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

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

Prevention and treatment of respiratory infections remain an important health care challenge as the US population ages, contains more susceptible or high-risk people, and encounters new pathogens or antibiotic resistant bacteria. Reasonably protective vaccines against very common microbes are available for childhood and adult immunization, but, generally, these are underutilized. A broader definition of higher risk individuals is evolving, which will include more for immunization. Different approaches to vaccine development through design of new component vaccines are necessary. This review has updated host defense mechanisms at three levels in the human respiratory tract: naso-oropharynx (upper airways), conducting airways, and alveolar space. Examples of representative pathogenic microbes have been inserted at the respective airway segment where they may colonize or create infection (influenza, measles virus, Porphyromonas gingivalis causing periodontitis, Bordetella pertussis, Chlamydia pneumoniae, Streptococcus pneumoniae, and Bacillus anthracis ). Hopefully, microbe-host interactions will suggest new approaches for preventing these kinds of infections.
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PMID:Modulating airway defenses against microbes. 1198 2

Case-control studies and a few prospective studies have indicated that chronic infections may add to the risk of stroke and that acute infections may act as trigger factors for stroke. Such chronic infections include periodontal disease, infection with Chlamydia pneumoniae or Helicobacter pylori, and chronic bronchitis. A causal role of these infectious diseases has not been proved, given conflicting study results, possible residual confounding in observational studies, and the lack of evidence from interventional trials. Therefore, special treatment regimens for stroke prevention based on serologic or genomic evidence of infection are not indicated outside of randomized studies at present. However, the preliminary available evidence suggests that in patients with previous cerebral ischemia, clinically diagnosed chronic infections should be taken seriously and should receive the treatment that is indicated according to current guidelines. This may include appropriate treatment of moderate or severe periodontitis and of chronic bronchitis. Inflammatory parameters (eg, C-reactive protein, leukocyte count, fibrinogen) are independently associated with the risk of first or recurrent stroke. The question of whether these indexes are causally related to stroke or merely represent risk markers is not sufficiently clarified. Their use in monitoring individual risk in daily clinical practice is limited at present by the lack of clearly defined therapeutic strategies to modify these parameters, although statins and other drugs can influence inflammatory markers. Observational studies have shown that influenza vaccination is significantly and independently associated with a reduced risk of stroke and myocardial infarction. Although interventional studies in stroke are lacking, it is recommendable that in accordance with current guidelines patients with previous vascular disease, including stroke, patients with high risk of stroke, and all subjects above age 60, receive an influenza vaccination annually.
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PMID:Role of anti-infective strategies in the prevention of stroke. 1600 50

Increasing evidence has linked the anaerobic bacteria forming periodontopathic biofilms with aspiration pneumonia in elderly persons. In experiments designed to eliminate the potent respiratory pathogens forming biofilms in the oral cavity, we have shown that the mechanical and chemical oral cleansing using povidone-iodine effectively reduced the detection rates and numbers of methicillin-sensitive Staphylococcus species, Streptococcus pneumoniae, and Haemophilus influenzae in patients scheduled to undergo oral surgery requiring endotracheal intubation. We confirmed the pathogenicity of periodontopathic anaerobic bacteria for aspiration pneumonia in an experimental mouse model. Based upon the finding of the coexistence of Porphyromonas gingivalis with Treponema denticola in chronic periodontitis lesions, we innoculated a mixed culture of P. gingivalis and T. denticola into the mouse trachea; the resulting infection induced inflammatory cytokine production and caused pneumonia. In another series of investigations, professional oral health care (POHC), mainly cleansing administered by dental hygienists once a week for 24 months to elderly persons requiring daily care, resulted in the reduction of the number of total anaerobes, Candida albicans, and Staphylococcus species and in the number of cases of fatal aspiration pneumonia. We also found that the POHC treatment of elderly persons for 6 months in the winter season reduced the salivary levels of protease, trypsin-like activity, and neuraminidase and also decreased the frequency of influenza cases.
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PMID:Involvement of periodontopathic anaerobes in aspiration pneumonia. 1627 88

There is increasing evidence that, in addition to conventional risk factors, acute and chronic infectious diseases increase the risk of stroke. Acute infection, mainly respiratory, and both bacterial and viral infection, represent temporarily active trigger factors for cerebral ischemia. Chronic infectious diseases that may increase the risk of stroke include periodontitis, chronic bronchitis and infections with microbial antigens, such as Helicobacter pylori and Chlamydia pneumoniae. From observational studies, there is evidence that vaccination against influenza is associated with a reduced risk of stroke, myocardial infarction and all-cause mortality. This report provides an overview on the influence of infection on stroke risk and potential anti-infective strategies that may play a future role in stroke prevention.
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PMID:The effect of infections and vaccinations on stroke risk. 1646 97

