Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Feb 9:7:53.
doi: 10.3389/fmicb.2016.00053. eCollection 2016.

Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line

Kah Yan How  1 , Keang Peng Song  2 , Kok Gan Chan  1
Affiliations
Review

Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line

Kah Yan How et al. Front Microbiol. .

Abstract

Periodontal disease represents a group of oral inflammatory infections initiated by oral pathogens which exist as a complex biofilms on the tooth surface and cause destruction to tooth supporting tissues. The severity of this disease ranges from mild and reversible inflammation of the gingiva (gingivitis) to chronic destruction of connective tissues, the formation of periodontal pocket and ultimately result in loss of teeth. While human subgingival plaque harbors more than 500 bacterial species, considerable research has shown that Porphyromonas gingivalis, a Gram-negative anaerobic bacterium, is the major etiologic agent which contributes to chronic periodontitis. This black-pigmented bacterium produces a myriad of virulence factors that cause destruction to periodontal tissues either directly or indirectly by modulating the host inflammatory response. Here, this review provides an overview of P. gingivalis and how its virulence factors contribute to the pathogenesis with other microbiome consortium in oral cavity.

Keywords: Porphyromonas gingivalis; gingivitis; inflammatory response; oral pathogen; periodontal disease; virulence factors.

PubMed Disclaimer

Figures

FIGURE 1
FIGURE 1
A simplified representation showing the association of chronic periodontal inflammation and pathogenesis of cardiovascular disease. Adapted from Bartold and Narayanan (2006).
FIGURE 2
FIGURE 2
Black-pigmented colonies of periodontopathogen P. gingivalis on horse blood agar. The pigment is thought to be related to accumulation of hemin (oxidized form of heme) on the cell surface when grown on blood agar.
FIGURE 3
FIGURE 3
P. gingivalis manipulation of dendritic cell entry using minor fimbriae Mfa1 and accessory proteins. The adhesive properties of fimbriae allows P. gingivalis to evade host cells and escape the host immune surveillance. Adapted from Zenobia and Hajishengallis (2015).
FIGURE 4
FIGURE 4
Schematic structure of lipopolysaccharide (LPS) of the outer membrane of P. gingivalis. Adapted from Ogawa and Yagi (2010).
See this image and copyright information in PMC

References

    1. Aas J. A., Paster B. J., Stokes L. N., Olsen I., Dewhirst F. E. (2005). Defining the normal bacterial flora of the oral cavity. J. Clin. Microbiol. 43 5721–5732. 10.1128/JCM.43.11.5721-5732.2005 - DOI - PMC - PubMed
    1. Ali R. W., Velcescu C., Jivanescu M. C., Lofthus B., Skaug N. (1996). Prevalence of 6 putative periodontal pathogens in subgingival plaque samples from Romanian adult periodontitis patients. J. Clin. Periodontol. 23 133–139. 10.1111/j.1600-051X.1996.tb00546.x - DOI - PubMed
    1. Ali T., Abidin K. Z. (2012). Relationship of periodontal disease to pre-term low birth weight infants in a selected population–a prospective study. Community Dent. Health 29 100–105. - PubMed
    1. Al-Qutub M. N., Braham P. H., Karimi-Naser L. M., Liu X., Genco C. A., Darveau R. P. (2006). Hemin-dependent modulation of the lipid A structure of Porphyromonas gingivalis lipopolysaccharide. Infect. Immun. 74 4474–4485. 10.1128/IAI.01924-05 - DOI - PMC - PubMed
    1. Amano A. (2007). Disruption of epithelial barrier and impairment of cellular function by Porphyromonas gingivalis. Front. Biosci. 12:3965–3974. 10.2741/2363 - DOI - PubMed