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      Periodontal and inflammatory bowel diseases: Is there evidence of complex pathogenic interactions?

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          Abstract

          Periodontal disease and inflammatory bowel disease (IBD) are both chronic inflammatory diseases. Their pathogenesis is mediated by a complex interplay between a dysbiotic microbiota and the host immune-inflammatory response, and both are influenced by genetic and environmental factors. This review aimed to provide an overview of the evidence dealing with a possible pathogenic interaction between periodontal disease and IBD. There seems to be an increased prevalence of periodontal disease in patients with IBD when compared to healthy controls, probably due to changes in the oral microbiota and a higher inflammatory response. Moreover, the induction of periodontitis seems to result in gut dysbiosis and altered gut epithelial cell barrier function, which might contribute to the pathogenesis of IBD. Considering the complexity of both periodontal disease and IBD, it is very challenging to understand the possible pathways involved in their coexistence. In conclusion, this review points to a complex pathogenic interaction between periodontal disease and IBD, in which one disease might alter the composition of the microbiota and increase the inflammatory response related to the other. However, we still need more data derived from human studies to confirm results from murine models. Thus, mechanistic studies are definitely warranted to clarify this possible bidirectional association.

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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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              Ulcerative colitis.

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                Author and article information

                Journal
                World J Gastroenterol
                World J. Gastroenterol
                WJG
                World Journal of Gastroenterology
                Baishideng Publishing Group Inc
                1007-9327
                2219-2840
                21 September 2016
                21 September 2016
                : 22
                : 35
                : 7963-7972
                Affiliations
                Ronaldo Lira-Junior, Carlos Marcelo Figueredo, Department of Periodontology, Faculty of Odontology, Rio de Janeiro State University, Rio de Janeiro, RJ 20551-030, Brazil
                Author notes

                Author contributions: Lira-Junior R and Figueredo CM contributed equally to this manuscript; both authors conceived the paper, performed the literature search and interpretation, wrote the article, and gave final approval of the manuscript.

                Correspondence to: Dr. Carlos Marcelo Figueredo, Department of Periodontology, Faculty of Odontology, Rio de Janeiro State University, Boulevard 28 de Setembro 157, 20 Andar, Vila Isabel, Rio de Janeiro, RJ 20551-030, Brazil. cmfigueredo@ 123456hotmail.com

                Telephone: +55-21-28688282

                Article
                jWJG.v22.i35.pg7963
                10.3748/wjg.v22.i35.7963
                5028810
                27672291
                c8ee5eef-debc-490d-950e-3cf9b985bd4a
                ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.

                This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

                History
                : 29 March 2016
                : 29 June 2016
                : 1 August 2016
                Categories
                Review

                periodontal disease,inflammatory bowel disease,crohn’s disease,ulcerative colitis,inflammation

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