Stroke is among the most common causes of death and persisting disability and therefore represents a great social and economic burden worldwide. In order to lower this burden it is essential to identify risk factors and respective preventive strategies. Besides the established stroke risk factors (e.g. hypertension, diabetes, hypercholesterolemia, atrial fibrillation) both acute and chronic infectious diseases have emerged as risk factors for stroke. Mainly acute respiratory tract infection but also urinary tract infections independently increase the risk of ischemic stroke. Such additional risk was shown to be highest for infection within 3 days before ischemia and the risk steadily declines with increasing time intervals between infection and stroke. Associations between stroke incidence and mortality and influenza epidemics have been demonstrated. Observational studies showed an inverse association between influenza vaccination and stroke risk; however, interventional studies in this field have not been performed so far. Chronic infections, presently discussed as stroke risk factors mainly include periodontitis and infections with Helicobacter pylori (Hp) and Chlamydia pneumoniae (Cp). Although most respective studies identified these infectious diseases as independent stroke risk factors interventional trials have not been performed so far and causality is not proven, yet. There is preliminary evidence that the number of pathogens to which a subject had been exposed to rather than single pathogens are associated with the risk of stroke or other cardiovascular diseases. Chronic infectious diseases are treatable conditions and their identification as causal contributors to stroke risk could offer new avenues in stroke prevention.
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PMID:Infection, its treatment and the risk for stroke. 1935 97

The occurrence of stroke in populations is incompletely explained by traditional vascular risk factors. Data from several case-control studies and one large study using case series methodology indicate that recent infection is a temporarily acting, independent trigger factor for ischemic stroke. Both bacterial and viral infections, particularly respiratory tract infections, contribute to this association. A causal role for infection in stroke is supported by a graded temporal relationship between these conditions, and by multiple pathophysiological pathways linking infection and inflammation, thrombosis, and stroke. Furthermore, observational studies suggest that influenza vaccination confers a preventive effect against stroke. Case-control and prospective studies indicate that chronic infections, such as periodontitis, chronic bronchitis and infection with Helicobacter pylori, Chlamydia pneumoniae or Cytomegalovirus, might increase stroke risk, although considerable variation exists in the results of these studies, and methodological issues regarding serological results remain unresolved. Increasing evidence indicates that the aggregate burden of chronic and/or past infections rather than any one single infectious disease is associated with the risk of stroke. Furthermore, genetic predispositions relating to infection susceptibility and the strength of the inflammatory response seem to co-determine this risk. Here, we summarize and analyze the evidence for common acute and chronic infectious diseases as stroke risk factors.
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PMID:Common infections and the risk of stroke. 2106 Mar 40

Smoking has substantial local and systemic adverse effects on the immune system, respiratory tract and skin and soft tissues. Smokers are at increased risk of invasive pneumococcal disease, pneumonia, periodontitis, surgical infections, tuberculosis, influenza and meningococcal disease. The results of several studies indicate that smokers with periodontitis or tuberculosis suffer more severe disease. Data on the impact of smoking on sepsis and pneumonia are controversial and limited, and systematic data regarding the outcome of the majority of infections in smokers are scarce. Abundant data indicate that children exposed to environmental tobacco smoke (ETS) suffer from more severe infections. However, information regarding the effects of ETS on the outcome of infections in adults is limited. Various aspects of the relation between smoking and the outcome of bacterial infection (e.g. potential dose-dependent effects and the interactions between smoking and other environmental factors that may affect the course of infectious diseases) remain to be established.
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PMID:Smoking and the outcome of infection. 2117 3

Relatively recently discovered, human metapneumovirus (HMPV) is a human pathogen with worldwide prevalence, accounting for a substantial percentage of respiratory tract diseases. Concurrent viral and bacterial infections enable intricate mechanisms of cooperation between pathogens, which complicate the symptoms and outcome of the disease. Such bilateral interactions are based on the modulation of bacterial growth on epithelium pathologically altered during viral illness and the modulation of immune responses, as well as the enhancement of virus replication by bacterial virulence factors. This study showed that proteases produced by Porphyromonas gingivalis, a Gram-negative bacterium implicated in the development of periodontitis, named gingipains, facilitated HMPV replication in LLC-MK2 cells and may contribute to HMPV pathogenicity in patients with periodontitis. Gingipains at low nanomolar concentrations enabled HMPV replication and allowed virus propagation in vitro. In contrast to previously published data for influenza virus, however, Staphylococcus aureus proteases and human neutrophil elastase did not affect virus replication.
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PMID:Porphyromonas gingivalis enzymes enhance infection with human metapneumovirus in vitro. 2171 99

The interactions between obesity and infectious diseases have recently received increasing recognition as emerging data have indicated an association between obesity and poor outcome in pandemic H1N1 influenza infection. Obesity is an established risk factor for surgical-site infections, nosocomial infections, periodontitis and skin infections. Several studies indicate that acute pancreatitis is more severe in the obese. Data are controversial and limited as regards the association between obesity and the risk and outcome of community-acquired infections such as pneumonia, bacteremia and sepsis and obesity and the course of HIV infection. As the cause-effect relationship between obesity and infection remains obscure in many infectious diseases, further studies are warranted. The consequences of obesity may have substantial effects on the global burden of infectious diseases.
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PMID:Obesity and the risk and outcome of infection. 2254 72


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