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      Porphyromonas gingivalis: Major Periodontopathic Pathogen Overview

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          Abstract

          Porphyromonas gingivalis is a Gram-negative oral anaerobe that is involved in the pathogenesis of periodontitis and is a member of more than 500 bacterial species that live in the oral cavity. This anaerobic bacterium is a natural member of the oral microbiome, yet it can become highly destructive (termed pathobiont) and proliferate to high cell numbers in periodontal lesions: this is attributed to its arsenal of specialized virulence factors. The purpose of this review is to provide an overview of one of the main periodontal pathogens— Porphyromonas gingivalis. This bacterium, along with Treponema denticola and Tannerella forsythia, constitute the “red complex,” a prototype polybacterial pathogenic consortium in periodontitis. This review outlines Porphyromonas gingivalis structure, its metabolism, its ability to colonize the epithelial cells, and its influence upon the host immunity.

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          Life below the gum line: pathogenic mechanisms of Porphyromonas gingivalis.

          Porphyromonas gingivalis, a gram-negative anaerobe, is a major etiological agent in the initiation and progression of severe forms of periodontal disease. An opportunistic pathogen, P. gingivalis can also exist in commensal harmony with the host, with disease episodes ensuing from a shift in the ecological balance within the complex periodontal microenvironment. Colonization of the subgingival region is facilitated by the ability to adhere to available substrates such as adsorbed salivary molecules, matrix proteins, epithelial cells, and bacteria that are already established as a biofilm on tooth and epithelial surfaces. Binding to all of these substrates may be mediated by various regions of P. gingivalis fimbrillin, the structural subunit of the major fimbriae. P. gingivalis is an asaccharolytic organism, with a requirement for hemin (as a source of iron) and peptides for growth. At least three hemagglutinins and five proteinases are produced to satisfy these requirements. The hemagglutinin and proteinase genes contain extensive regions of highly conserved sequences, with posttranslational processing of proteinase gene products contributing to the formation of multimeric surface protein-adhesin complexes. Many of the virulence properties of P. gingivalis appear to be consequent to its adaptations to obtain hemin and peptides. Thus, hemagglutinins participate in adherence interactions with host cells, while proteinases contribute to inactivation of the effector molecules of the immune response and to tissue destruction. In addition to direct assault on the periodontal tissues, P. gingivalis can modulate eucaryotic cell signal transduction pathways, directing its uptake by gingival epithelial cells. Within this privileged site, P. gingivalis can replicate and impinge upon components of the innate host defense. Although a variety of surface molecules stimulate production of cytokines and other participants in the immune response, P. gingivalis may also undertake a stealth role whereby pivotal immune mediators are selectively inactivated. In keeping with its strict metabolic requirements, regulation of gene expression in P. gingivalis can be controlled at the transcriptional level. Finally, although periodontal disease is localized to the tissues surrounding the tooth, evidence is accumulating that infection with P. gingivalis may predispose to more serious systemic conditions such as cardiovascular disease and to delivery of preterm infants.
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            Porphyromonas gingivalis: an invasive and evasive opportunistic oral pathogen.

            Porphyromonas gingivalis is a Gram-negative oral anaerobe that is involved in the pathogenesis of periodontitis, an inflammatory disease that destroys the tissues supporting the tooth, eventually leading to tooth loss. Porphyromonas gingivalis has can locally invade periodontal tissues and evade the host defence mechanisms. In doing so, it utilizes a panel of virulence factors that cause deregulation of the innate immune and inflammatory responses. The present review discusses the invasive and evasive strategies of P. gingivalis and the role of its major virulence factors in these, namely lipopolysaccharide, capsule, gingipains and fimbriae. Moreover, the role of P. gingivalis as a 'keystone' biofilm species in orchestrating a host response, is highlighted. © 2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.
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              Variations of Porphyromonas gingivalis fimbriae in relation to microbial pathogenesis.

              Periodontal disease is an infectious disorder caused by a small subset of periodontal pathogens including Porphyromonas gingivalis. Accumulated evidences show that the expression of P. gingivalis heterogenic virulence properties is dependent on its clonal diversity. P. gingivalis expresses two distinct fimbria molecules, major and minor fimbriae, on its cell surfaces, both of which seem to be involved in the development of periodontitis. In this short review, variations of fimbriae in relation to microbial pathogenesis are discussed. Our recent findings are summarized to elucidate the relationship between clonal variation of fimbriae and bacterial pathogenicity of various strains. Major fimbriae were classified into six types (I to V and Ib) based on the diversity of fimA genes encoding FimA (a subunit of major fimbriae). A majority of periodontitis patients were found to carry type II fimA organisms, followed by type IV, and type II fimA organisms were significantly occurred with more severe forms of periodontitis. Studies of clones with type II fimA have revealed significantly greater adhesive and invasive capabilities to epithelial cells than other fimA type clones. Minor fimbriae induced interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) cytokine expression in macrophages and were suggested to be a causative factor of alveolar bone resorption in animal models. The clonal diversity of minor fimbriae is unclear, however, distinct minor fimbria molecules were found in different strains. The fimbria variations may have an influence on the development of periodontal disease.
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                Author and article information

                Journal
                J Immunol Res
                J Immunol Res
                JIR
                Journal of Immunology Research
                Hindawi Publishing Corporation
                2314-8861
                2314-7156
                2014
                25 March 2014
                : 2014
                : 476068
                Affiliations
                Institute of Clinical and Experimental Dental Medicine, First Faculty of Medicine and General University Hospital, Charles University, Karlovo Namesti 32, 12000 Prague, Czech Republic
                Author notes
                *Stepan Podzimek: podzimek@ 123456vus.cz

                Academic Editor: Clelia M. Riera

                Article
                10.1155/2014/476068
                3984870
                24741603
                0f946599-6a18-4577-a212-a03bba77a718
                Copyright © 2014 Jaroslav Mysak et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 8 November 2013
                : 21 February 2014
                : 21 February 2014
                Categories
                Review Article

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