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. 2019;7(3):e1651158.
doi: 10.1080/21688370.2019.1651158. Epub 2019 Aug 7.

Gingival epithelial barrier: regulation by beneficial and harmful microbes

Affiliations

Gingival epithelial barrier: regulation by beneficial and harmful microbes

Naoki Takahashi et al. Tissue Barriers. 2019.

Abstract

The gingival epithelium acts as a physical barrier to separate the biofilm from the gingival tissue, providing the first line of defense against bacterial invasion in periodontal disease. Disruption of the gingival epithelial barrier, and the subsequent penetration of exogenous pathogens into the host tissues, triggers an inflammatory response, establishing chronic infection. Currently, more than 700 different bacterial species have been identified in the oral cavity, some of which are known to be periodontopathic. These bacteria contribute to epithelial barrier dysfunction in the gingiva by producing several virulence factors. However, some bacteria in the oral cavity appear to be beneficial, helping gingival epithelial cells maintain their integrity and barrier function. This review aims to discuss current findings regarding microorganism interactions and epithelial barrier function in the oral cavity, with reference to investigations in the gut, where this interaction has been extensively studied.

Keywords: Epithelium; adherens junctions; periodontal disease; porphyromonas gingivalis; tight junctions.

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Figures

Figure 1.
Figure 1.
Structure of cell-to-cell adherence in gingival epithelial cells. TJ: tight junctions (occludin, claudin, ZO-1, ZO-2, ZO-3), AJ: adherens junctions (cadherin), GJ: gap junctions (connexin), D: desmosome, H: hemidesmosome
Figure 2.
Figure 2.
Possible mechanisms of beneficial microbes on gingival epithelial barrier function. Beneficial bacteria can either induce antimicrobial peptides (AMPs) through host immune response or express direct antimicrobial activity against barrier-disrupting pathogens. Beneficial bacteria and their derivatives (e.g., HYA) maintain the epithelial barrier by enhancing tight junction (TJ)-related gene expression. In addition, beneficial bacteria develop a favorable microenvironment that reduces the viability of barrier-disrupting pathogens. Altogether, both direct and indirect pathways regulated by beneficial bacteria are positively associated with maintenance of gingival epithelial barrier.

References

    1. Turner JR. Intestinal mucosal barrier function in health and disease. Nat Rev Immunol. 2009;9(11):799–809. doi:10.1038/nri2653. - DOI - PubMed
    1. König J, Wells J, Cani PD, García-Ródenas CL, MacDonald T, Mercenier A, Whyte J, Troost F, Brummer RJ. Human intestinal barrier function in health and disease. Clin Transl Gastroenterol. 2016;7(10):e196. doi:10.1038/ctg.2016.54. - DOI - PMC - PubMed
    1. Bruewer M, Samarin S, Nusrat A. Inflammatory bowel disease and the apical junctional complex. Ann N Y Acad Sci. 2006;1072(1):242–252. doi:10.1196/annals.1326.017. - DOI - PubMed
    1. Löe H, Theilade E, Jensen SB. Experimental Gingivitis in Man. J Periodontol. 1965;36(3):177–187. doi:10.1902/jop.1965.36.3.177. - DOI - PubMed
    1. Ye P, Chapple CC, Kumar RK, Hunter N. Expression patterns of E-cadherin, involucrin, and connexin gap junction proteins in the lining epithelia of inflamed gingiva. J Pathol. 2000;192(1):58–66. doi:10.1002/1096-9896(2000)9999:9999<::AID-PATH740>3.0.CO;2-1. - DOI - PubMed

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