis that periodontal diseases, which are chronic Gramnegative infections, represent a previously unrecognized risk factor for atherosclerosis and thromboembolic events. Previous studies have demonstrated an association between periodontal disease severity and risk of coronary heart disease and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis. We further suggest that periodontal disease, once established, provides a biological burden of endotoxin (lipopolysaccharide) and inflammatory cytokines (especially TxA , IL-1β, PGE , and TNF-α) which serve to initiate and exacerbate atherogenesis' and thromboembolic events. A cohort study was conducted using combined data from the Normative Aging Study and the Dental Longitudinal Study sponsored by the United States Department of Veterans Affairs. Mean bone loss scores and worst probing pocket depth scores per tooth were measured on 1,147 men during 1968 to 1971. Information gathered during follow-up examinations showed that 207 men developed coronary heart disease (CHD), 59 died of CHD, and 40 had strokes. Incidence odds ratios adjusted for established cardiovascular risk factors were 1.5, 1.9, and 2.8 for bone loss and total CHD, fatal CHD, and stroke, respectively. Levels of bone loss and cumulative incidence of total CHD and fatal CHD indicated a biologic gradient between severity of exposure and occurrence of disease. J Periodontol 1996;67:1123-1137.

Objectives To determine if rates of tooth loss, periodontal disease progression and caries incidence predict cognitive decline in men. Design Prospective study. Setting Community-dwelling men enrolled in the VA Dental Longitudinal Study. Participants Five hundred ninety-seven dentate men, aged 28–70 years at the study baseline, who have been followed up to 32 years. Measurements Oral examinations were conducted approximately every 3 years. Periodontal disease measures included probing pocket depth and radiographic alveolar bone height. Participants underwent cognitive testing beginning in 1993. Low cognitive statuses were defined as <25 points or <90% of the age and education-specific median on the MiniMental State Examination, and < 10 points on a Spatial Copying Task. Results Each tooth lost per decade since the baseline dental examination increased the risks of low MiniMental score (HR= 1.09, 95% CI=1.01, 1.18) and low spatial copying score (HR=1.12, CI= 1.05, 1.18). Risks were elevated per additional tooth with progression of alveolar bone loss (spatial copying: HR=1.03, CI= 1.01, 1.06), probing pocket depth (MiniMental: HR=1.04, CI= 1.01, 1.09; spatial copying: HR=1.04, CI= 1.01, 1.06) and caries (spatial copying: HR=1.05, CI= 1.01, 1.08). Risks were consistently higher among men who were older than 45.5 years at baseline than in younger men. Conclusion Risk of cognitive decline in older men increases as more teeth are lost. Periodontal disease and caries, major reasons for tooth loss, are also related to cognitive decline.

Self-reports provide reasonably valid estimates for numbers of remaining teeth, fillings, root canal therapy, and fixed and removable prostheses. However, they appear to be less useful for the assessment of dental caries and periodontal disease in the two populations we have studied. There remains a need and potential to further develop self-report oral health measures that are valid for use in large population studies. Such self-report measures would yield great cost and time savings.

Background-Several epidemiological studies have suggested periodontitis as a risk factor for coronary heart disease (CHD), but results have been inconsistent. Methods and Results-We evaluated the association between clinical and radiographic measures of periodontitis, edentulism, and incident CHD (angina, myocardial infarction, or fatal CHD) among 1203 men in the VA Normative Aging and Dental Longitudinal Studies who were followed up with triennial comprehensive medical and dental examinations up to 35 years (median 24 years). Cox proportional hazards models with time-varying effects of exposure and potential confounders were fit. We found a significant dose-dependent association between periodontitis and CHD incidence among men Ͻ60 years of age (hazard ratio 2.12, 95% confidence interval 1.26 to 3.60 comparing highest versus lowest category of radiographic bone loss, P for trendϭ0.02), independent of age, body mass index, smoking, alcohol intake, diabetes mellitus, fasting glucose, total cholesterol, high-density lipoprotein cholesterol, triglycerides, hypertension, systolic and diastolic blood pressure, education, marital status, income, and occupation. No association was found among men Ͼ60 years of age. Similar results were found when the sum of probing pocket depths was used as a measure of periodontitis. Among men Ն60 years of age, edentulous men tended to have a higher risk of CHD than dentate men in the lowest bone loss (hazard ratio 1.61, 95% confidence interval 0.95 to 2.73) and lowest pocket depth (hazard ratio 1.72, 95% confidence interval 1.03 to 2.85) categories, independent of confounders. Conclusions-Chronic periodontitis is associated with incidence of CHD among younger men, independent of established cardiovascular risk factors. (Circulation. 2008;117:1668-1674.)

This paper evaluates the current information on the relationship between oral disease (specifically periodontitis) and atherosclerosis/coronary heart disease (CHD) to determine whether the information is sufficient to conclude that periodontitis is a risk factor for atherosclerosis/CHD. As background for this evaluation, the term "risk factor" is defined, and the 3 criteria used to establish exposures as risk factors are reviewed. In addition, epidemiologic criteria for defining an exposure as causal are presented. The available evidence then is evaluated according to the criteria for causality, which are extensions of the criteria for establishing a risk factor. This review is done in the context of the relationship between atherosclerosis/CHD and inflammation. A number of findings are briefly reviewed that link inflammation and atherosclerosis/CHD, such as: 1) prior flu-like symptoms were more common in cases of myocardial infarction than in concurrently sampled controls; 2) high levels of cytomegalovirus antibody titers were associated with elevated carotid intimal-medial wall thickness 18 years later; 3) prior infection with cytomegalovirus was a strong independent risk factor for restenosis after coronary atherectomy; 4) dental infections were more common in cases of cerebral infarction compared to community controls matched on age and sex; and 5) the gingival index was significantly correlated with fibrinogen and white cell counts in periodontal patients and controls, adjusted for age, smoking, and socioeconomic status. Three case-control studies and 5 longitudinal studies investigating the relationship between dental conditions and atherosclerosis/CHD are reviewed in terms of strength of associations, consistency of associations, specificity. of associations, time sequence between exposure and outcome, and degree of exposure and outcome. Related to the last criterion, new findings are presented which indicate that the extent of the periodontal infection, a measure reflecting microbial burden, also is related to onset of new CHD events. Our previously published model describing the potential biological mechanisms underlying the associations found is reviewed. This model places the associations into a context of an intrinsic or acquired hyperinflammatory monocyte trait that results in a more intense inflammatory response to lipopolysaccharide (LPS) challenges, such as periodontal infections. This hyperinflammatory response may promote atheroma formation and thromboembolic events. finally, new findings from ongoing animal studies are presented, indicating that high fat diets in atherosclerotic-susceptible mice induce greater inflammatory responses to Porphyromonas gingivalis challenges. We conclude that the available evidence does allow an interpretation of periodontitis being a risk factor for atherosclerosis/CHD. This conclusion, however. is made with some qualifications. While the associations found across a wide variety of subjects are remarkably consistent, for the most part they are represented by incid...