Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology
Open accessAbstract
Summary: Recent advancements in the periodontal research field are consistent with a new model of pathogenesis according to which periodontitis is initiated by a synergistic and dysbiotic microbial community rather than by select ‘periopathogens’, such as the ‘red complex’. In this polymicrobial synergy, different members or specific gene combinations within the community fulfill distinct roles that converge to shape and stabilize a disease‐provoking microbiota. One of the core requirements for a potentially pathogenic community to arise involves the capacity of certain species, termed ‘keystone pathogens’, to modulate the host response in ways that impair immune surveillance and tip the balance from homeostasis to dysbiosis. Keystone pathogens also elevate the virulence of the entire microbial community through interactive communication with accessory pathogens. Other important core functions for pathogenicity require the expression of diverse molecules (e.g. appropriate adhesins, cognate receptors, proteolytic enzymes and proinflammatory surface structures/ligands), which in combination act as community virulence factors to nutritionally sustain a heterotypic, compatible and proinflammatory microbial community that elicits a non‐resolving and tissue‐destructive host response. On the basis of the fundamental concepts underlying this model of periodontal pathogenesis, that is, p olymicrobial s ynergy and d ysbiosis, we term it the PSD model.
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Key species in oral biofilm are recognized as etiological agents in the development of periodontal disease, including the red complex bacteria T forsythia, Treponema denticola, and P gingivalis, which drive periodontal disease pathogenesis by orchestrating restructure of the microbiota and promoting inflammation.
“Key species in oral biofilm are recognized as etiological agents in the development of periodontal disease: these species include the red complex bacteria—T forsythia, Treponema denticola, and P gingivalis—that exhibit the capacity to drive the processes involved in periodontal disease pathogenesis by orchestrating restructure of the microbiota and promoting inflammation.178”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [178]
States of oral disease are induced by dysbiosis of the oral microbiome.
“Conversely, states of oral disease are induced by dysbiosis of the oral microbiome.178, 179”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [178]
Such interactions demonstrate the role of microbial interactions in promoting disease via multifaceted physical and metabolic interactions that are the cornerstone of the polymicrobial synergy and dysbiosis model.
“Such interactions demonstrate the role of microbial interactions in promoting disease via multifaceted physical and metabolic interactions that are the cornerstone of the polymicrobial synergy and dysbiosis model.178”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [178]
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<i>Filifactor alocis</i> : Recent Insights and Advances
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- Authors
- Hajishengallis, G., & Lamont, R. J.
- Affiliations
- University of Pennsylvania (US)
- University of Louisville (US)
- Corresponding author
- Hajishengallis, G.
- Venue
- Molecular Oral Microbiology
- Publisher
- Wiley
- Published
- 2012-09-03
- Volume
- 27
- Issue
- 6
- Pages
- 409-419
- ISSN
- 2041-1006 (ISSN-L)
- 2041-1014
- PMC
- PMC3653317
- OpenAlex
- W2074150122
- Cited by
- 1,267
- References
- 97
- Citations by year
- 2026: 121 · 2025: 96 · 2024: 125 · 2023: 102 · 2022: 111 · 2021: 134 · 2020: 102 · 2019: 103 · 2018: 78 · 2017: 86 · 2016: 65 · 2015: 64 · 2014: 51 · 2013: 23 · 2012: 3
- FWCI
- 8.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Oral Microbiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Fonds pour la Formation à la Recherche dans l’Industrie et dans l’Agriculture
- National Institute of Dental and Craniofacial Research (R01DE018292, DE17138, R01DE015254, R01DE017921, DE 11111, R37DE011111, DE18292, DE21685, DE16690, DE12505, R21DE022867, RC4DE021580, DE22867, R01DE016690, R01DE021685, R01DE017138, DE15254, DE21580, R01DE012505, R01DE011111, DE17921)
- Topics
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacterial biofilms and quorum sensing
- Health Sciences › Medicine › Urology › Periodontal Regeneration and Treatments
- Keywords
- periodontitis, periodontal disease etiology, dysbiosis, red complex, host immune response, host-pathogen interaction, periodontal microbiota
- MeSH terms
- Bacteria, Humans, Periodontitis, Symbiosis, Virulence, Inflammation Mediators, Host-Pathogen Interactions, Immune Evasion, Microbial Consortia
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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