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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During episodes of dental bacteremia, viridans group streptococci encounter platelets. Among these microorganisms, certain Streptococcus sanguis induce human and rabbit platelets to aggregate in vitro. In experimental rabbits, circulating streptococci induced platelets to aggregate, triggering the accumulation of platelets and fibrin into the heart valve vegetations of endocarditis. At necropsy, affected rabbit hearts showed ischemic areas. We therefore hypothesized that circulating S. sanguis might cause coronary thrombosis and signs of myocardial infarction (MI). Signs of MI were monitored in rabbits after infusion with platelet-aggregating doses of 4 to 40 x 10(9) cells of S. sanguis 133-79. Infusion resulted in dose-dependent changes in electrocardiograms, blood pressure, heart rate, and cardiac contractility. These changes were consistent with the occurrence of MI. Platelets isolated from hyperlipidemic rabbits showed an accelerated in vitro aggregation response to strain 133-79. Cultured from immunosuppressed children with septic shock and signs of disseminated intravascular coagulation, more than 60% of isolates of viridans streptococci induced platelet aggregation when tested in vitro. The data are consistent with a thrombogenic role for S. sanguis in human disease, contributing to the development of the vegetative lesion in infective endocarditis and a thrombotic mechanism to explain the additional contributed risk of periodontitis to MI.
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PMID:Effects of oral flora on platelets: possible consequences in cardiovascular disease. 891 Aug 32

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 incidence odds ratios around 2.0. While this level of association would result in oral conditions contributing to a large number of CHD cases, it is possible that associations of this magnitude are due to bias in the study designs. In addition, some studies report that periodontitis is associated with all-cause mortality and low birth weight infants. These multiple associations detract from the credibility of periodontitis as a risk factor, as specificity of association is more often related to causality. However, all-cause mortality may largely be driven by mortality from cardiovascular events: and some exposures, such as smoking. are indeed risk factors for multiple conditions. On the other hand, current findings regarding the associations between oral conditions and atherosclerosis/CHD imply that the criteria for causality may be met in the not-too-distant future.
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PMID:Periodontitis: a risk factor for coronary heart disease? 972 97

Cardiovascular diseases, including atherosclerosis and myocardial ischemia, occur as a result of a complex set of genetic and environmental factors. During periodontitis, dental plaque microorganisms may disseminate through the blood to infect the vascular endothelium and contribute to the occurrence of atherosclerosis and risk of myocardial ischemia and infarction. Myocardial ischemia and infarction are often preceded by acute thromboembolic events. In an in vitro model of thrombosis, certain dental plaque bacteria induce platelets to aggregate. Aggregation of platelets is induced by the platelet aggregation-associated protein [PAAPJ expressed on plaque bacteria, including Streptococcus sanguis and Porphyromonas gingivalis. Intravenous infusion of S. sanguis into rabbits has been shown previously to cause changes in the electrocardiogram (ECG), heart rate, blood pressure, and cardiac contractility. These changes are consistent with the occurrence of myocardial infarction. The ECG changes are now shown to begin within 30 seconds after infusion of PAAP+ S. sanguis, followed by alterations in blood pressure and respiratory rate. These changes occurred intermittently over a 30-minute period and changed within one heartbeat to a normal pattern and suddenly back to abnormal. Intermittent ECG abnormalities were seen in 13 of 15 rabbits, including left axis deviation, ST-segment depression, preventricular contractions, alternans, and bigemnia. Dose-dependent thrombocytopenia, accumulation of 111Indium-labeled platelets in the lungs, and tachypnea also occurred. No changes occurred with the PAAp- strain. The data indicated that PAPP+ S. sanguis interacts with circulating platelets, inducing thromboemboli to cause the pulmonary and cardiac abnormalities. During periodontitis, therefore, PAAP+ S. sanguis and P. gingivalis bacteremia may contribute to the chance of acute thromboembolic events.
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PMID:Dental plaque, platelets, and cardiovascular diseases. 972 99

