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Louise Parker Bench D 31/08/2016

Classification

Higher order taxa

Bacteria – Domain – Bacteroidetes – Bacteroidetes – Bacteroidales – Porphyromonadaceae – Porphyromonas

Species

Species: Porphyromonas gingivalis
Strain: strain 2561 = ATCC 33277= CCUG 25893 = CCUG 25928 = CIP 103683 = DSM 20709 = JCM 12257 = NCTC 11834. 

Description and significance

Porphyromonas gingivalis is a Gram-negative anaerobe. It is a major causative agent of the initiation and progression of periodontal disease, a main cause of tooth loss ^[1]. P. gingivalis is an opportunistic pathogen found in the subgingival sulcus of the human oral cavity ^[2]. Along with T. denticola and T. forsythia, P. gingivalis forms the red bacterial complex which is often seen in advanced periodontal lesions (^[2]. P. gingivalis is strongly associated with gingival recession, increased sulcular pocket depth and bleeding upon probing (Molecular analysis of bacteria in periodontitis: evaluation of clone libraries, novel phylotypes and putative pathogens). The bacterium has also been found in healthy individuals, at a prevalence of 10-25%. P. gingivalis is found in those with periodontitis at a prevalence of 79%-90%. Epidemiological studies have shown that strains vary in association with human disease and virulence in animal models. Strains W83, W50, ATCC 49417, A7A1 have been classified as virulence, whereas avirulent strains include 381, 33277 and 23A4 ^[4].
P. gingivalis is obligately anaerobic and does not form spores ^[5]. Cells are non-motile rods 0.5 by 1-2um in broth ^[5]. On blood agar, colonies are black-pigmented smooth, shiny, convex and 1-2mm in diameter ^[5].
Periodontal disease is the most common cause of infectious inflammatory disease. The majority of the population is affected by mild periodontal disease and 5-8% suffer from more severe forms ^[6]. Periodontal disease has also been linked with increased risk of cardiovascular disease ^[6].

Genome structure

The Porphyromonas gingivalis strain W83 has a 2,343,479bp genome sequence ^[7]. It has an average G+C content of 48.3%. 1,990 open reading frames were identified in the genome, making up 85% of the genome ^[7]. 1,075 of these were assigned biological role categories. Repetitive elements make up approximately 6% of the genome and are mainly DNA repeats and transposable elements. Analysis of this genome has shown that P. gingivalis is able to metabolise many amino acids and generate products toxic to the human host which aids development of periodontitis ^[7].

Cell structure and metabolism

Cell wall: P. gingivalis has a gram-negative cell wall consisting of an inner membrane, thin peptidoglycan layer and outer membrane. The peptidoglycan layer contains lysine as the diamino acid^[5].

Biofilm formation: In addition to infecting gingival cells, P gingivalis is able to inhabit subgingival dental biofilms ^[8]. The bacterium is a late coloniser, attracted to the biofilm by intermediate colonisers such as Fusobacterium nucleatum^[8]. P. gingivalis is able to increase the virulence of biofilms even in low numbers. It does this by subverting host responses, altering biofilm community structures and enabling an increase in bacterial load ^[8]. For these reasons it is termed a ‘keystone’ pathogen. When studied in mice, P. gingivalis was not found to cause disease in isolation ^[8]. Thus it is thought that relationships with other microbes are necessary for P. gingivalis to use its full potential for pathogenicity.

Fimbriae: Fimbriae are surface appendages that protrude from the outer membrane of most strains of P. gingivalis ^[2]. The bacteria express fimbriae of two types, made up of FimA protein and Mfa protein. Both types are thought to contribute to periodontal disease, and when fimbriae is not expressed, binding to and invasion of host cells is disrupted^[2]. Fimbriae also mediate adhesion to extracellular matrix proteins and commensal bacteria including Streptococci and Actinomyces viscosus^[2].

Capsule: Capsule is also thought to contribute to virulence ^[2]. While its chemical composition varies between strains, strains without capsule have been found to mainly cause non-invasive localised abscesses in animal models^[2]. They are also associated with increased phagocytosis and killing by macrophages and dendritic cells. Virulent strains of P. gingivalis W83 and W50 have a thicker capsule then less virulenct strains, which is linked to decreased production of leukocyctes^[2]. Capsule type also influences initial adhesion to periodontal pocket epithelial cells^[2].

Metabolic function: P. gingivalis requires anaerobic conditions for growth, in addition to heme or hemin and vitamin K ^[9]. The black colour seen when P. gingivalis is grown on blood media is associated with heme accumulating on the cell surface. When grown on heme-limited media, it becomes less virulent ^[9]. The bacterium gains energy by fermentation of amino acids. This is crucial as sugars are not abundant in deep periodontal pockets where P. gingivalis is found^[9].

