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Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases

Identifieur interne : 000063 ( Istex/Corpus ); précédent : 000062; suivant : 000064

Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases

Auteurs : Maurizio S. Tonetti ; Thomas E. Van Dyke

Source :

RBID : ISTEX:13327CE8D945B912A6ECC19A207C0B4321C7EC6E

English descriptors

Abstract

This consensus report is concerned with the association between periodontitis and atherosclerotic cardiovascular disease (ACVD). Periodontitis is a chronic multifactorial inflammatory disease caused by microorganisms and characterized by progressive destruction of the tooth supporting apparatus leading to tooth loss; as such, it is a major public health issue.

Url:
DOI: 10.1111/jcpe.12089

Links to Exploration step

ISTEX:13327CE8D945B912A6ECC19A207C0B4321C7EC6E

Le document en format XML

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<p>This consensus report is concerned with the association between periodontitis and atherosclerotic cardiovascular disease (
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Aims
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Plausibility
<p>Periodontitis leads to entry of bacteria in the blood stream. The bacteria activate the host inflammatory response by multiple mechanisms. The host immune response favors atheroma formation, maturation and exacerbation.</p>
Epidemiology
<p>In longitudinal studies assessing incident cardiovascular events, statistically significant excess risk for
<hi rend="fc">ACVD</hi>
was reported in individuals with periodontitis. This was independent of established cardiovascular risk factors. The amount of the adjusted excess risk varies by type of cardiovascular outcome and across populations by age and gender. Given the high prevalence of periodontitis, even low to moderate excess risk is important from a public health perspective.</p>
Intervention
<p>There is moderate evidence that periodontal treatment: (i) reduces systemic inflammation as evidenced by reduction in C‐reactive protein (
<hi rend="fc">CRP</hi>
) and improvement of both clinical and surrogate measures of endothelial function; but (ii) there is no effect on lipid profiles – supporting specificity. Limited evidence shows improvements in coagulation, biomarkers of endothelial cell activation, arterial blood pressure and subclinical atherosclerosis after periodontal therapy. The available evidence is consistent and speaks for a contributory role of periodontitis to
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<hi rend="fc">ACVD</hi>
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<hi rend="fc">ACVD</hi>
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Conclusions
<p>It was concluded that: (i) there is consistent and strong epidemiologic evidence that periodontitis imparts increased risk for future cardiovascular disease; and (ii) while in vitro, animal and clinical studies do support the interaction and biological mechanism, intervention trials to date are not adequate to draw further conclusions. Well‐designed intervention trials on the impact of periodontal treatment on prevention of
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