Recent studies have shown that acute infections, especially of the respiratory tract, are an important risk factor for cerebral ischemia. Additionally we know that chronic dental infections may be a risk for myocardial infarction and artherosclerosis. However, the connection between stroke and dental infections has hardly been examined so far. Therefore we performed a case-control study using a standardized questionaire and examination. We investigated 66 patients consecutive to a acute cerebral ischemia/stroke and 60 age- and sex-matched nonstroke neurological patients as a control group. Dental status was determined by a so called total dental index (TDI) which reflects primarily caries, periodontitis, periapical lesions, devital and missing teeth as well as by a panoramic index (PI). Specifically, older patients with cerebrovascular ischemia tended to have a significantly worse dental status and had more severe periodontitis and periapical lesions than control subjects. A predefined poor dental status was associated with cerebrovascular ischemia independent from other vascular risk factors and social status. In conclusion, poor dental health, mainly resulting from chronic dental infections, may be associated with an increased risk for cerebrovascular ischemia. The results must now be verified in larger studies. As chronic dental infections are a common and also easily treatable factor, their identification as a risk factor for stroke would be quite important in the field of preventive medicine.
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PMID:[Odontogenic focus as the etiology of cerebral ischemia]. 988 Oct 1

Recent evidence has established an association between chronic periodontitis and cardiovascular disease. Periodontitis is a chronic inflammatory disease caused by a small group of gram-negative bacteria, of which Porphyromonas gingivalis is considered an important causative agent. It has been proposed that dental plaque bacteria and their products can disseminate into the bloodstream from the site of infection and promote thromboembolic events associated with atherosclerosis and myocardial infarction. In this regard, Streptococcus sanguis and P. gingivalis have been shown to induce platelet aggregation in vitro. Here we report that P. gingivalis was able to induce platelet aggregation, and that oral strains of Actinobaillus actinomycetemcomitans, Bacteroides forsythus, Campylobacter rectus, Fusobacterium nucleatum, Prevotella intermedia and Trepenoma denticola failed to aggregate platelets when tested for platelet aggregation activity under similar conditions. Additionally, we show that vesicles (outer membrane evaginations that are shed into the environment by the bacteria) of P. gingivalis are potent inducers of mouse platelet aggregation in vitro. In summary, our data show that i) initial adherence of the bacterium to platelet may be facilitated by P. gingivalis fimbriae and ii) P. gingivalis vesicles possess platelet aggregation-inducing activity.
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PMID:Porphyromonas gingivalis platelet aggregation activity: outer membrane vesicles are potent activators of murine platelets. 1115 38

Periodontal infections in individuals with pre-existing heart disease are believed to increase the risk for future coronary heart disease (CHD) events. The goal of this study was to search for an association between periodontitis and CHD events among individuals with pre-existing heart disease, reported in the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Dentate adults (n = 636) with a history of pre-existing cardiovascular disease were followed for CHD events. The presence of periodontitis and gingivitis did not increase CHD risk among these at-risk individuals (hazard ratio [HR], 0.97, and 95% confidence interval [CI], 0.72-1.31; and HR, 1.09, and 95% CI, 0.79-1.50, respectively). When limited to individuals with a self-reported prior heart attack, periodontitis was associated with a 34% decreased CHD risk (HR, 0.66; 95% CI, 0.42-1.05). It is concluded that periodontitis or gingivitis does not elevate CHD risk among individuals with a prior heart attack or self-reported pre-existing cardiovascular disease.
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PMID:Pre-existing cardiovascular disease and periodontitis: a follow-up study. 1209 24

