Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases

Aims In this article, inflammatory mechanisms that link periodontal diseases to cardiovascular diseases are reviewed. Methods This article is a literature review. Results Studies in the literature implicate a number of possible mechanisms that could be responsible for increased inflammatory response...

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Bibliographic Details
Published inJournal of clinical periodontology Vol. 40; no. s14; pp. S51 - S69
Main Authors Schenkein, Harvey A., Loos, Bruno G.
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.04.2013
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Summary:Aims In this article, inflammatory mechanisms that link periodontal diseases to cardiovascular diseases are reviewed. Methods This article is a literature review. Results Studies in the literature implicate a number of possible mechanisms that could be responsible for increased inflammatory responses in atheromatous lesions due to periodontal infections. These include increased systemic levels of inflammatory mediators stimulated by bacteria and their products at sites distant from the oral cavity, elevated thrombotic and hemostatic markers that promote a prothrombotic state and inflammation, cross‐reactive systemic antibodies that promote inflammation and interact with the atheroma, promotion of dyslipidemia with consequent increases in pro‐inflammatory lipid classes and subclasses, and common genetic susceptibility factors present in both disease leading to increased inflammatory responses. Conclusions Such mechanisms may be thought to act in concert to increase systemic inflammation in periodontal disease and to promote or exacerbate atherogenesis. However, proof that the increase in systemic inflammation attributable to periodontitis impacts inflammatory responses during atheroma development, thrombotic events or myocardial infarction or stroke is lacking.
Bibliography:istex:E4D4B3F2D316D5171279036C0AF2E7C46B8F1450
ArticleID:JCPE12060
ark:/67375/WNG-JCH5C5L5-8
Conflict of interest and source of funding statement
The authors declare no conflict of interest. The workshop was funded by an unrestricted educational grant from Colgate‐Palmolive to the European Federation of Periodontology and the American Academy of Periodontology.
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SourceType-Scholarly Journals-1
ObjectType-Feature-3
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ObjectType-Review-1
ISSN:0303-6979
1600-051X
DOI:10.1111/jcpe.12060