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Porphyromonas Gingivalis: A Microbe Enigma

Porphyromonas gingivalis is able to use various deliberate mechanisms to resist, weaken, or manipulate host immune responses.

Despite the presence of more than 500 bacterial species in human subgingival biofilm, extensive study has shown that Porphyromonas gingivalis is the predominant etiologic bacterium contributing to chronic periodontitis.1,2 P. gingivalis is rightly termed the “keystone pathogen” because of its ability to use various deliberate mechanisms to resist, weaken, or manipulate host immune responses.3–5 P. gingivalis depends on the presence of other biofilm bacteria and the bacterial dysbiosis it initiates.

A groundbreaking study in germ-free mice inoculated with P. gingivalis demonstrated its inability to cause periodontitis alone. This research also highlighted the requirement of the intact complement system as part of host immune response in the development of P. gingivalis-induced disease. Mice without functioning C3a/C5a receptors were resistant to developing periodontitis, emphasizing the critical role of these complement signaling pathways and their required manipulation by P. gingivalis in periodontal diseases.6,7

Considering its many adaptive strategies to maintain virulence, P. gingivalis is truly a microbe enigma, much like the bacterium Helicobacter pylori found in the stomach and small intestine. Among its abilities to modify the microbiome’s environment are altering pH imbalances, rectifying oxygen stress, optimizing temperatures, and overcoming countless antagonistic antibacterial peptides and bacteriophages. Recent research into the genome sequencing of P. gingivalis revealed its use of various amino-acid catabolic pathways as an action to resist acidic pH stress in the microbiome. Following the digestion of amino acids, P. gingivalis generates ammonia as a byproduct, which can alter the microbiome from an acidic to neutral pH—ideal for cell proliferation.8

Modifying the functionality of the commensal environment through its virulence factors, P. gingivalis is capable of adapting to a rapidly shifting nutritional environment of “feast or famine” to ensure its nutritional demands for survival.8 As an inflammophilic and asaccharolytic organism, P. gingivalis amasses metabolic and nutritional needs of carbon and nitrogen by digesting peptide accretions from tissue-damaging metabolites, enzymes, and proinflammatory cytokines produced during host inflammation.3,8

P. gingivalis maintains a favorable inflammatory nutrient-rich environment by producing and utilizing its gingipain protease (Arg-gingipain); however, it can transition to using another protease (Lys-gingipain) to ameliorate the negative effects of too high an inflammatory response, highlighting the microbe’s adaptability to its environment.3,2


  1. How KY, Song KP, Chan KG. Porphyromonas gingivalis: an overview of periodontopathic pathogen below the gum line. Front Microbiol. 2016;7:53.
  2. Mei F, Xie M, Huang X, et al. Porphyromonas gingivalis and its systemic impact: current status. pathogens. 2020;9:944.
  3. Chopra A, Bhat SG, Sivaraman K. Porphyromonas gingivalis adopts intricate and unique molecular mechanisms to survive and persist within the host: a critical update. J Oral Microbiol. 2020;12:1801090.
  4. Moradali MF, Ghods S, Angelini TE, Davey ME. Amino acids as wetting agents: surface translocation by Porphyromonas gingivalis. ISME J. 2019;13:1560–1574.
  5. Bereta G, Goulas T, MadeJ M, et al. Structure, function, and inhibition of a genomic/​clinical variant of Porphyromonas gingivalis peptidylarginine deiminase. Protein Sci. 2019;28:478-486.
  6. Hajishengallis G, Liang S, Payne MA, et al. A low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and the complement pathway. Cell Host Microbe. 2011;10:497–506.
  7. Hajishengallis G, Lamont RJ. Breaking bad: manipulation of the host response by Porphyromonas gingivalis. Eur J Immunol. 2014;44:328–338.
  8. Nara PL, Sindelar D, Penn MS, Potempa J, Griffin WST. Porphyromonas gingivalis outer membrane vesicles as the major driver of and explanation for neuropathogenesis, the cholinergic hypothesis, iron dyshomeostasis, and salivary lactoferrin in Alzheimer’s disease. J Alzheimers Dis JAD. 2021;82:1417–1450.

This information originally appeared in Marsh I, Matthews A. The pathogenicity of Porphyromonas gingivalis. Dimensions of Dental Hygiene. 2022;20(10)34-37.

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