Ecology

P. gingivalis is an obligate anaerobe found mainly in the human oral cavity. It has been found among epithelial cells obtained from periodontal pockets, gingival crevices and buccal mucosa collected from individuals with both periodontitis and healthy gingivae ^[10]. P. gingivalis has also been found in the upper gastrointestinal system, respiratory tract, colon^[10] and vagina ^[11]. P. gingivalis is found uncommonly and in low numbers in healthy individuals compared to those with disease ^[6]. As a keystone pathogen, uses a number of virulence factors including fimbriae, degradative enzymes, exopolysaccharide capsule and atypicaly lipopolysaccharide^[6]. P. gingivalis also uses gingipains, a group of cysteine proteases which have trypsin-like proteolytic activity outside of the cell. These cleave host proteins and result in tissue damage and disruption of the immune response^[6].

Pathology

P. gingivalis is one of the major causes of periodontal disease. Periodontal disease is the inflammation of the gingiva, alveolar bone, periodontal ligament and cementum^[2]. Periodontal diseases comprise gingival disease, the inflammation of gingival tissues, and the more severe periodontitis^[2]. Periodontitis is the irreversible inflammation of the periodontal tissues induced by plaque^[2]. It can destroy the periodontal ligament and alveolar bone and cause migration of the epithelial ligament. This in turn results in a periodontal pocket, upon which bacteria can colonise and subginigival plaque can form^[2]. In a study of patients with chronic periodontitis, 87.75% of subgingival plaque samples contained P. gingivalis^[2].
Periodontal disease has been linked with rheumatoid arthritis^[6]. Rheumatoid arthritis is a systematic autoimmune disease associated with debilitating joint destruction and chronic inflammation^[6]. Periodontal destruction and joint destruction are known to have common pathogenic mechanisms and are thought to influence each other^[6]. Individuals with Periodontal disease show increased chance of developing rheumatoid arthritis^[6]. Periodontal disease has also been linked with cardiovascular disease, and P. gingivalis has been found in atherosclerotic plaques ^[1].

Application to biotechnology

Bioengineering, biotechnologically relevant enzyme/compound production, drug targets,…

Current research

Summarise some of the most recent discoveries regarding this species.

References

1. Naito, M., Hirakawa, H., Yamashita, A., Ohara, N., Shoji, M., Yuritake, H., Nakayama, K., Toh, H., Yoshimura, F., Kuhara, S., Hattori, M., Hayashi, T. and Nakayama, K. (2008) Determination of the Genome Sequence of Porphyromonas gingivalis Strain ATCC 33277 and Genomic Comparison with Strain W83 Revealed Extensive Genome Rearrangements in P. gingivalis. DNA Res 4:215-225.

2. How, K. Y., Song, K. P. and Chan, K. G. (2016) Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line. Front Microbiol, 7: 53.

3. Hutter G., Schlagenhauf, U., Valenza, G., Horn, M., Burgemeister, S., Claus, H. and Vogel, U. (2003) Molecular analysis of bacteria in periodontitis: evaluation of clone libraries, novel phylotypes and putative pathogens. Microbiology, 149: 67-75.

4. Igboin, C. O., Griffen, A. L. and Leys, E. J. (2009) Porphyromonas gingivalis strain diversity. J Clin Microbiol, 47,: 3073-81.

5. Shah N, H., Collins D, M. (1988) Proposal for Reclassification of Bacteroides asaccharolyticus, Bacteroides gingivalis, and Bacteroides endodontalis in a New Genus, Porphyromonas.Int J Syst Evol Microbiol 38 :128-131.

6. Farquharson, D., Butcher, J. P., and Culshaw, S. (2012) Periodontitis, Porphyromonas, and the pathogenesis of rheumatoid arthritis. Mucosal Immunol 5:112-20

7. Nelson, K.E., Fleischmann, R.D., Deboy, R.T., Paulsen, I.T., Fouts, D.E., Eisen, J.A., et al. (2003) Complete Genome Sequence of the Oral Pathogenic Bacterium Porphyromonas gingivalis Strain W83. J Bacteriol 185: 5591–5601.

8. Sakanaka, A., Takeuchi, H., Kuboniwa, M. and Amano, A. (2016) Dual lifestyle of Porphyromonas gingivalis in biofilm and gingival cells. Microb Pathog 94: 42-7.

9. Bos, M. P., Robert, V., & Tommassen, J. (2007) Biogenesis of the Gram-Negative Bacterial Outer Membrane. Annual Review of Microbiology, 61(1), 191-214. doi:10.1146/annurev.micro.61.080706.093245

10. Ogrendik, M. (2013) Rheumatoid arthritis is an autoimmune disease caused by periodontal pathogens. Int J Gen Med 6: 383-386\

11. Cassini, M. A., Pilloni, A., Condo, S. G., Vitali, L. A., Pasquantonio, G., and Cerroni, L. (2013) Periodontal bacteria in the genital tract: are they related to adverse pregnancy outcome? Int J Immunopathol Pharmacol 26: 931-9.

This page is written by Louise Parker for the MICR3004 course, Semester 2, 2016