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Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
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Porphyromonas gingivalis disturbs host-commensal homeostasis by changing complement function.

Ingar Olsen1, John D Lambris2, George Hajishengallis3

  • 1Department of Oral Biology, Faculty of Dentistry, University of Oslo, Oslo, Norway.

Journal of Oral Microbiology
|July 28, 2017
PubMed
Summary

Porphyromonas gingivalis, a keystone pathogen, orchestrates complement-driven inflammation and oral dysbiosis. Animal models show it disrupts microbial balance, causing bone loss, but human relevance requires further study.

Keywords:
P. gingivalisanimal modelcommensal microbiotacomplementkeystone pathogenperiodontitis

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Area of Science:

  • Microbiology
  • Immunology
  • Oral Health

Background:

  • Porphyromonas gingivalis is a Gram-negative anaerobic rod implicated in dysbiotic inflammation.
  • Its role in manipulating complement-Toll-like receptor crosstalk has been observed in animal models.
  • P. gingivalis may act as a keystone pathogen, disproportionately impacting microbial communities.

Purpose of the Study:

  • To review the literature on Porphyromonas gingivalis's role in dysbiotic inflammation.
  • To discuss the extrapolation of findings from animal models to human health.
  • To evaluate P. gingivalis as a keystone pathogen in periodontal disease.

Main Methods:

  • Literature review of studies on Porphyromonas gingivalis and oral microbiota.
  • Analysis of animal models demonstrating P. gingivalis's effects on innate immunity and microbial composition.
  • Examination of the concept of keystone pathogens in the context of P. gingivalis.

Main Results:

  • P. gingivalis interferes with innate immunity at low colonization levels.
  • It alters oral commensal microbiota composition, leading to dysbiosis.
  • Dysbiosis disrupts host-microbial homeostasis and causes inflammatory bone loss in animal models.

Conclusions:

  • Porphyromonas gingivalis exhibits keystone pathogen characteristics.
  • Its capacity to orchestrate dysbiotic inflammation and bone loss is supported by animal studies.
  • Further research is needed to confirm the direct extrapolation of these findings to human periodontal disease.