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Review
. 2018 Mar-Apr;22(2):101-106.
doi: 10.4103/jisp.jisp_385_17.

Polymicrobial synergy and dysbiosis: An overview

Hawaabi Faqeer Mohd Shaikh  1 , Suvarna Hanmantgouda Patil  1 , Tanvi Shyamsundar Pangam  1 , Khushboo Vijaysinh Rathod  1
Affiliations
Review

Polymicrobial synergy and dysbiosis: An overview

Hawaabi Faqeer Mohd Shaikh et al. J Indian Soc Periodontol. 2018 Mar-Apr.

Abstract

The oral fissure is immensely inhabited with a number of polymicrobial colonies similar to the intestinal system. Periodontitis is a dysbiotic disease resulting from deviation in subgingival Gram-positive bacteria to Gram-negative bacteria shift from Gram-positive bacteria. The development of periodontal dysbiosis occurs over a broadened timeframe, which slowly turns the symbiotic association of host and microbe to pathogenic. This review highlights a recent paradigm of periodontitis progression has been postulated which challenges the traditional concept of periodontitis being induced by few particular periopathogens such as belonging to red complex, but by a more comprehensive dysbiotic-synergistic community.

Keywords: Dysbiosis; keystone pathogens; polymicrobial synergy; polymicrobial synergy and dysbiosis model.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Figure 1
Figure 1
Downregulation of chemokines by Porphyromonas gingivalis. TLR – Toll like receptors; F. Nucleatum – Fusobacterium nucleatum; IRF – Interferon-Regulatory Factor; IP – Interferon gamma-induced protein; IL – Interleukin
Figure 2
Figure 2
Disruption of neutrophil function and dysbiosis by Porphyromonas gingivalis. TLR – Toll like receptors; MAL – MyD88-Adaptor Like; C5aR – Complement 5a Receptor; Smurf – Smad ubiquitination regulatory factor; P13K – Phosphoinositide 3-kinase; RhoA – Ras homolog gene family, member A; MyD88 – Myeloid differentiation primary response 88
Figure 3
Figure 3
The polymicrobial synergy and dysbiosis model of periodontal disease etiology
See this image and copyright information in PMC

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