Dental disease and risk of coronary heart disease and mortality.
TL;DR: Dental disease is associated with an increased risk of coronary heart disease, particularly in young men, and may be a more general indicator of personal hygiene and possibly health care practices.
Abstract: OBJECTIVE--To investigate a reported association between dental disease and risk of coronary heart disease. SETTING--National sample of American adults who participated in a health examination survey in the early 1970s. DESIGN--Prospective cohort study in which participants underwent a standard dental examination at baseline and were followed up to 1987. Proportional hazards analysis was used to estimate relative risks adjusted for several covariates. MAIN OUTCOME MEASURES--Incidence of mortality or admission to hospital because of coronary heart disease; total mortality. RESULTS--Among all 9760 subjects included in the analysis those with periodontitis had a 25% increased risk of coronary heart disease relative to those with minimal periodontal disease. Poor oral hygiene, determined by the extent of dental debris and calculus, was also associated with an increased incidence of coronary heart disease. In men younger than 50 years at baseline periodontal disease was a stronger risk factor for coronary heart disease; men with periodontitis had a relative risk of 1.72. Both periodontal disease and poor oral hygiene showed stronger associations with total mortality than with coronary heart disease. CONCLUSION--Dental disease is associated with an increased risk of coronary heart disease, particularly in young men. Whether this is a causal association is unclear. Dental health may be a more general indicator of personal hygiene and possibly health care practices.
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TL;DR: It is suggested that periodontal disease, once established, provides a biological burden of endotoxin (lipopolysaccharide) and inflammatory cytokines (especially TxA2, IL-1β, PGE2, and TNF-α) which serve to initiate and exacerbate atherogenesis' and thromboembolic events.
Abstract: 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 TxA2 , IL-1β, PGE2 , 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.
1,444 citations
TL;DR: APR-induced alterations initially protect the host from the harmful effects of bacteria, viruses, and parasites, however, if prolonged, these changes in the structure and function of lipoproteins will contribute to atherogenesis.
1,328 citations
TL;DR: periodontal pathogens are present in atherosclerotic plaques where, like other infectious microorganisms such as C. pneumoniae, they may play a role in the development and progression of atherosclerosis leading to coronary vascular disease and other clinical sequelae.
Abstract: Background: Recent studies suggest that chronic infections including those associated with periodontitis increase the risk for coronary vascular disease (CVD) and stroke. We hypothesize that oral microorganisms including periodontal bacterial pathogens enter the blood stream during transient bacteremias where they may play a role in the development and progression of atherosclerosis leading to CVD. Methods: To test this hypothesis, 50 human specimens obtained during carotid endarterectomy were examined for the presence of Chlamydia pneumoniae, human cytomegalovirus, and bacterial 16S ribosomal RNA using specific oligonucleotide primers in polymerase chain reaction (PCR) assays. Approximately 100 ng of chromosomal DNA was extracted from each specimen and then amplified using standard conditions (30 cycles of 30 seconds at 95°C, 30 seconds at 55°C, and 30 seconds at 72°C). Bacterial 16S rDNA was amplified using 2 synthetic oligonucleotide primers specific for eubacteria. The PCR product generated with the e...
1,065 citations
TL;DR: The mechanism of action of possible risk factors, such as smoking and diabetes on the host, and the evidence that host modulating agents will be effective in prevention or treatment of periodontal diseases are studied.
Abstract: Question Set 1. What are the important destructive mechanisms in periodontal diseases? 2. What are the important protective mechanisms in periodontal diseases? 3. What are the important genetic factors and what is the state-of-the art relative to assessing these genetic factors in periodontal diseases? 4. What do we know about the mechanism of action of possible risk factors, such as smoking and diabetes on the host? 5. What is the evidence that host modulating agents will be effective in prevention or treatment ofperiodontal diseases?
995 citations
TL;DR: The purpose of this review is to evaluate the current status of oral infections, especially periodontitis, as a causal factor for systemic diseases.
Abstract: Recently, it has been recognized that oral infection, especially periodontitis, may affect the course and pathogenesis of a number of systemic diseases, such as cardiovascular disease, bacterial pneumonia, diabetes mellitus, and low birth weight. The purpose of this review is to evaluate the current status of oral infections, especially periodontitis, as a causal factor for systemic diseases. Three mechanisms or pathways linking oral infections to secondary systemic effects have been proposed: (i) metastatic spread of infection from the oral cavity as a result of transient bacteremia, (ii) metastatic injury from the effects of circulating oral microbial toxins, and (iii) metastatic inflammation caused by immunological injury induced by oral microorganisms. Periodontitis as a major oral infection may affect the host9s susceptibility to systemic disease in three ways: by shared risk factors; subgingival biofilms acting as reservoirs of gram-negative bacteria; and the periodontium acting as a reservoir of inflammatory mediators. Proposed evidence and mechanisms of the above odontogenic systemic diseases are given.
