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      Periodontal Disease: A Risk Factor for Diabetes and Cardiovascular Disease

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          Abstract

          Periodontitis is a chronic inflammatory disease, initiated by the presence of a bacterial biofilm, called dental plaque, which affects both the periodontal ligaments and bone surrounding teeth. In the last decades, several lines of evidence have supported the existence of a relationship between periodontitis and systemic health. For instance, as periodontitis acts within the same chronic inflammatory model seen in cardiovascular disease (CVD), or other disorders, such as diabetes, several studies have suggested the existence of a bi-directional link between periodontal health and these pathologies. For instance, people with diabetes are more susceptible to infections and are more likely to suffer from periodontitis than people without this syndrome. Analogously, it is now evident that cardiac disorders are worsened by periodontitis, both experimentally and in humans. For all these reasons, it is very plausible that preventing periodontitis has an impact on the onset or progression of CVD and diabetes. On these grounds, in this review, we have provided an updated account on the current knowledge concerning periodontal disease and the adverse effects exerted on the cardiovascular system health and diabetes, informing readers on the most recent preclinical studies and epidemiological evidence.

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          Most cited references127

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          Heart Disease and Stroke Statistics—2019 Update: A Report From the American Heart Association

          Circulation, 139(10)
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            Periodontitis: a polymicrobial disruption of host homeostasis.

            Periodontitis, or gum disease, affects millions of people each year. Although it is associated with a defined microbial composition found on the surface of the tooth and tooth root, the contribution of bacteria to disease progression is poorly understood. Commensal bacteria probably induce a protective response that prevents the host from developing disease. However, several bacterial species found in plaque (the 'red-complex' bacteria: Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola) use various mechanisms to interfere with host defence mechanisms. Furthermore, disease may result from 'community-based' attack on the host. Here, I describe the interaction of the host immune system with the oral bacteria in healthy states and in diseased states.
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              Inflammatory and immune pathways in the pathogenesis of periodontal disease.

              The pathogenesis of periodontitis involves a complex immune/inflammatory cascade that is initiated by the bacteria of the oral biofilm that forms naturally on the teeth. The susceptibility to periodontitis appears to be determined by the host response; specifically, the magnitude of the inflammatory response and the differential activation of immune pathways. The purpose of this review was to delineate our current knowledge of the host response in periodontitis. The role of innate immunity, the failure of acute inflammation to resolve (thus becoming chronic), the cytokine pathways that regulate the activation of acquired immunity and the cells and products of the immune system are considered. New information relating to regulation of both inflammation and the immune response will be reviewed in the context of susceptibility to, and perhaps control of, periodontitis. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                20 March 2019
                March 2019
                : 20
                : 6
                : 1414
                Affiliations
                [1 ]Department of Translational Medical Sciences, Federico II University of Naples, 80131 Naples, Italy; liccardo.daniela@ 123456gmail.com (D.L.); nicola.ferrara@ 123456unina.it (N.F.); antonio.cittadini@ 123456unina.it (A.C.); giuseppe.rengo@ 123456unina.it (G.R.)
                [2 ]Center for Translational Medicine, Temple University, Philadelphia, PA 19140, USA
                [3 ]Department of Neurosciences, Reproductive and Odontostomatological Sciences, Federico II University of Naples, 80131 Naples, Italy; gianrico.spagnuolo@ 123456gmail.com
                [4 ]Institute of Dentistry, I.M. Sechenov First Moscow State Medical University, 119146 Moscow, Russia
                [5 ]Istituti Clinici Scientifici-ICS Maugeri S.p.A., 82037 Telese Terme (BN), Italy
                [6 ]Department of Prosthodontics and Dental Materials, School of Dental Medicine, University of Siena, 53100 Siena, Italy; carlorengo@ 123456alice.it
                Author notes
                [* ]Correspondence: alessandro.cannavo@ 123456unina.it ; Tel.: +39-0817-463-677
                Author information
                https://orcid.org/0000-0003-3769-9786
                https://orcid.org/0000-0001-8200-4942
                https://orcid.org/0000-0003-1127-0877
                https://orcid.org/0000-0002-9701-0437
                Article
                ijms-20-01414
                10.3390/ijms20061414
                6470716
                30897827
                031a9567-b74c-4f3c-a472-9d9ec9eb1d0d
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 09 February 2019
                : 18 March 2019
                Categories
                Review

                Molecular biology
                periodontitis,inflammation,bacteria,cardiovascular disease,diabetes
                Molecular biology
                periodontitis, inflammation, bacteria, cardiovascular disease, diabetes

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