Periodontitis and mechanisms of cardiometabolic risk: Novel insights and future perspectives
Periodontitis is an infectious and inflammatory disease of the tooth-supporting tissues caused by the accumulation of subgingival plaque and the action of specific periodontopathogenic bacteria. Periodontitis has been associated with cardiovascular diseases and considered a cardiovascular risk facto...
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Veröffentlicht in: | Biochimica et biophysica acta. Molecular basis of disease 2019-02, Vol.1865 (2), p.476-484 |
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Sprache: | eng |
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Zusammenfassung: | Periodontitis is an infectious and inflammatory disease of the tooth-supporting tissues caused by the accumulation of subgingival plaque and the action of specific periodontopathogenic bacteria. Periodontitis has been associated with cardiovascular diseases and considered a cardiovascular risk factor. Several mechanisms have been proposed to explain this association, such as the infection of atherosclerotic plaques by periodontal pathogens, the pro-atherogenic effect on the lipid profile, the systemic dissemination of pro-inflammatory mediators or the contribution to type 2 diabetes mellitus. Periodontal treatment has also been related to improvement in cardiometabolic risk variables, and oral hygiene techniques may be useful in reducing cardiometabolic risk. The aim of this review is to provide new and recent insights on the relationship between periodontitis and cardiometabolic risk, focusing on recent evidence. Comments on shared potential therapeutic targets, such as the role of glucagon-like peptide 1, are also highlighted.
•Periodontitis is associated with increased cardiovascular events.•Periodontal bacteria have an effect of atherosclerosis by infection of the plaque.•Inflammatory mediators and bacterial compounds from periodontitis may also interact with atherosclerosis.•Periodontal bacteria may elevate plasma lipid levels and lipoproteins.•Innovative therapies such as incretin-based drugs could be useful in both cardiovascular diseases and periodontitis. |
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ISSN: | 0925-4439 1879-260X |
DOI: | 10.1016/j.bbadis.2018.12.001 |