986 citations
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TL;DR: The association between poor dental health and acute myocardial infarction was investigated in two separate case-control studies and remained valid after adjustment for age, social class, smoking, serum lipid concentrations, and the presence of diabetes.
Abstract: Known risk factors for coronary heart disease do not explain all of the clinical and epidemiological features of the disease. To examine the role of chronic bacterial infections as risk factors for the disease the association between poor dental health and acute myocardial infarction was investigated in two separate case-control studies of a total of 100 patients with acute myocardial infarction and 102 controls selected from the community at random. Dental health was graded by using two indexes, one of which was assessed blind. Based on these indexes dental health was significantly worse in patients with acute myocardial infarction than in controls. The association remained valid after adjustment for age, social class, smoking, serum lipid concentrations, and the presence of diabetes. Further prospective studies are required in different populations to confirm the association and to elucidate its nature.
1,002 citations
TL;DR: The results suggest that chronic C. pneumoniae infection may be a significant risk factor for the development of coronary heart disease.
Abstract: ▪Objective:To investigate in the prospective Helsinki Heart Study, whether chronic Chlamydia pneumoniae infection, indicated by elevated antibody titers against the pathogen, chlamydial li...
806 citations
TL;DR: The results generally support the previously reported association between C pneumoniae infection and coronary heart disease, and caution should be used in interpreting the basis for this association.
Abstract: Objective. —To evaluate the association between prior infection withChlamydia pneumoniae, as measured by IgG antibody, and coronary artery disease. Design. —A population-based, case-control study. Setting. —Group Health Cooperative of Puget Sound, a Seattle-based health maintenance organization. Participants. —Men 55 years of age and younger and women 65 years of age and younger. Cases (n=171) were members of Group Health Cooperative undergoing diagnostic coronary angiography who had at least one coronary artery lesion occupying 50% or more of the luminal diameter. The population controls (n=120) were Group Health Cooperative members without known coronary heart disease. Main Outcome Measure. —The adjusted odds ratio (OR) for coronary artery disease associated with priorCpneumoniaeinfection as measured by the presence of IgG antibody. Results. —After adjusting for age, gender, and calendar quarter of blood drawing, the OR for coronary artery disease associated with the presence of antibody was 2.6 (95% confidence interval, 1.4 to 4.8). The association was limited to cigarette smokers, in whom the OR was 3.5 (95% confidence interval, 1.7 to 7.0). Among never-smokers, the OR was 0.8 (95% confidence interval, 0.3 to 1.9). When cases and controls were restricted to those assayed concurrently, the adjusted OR (smokers and nonsmokers combined) was 4.2 (95% confidence interval, 1.8 to 10.0). Adjustment for serum cholesterol, hypertension, alcohol use, diabetes, and socioeconomic status did not change these results. Only a weak association was found when cases were compared with 63 subjects whose angiographic results were normal (OR, 1.2; 95% confidence interval, 0.6 to 2.2). Conclusions. —These results generally support the previously reported association betweenCpneumoniaeinfection and coronary heart disease. However, caution should be used in interpreting the basis for this association. (JAMA. 1992;268:68-72)
453 citations
Journal Article•
TL;DR: Differences were noted in the risk profiles for various manifestations of cardiovascular disease (CVD) that occurred before the age of 65 during the first 30 years of follow-up of the 5070 subjects of the original Framingham cohort, highlighting the need for future studies to distinguish better between those factors that precipitate cardiovascular events and those that relate to the pathogenesis of the underlying atherosclerosis.
Abstract: Substantial differences were noted in the risk profiles for various manifestations of cardiovascular disease (CVD) that occurred before the age of 65 during the first 30 years of follow-up of the 5070 subjects of the original Framingham cohort. Hypertension contributed most consistently to short-term risk of all manifestations of CVD. Differences were noted between the sexes and age groups in both the univariate and multivariate analyses. These patterns have biological, clinical, and statistical significance, particularly as they relate to the need for future studies to distinguish better between those factors that precipitate cardiovascular events and those that relate to the pathogenesis of the underlying atherosclerosis.
338 citations
01 Feb 1973
327 citations