» Articles » PMID: 22036469

Low-abundance Biofilm Species Orchestrates Inflammatory Periodontal Disease Through the Commensal Microbiota and Complement

Overview
Publisher Cell Press
Date 2011 Nov 1
PMID 22036469
Citations 569
Authors
Affiliations
Soon will be listed here.
Abstract

Porphyromonas gingivalis is a low-abundance oral anaerobic bacterium implicated in periodontitis, a polymicrobial inflammatory disease, and the associated systemic conditions. However, the mechanism by which P. gingivalis contributes to inflammation and disease has remained elusive. Here we show that P. gingivalis, at very low colonization levels, triggers changes to the amount and composition of the oral commensal microbiota leading to inflammatory periodontal bone loss. The commensal microbiota and complement were both required for P. gingivalis-induced bone loss, as germ-free mice or conventionally raised C3a and C5a receptor-deficient mice did not develop bone loss after inoculation with P. gingivalis. These findings demonstrate that a single, low-abundance species can disrupt host-microbial homeostasis to cause inflammatory disease. The identification and targeting of similar low-abundance pathogens with community-wide impact may be important for treating inflammatory diseases of polymicrobial etiology.

Citing Articles

Gum-on-a-Chip Exploring Host-Microbe Interactions: Periodontal Disease Modeling and Drug Discovery.

Hu Q, Acharya A, Shum H, Leung W, Pelekos G J Tissue Eng. 2025; 16:20417314251314356.

PMID: 40078219 PMC: 11898034. DOI: 10.1177/20417314251314356.


An in vitro model demonstrating homeostatic interactions between reconstructed human gingiva and a saliva-derived multispecies biofilm.

Shang L, Roffel S, Slomka V, DAgostino E, Metris A, Buijs M Microbiome. 2025; 13(1):58.

PMID: 40022258 PMC: 11869481. DOI: 10.1186/s40168-025-02033-w.


Dysbiosis of Oral Microbiome: A Key Player in Oral Carcinogenesis? A Critical Review.

Devaraja K, Aggarwal S Biomedicines. 2025; 13(2).

PMID: 40002861 PMC: 11852717. DOI: 10.3390/biomedicines13020448.


Underscoring long-term host-microbiome interactions in a physiologically relevant gingival tissue model.

Adelfio M, Callen G, Diaz A, Paster B, He X, Hasturk H NPJ Biofilms Microbiomes. 2025; 11(1):9.

PMID: 39789014 PMC: 11718163. DOI: 10.1038/s41522-024-00641-2.


The Effect of Oral Care Product Ingredients on Oral Pathogenic Bacteria Transcriptomics Through RNA-Seq.

Hu P, Xie S, Shi B, Tansky C, Circello B, Sagel P Microorganisms. 2025; 12(12.

PMID: 39770870 PMC: 11728304. DOI: 10.3390/microorganisms12122668.


References
1.
Hajishengallis G, Lambris J . Crosstalk pathways between Toll-like receptors and the complement system. Trends Immunol. 2010; 31(4):154-63. PMC: 2849859. DOI: 10.1016/j.it.2010.01.002. View

2.
Chaves E, Jeffcoat M, Ryerson C, Snyder B . Persistent bacterial colonization of Porphyromonas gingivalis, Prevotella intermedia, and Actinobacillus actinomycetemcomitans in periodontitis and its association with alveolar bone loss after 6 months of therapy. J Clin Periodontol. 2001; 27(12):897-903. DOI: 10.1034/j.1600-051x.2000.027012897.x. View

3.
Tonetti M, Imboden M, Lang N . Neutrophil migration into the gingival sulcus is associated with transepithelial gradients of interleukin-8 and ICAM-1. J Periodontol. 1998; 69(10):1139-47. DOI: 10.1902/jop.1998.69.10.1139. View

4.
Wang M, Shakhatreh M, James D, Liang S, Nishiyama S, Yoshimura F . Fimbrial proteins of porphyromonas gingivalis mediate in vivo virulence and exploit TLR2 and complement receptor 3 to persist in macrophages. J Immunol. 2007; 179(4):2349-58. DOI: 10.4049/jimmunol.179.4.2349. View

5.
Markiewski M, DeAngelis R, Benencia F, Ricklin-Lichtsteiner S, Koutoulaki A, Gerard C . Modulation of the antitumor immune response by complement. Nat Immunol. 2008; 9(11):1225-35. PMC: 2678913. DOI: 10.1038/ni.1655. View