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Review
, 69 (1), 18-27

Microbial Protection and Virulence in Periodontal Tissue as a Function of Polymicrobial Communities: Symbiosis and Dysbiosis

Review

Microbial Protection and Virulence in Periodontal Tissue as a Function of Polymicrobial Communities: Symbiosis and Dysbiosis

Frank A Roberts et al. Periodontol 2000.

Abstract

This review discusses polymicrobial interactions with the host in both health and disease. As our ability to identify specific bacterial clonal types, with respect to their abundance and location in the oral biofilm, improves, we will learn more concerning their contribution to both oral health and disease. Recent studies examining host- bacteria interactions have revealed that commensal bacteria not only protect the host simply by niche occupation, but that bacterial interactions with host tissue can promote the development of proper tissue structure and function. These data indicate that our host-associated polymicrobial communities, such as those found in the oral cavity, co-evolved with us and have become an integral part of who we are. Understanding the microbial community factors that underpin the associations with host tissue that contribute to periodontal health may also reveal how dysbiotic periodontopathic oral communities disrupt normal periodontal tissue functions in disease. A disruption of the oral microbial community creates dysbiosis, either by overgrowth of specific or nonspecific microorganisms or by changes in the local host response where the community can now support a disease state. Dysbiosis provides the link between systemic changes (e.g. diabetes) and exogenous risk factors (e.g. smoking), and the dysbiotic community, and can drive the destruction of periodontal tissue. Many other risk factors associated with periodontal disease, such as stress, aging and genetics, are also likely to affect the microbial community, and more research is needed, utilizing sophisticated bacterial taxonomic techniques, to elucidate these effects on the microbiome and to develop strategies to target the dysbiotic mechanisms and improve periodontal health.

Figures

Fig. 1
Fig. 1
(A) Current knowledge of microbial influence on the junctional epithelium based on cumulative data from human and mouse studies. The architecture of junctional epithelium and the presence of neutrophils are similar between germ-free and conventional mice. Several molecules appear to change dramatically with the addition of bacteria but many are unchanged [14]. (B) Overview of current knowledge of microbial influence on the intestinal epithelium. The architecture of the intestinal tissue is changed markedly with the addition of bacteria: the crypts are deeper, the capillary network is more extensive, the mucus layer is reduced, cilia are shorter, and many differences are seen with immune cells and molecules as indicated [32]. The figure indicates the relative location and abundance of innate immune cells/molecules (*indicates changes due to microbial interactions confirmed in germ-free studies.) Reprinted with permission from Cell Host & Microbe 10, October, 2011 ©2011 Elsevier Inc.
Fig. 2
Fig. 2
Periodontal Health and Disease as a function of the periodontal oral community and the host response. Periodontal health results from a homeostatic balance between the oral microbial community amount and composition and the corresponding host response. Risk factors can alter this balance and create a dysbiotic oral microbial community with an altered oral commensal bacterial composition. Bacterial community changes which result in a dysfunctional host response include an increase the total number of bacteria (22) and/or the outgrowth of specific bacteria (31). Periodontal treatment regimens can restore homeostasis.

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