Epidemiological studies have implicated periodontitis (PD) as a risk factor for development of cardiovascular disease (CVD). Persistent infections such as periodontitis induce inflammatory and immune responses which may contribute to coronary atherogenesis, and, in conjunction with other risk factors, may lead to coronary heart disease (CHD). In this review, mechanisms are described that may help explain the association between periodontal infections and CHD. Periodontal diseases are bacterial infections associated with bacteremia, inflammation, and a strong immune response, all of which may represent significant risk factors for the development of atherogenesis, CHD, and myocardial infarction (MI). Several mechanisms may participate in this association, including those induced by oral organisms, and those associated with host response factors. This review will focus on host factors. Oral pathogens and inflammatory mediators (such as interleukin [IL]-1 and tumor necrosis factor [TNF]-alpha) from periodontal lesions intermittently reach the bloodstream inducing systemic inflammatory reactants such as acute-phase proteins, and immune effectors including systemic antibodies to periodontal bacteria. This review will describe the potential role of various inflammatory as well as immunologic factors that may play a role in periodontitis as a possible risk factor for CHD.
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PMID:The role of inflammatory and immunological mediators in periodontitis and cardiovascular disease. 1188 69

Conventional periodontal therapy consists of mechanical scaling and root planing, and surgical treatment. This is still the mainstay of periodontal treatment. Adjunctive antimicrobial treatments, both systemic and local delivery, are becoming more sophisticated and useful in the treatment of recurrent periodontitis. Also very promising are adjunctive treatments that modulate the host response and decrease levels of destructive pro-inflammatory cytokines or matrix metalloproteinases. Smoking is a major risk factor for periodontitis and has a profound impact on the progression of periodontal bone and attachment loss. In the interest of improved periodontal health patients should be encouraged to stop smoking. Finally bacterial endotoxins that stimulate the release of pro-inflammatory cytokines can have systemic effects and may lead to pre-term, low birthweight babies, and cardiovascular diseases such as atherosclerosis, myocardial infarction and stroke. Health professionals need to be cognisant of the effect dental health can have on systemic diseases and refer for treatment when appropriate to ensure that optimum oral and systemic health is achieved for their patients.
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PMID:Emerging concepts in periodontal therapy. 1246 98

The term periodontal medicine encompasses the study of the contribution of periodontal infections on several systemic conditions such as atherosclerosis, myocardial infarction, stroke, diabetes, and premature delivery. The early reports of a linkage between periodontitis and systemic conditions are gaining further support from additional epidemiological studies. The evidence continues to suggest that maternal periodontitis may bean important risk factor or risk indicator for pregnancies culminating in preterm low birth-weight deliveries. Potential mechanisms by which infectious challenge of periodontal origin and systemic inflammation may serve as a potential modifier of parturition are discussed. Furthermore, preliminary data are presented, supporting a hypothetical model in which periodontal pathogens disseminate systemically within the mother and gain access to the foetal compartment. Several aspects of this hypothetical model remain to be elucidated. Only the clarification of the mechanisms of pathogenesis of both periodontitis and premature deliveries will ultimately allow for accurate diagnoses and successful therapies. The concept of diagnosing and treating a periodontal patient to minimise the deleterious effects of this chronic infectious and inflammatory condition on systemic conditions represents both an unprecedented challenge and opportunity to our profession.
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PMID:Periodontal medicine: emerging concepts in pregnancy outcomes. 1266 80

Recent studies have shown that chronic odontogenic infections could pose a risk for myocardial infarction, cerebral ischemia, and arteriosclerosis. However, the correlation between urticaria and dental infections has rarely been examined so far. Therefore, we performed a case-control study using a standardized questionnaire and examination. We investigated 66 patients suffering from an acute or chronic urticaria and 65 age- and sex-matched healthy patients as a control group. Dental status was determined by a so-called total dental index (TDI) which primarily reflects caries, periodontitis, periapical lesions, and nonvital and missing teeth. All 66 patients were referred from the department of dermatology. After their treatment in hospital, all patients received a questionnaire with questions on intensity and localization of the urticaria. The TDI of the urticaria patients was slightly better ( n=66; 2.6+/-1.98) than that of the control group ( n=65, TDI=3.3+/-1.86). Subsequently, it was determined if the urticaria had receded after dental treatment. In conclusion, chronic dental infections do not seem to correlate with an increased risk for urticaria.
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PMID:[Odontogenic foci--possible etiology of urticaria?]. 1464 48


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