Document Detail


Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology.
MedLine Citation:
PMID:  23134607     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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, polymicrobial synergy and dysbiosis, we term it the PSD model.
Authors:
G Hajishengallis; R J Lamont
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2012-09-03
Journal Detail:
Title:  Molecular oral microbiology     Volume:  27     ISSN:  2041-1014     ISO Abbreviation:  Mol Oral Microbiol     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-08     Completed Date:  2013-12-11     Revised Date:  2014-02-17    
Medline Journal Info:
Nlm Unique ID:  101524770     Medline TA:  Mol Oral Microbiol     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  409-19     Citation Subset:  D    
Copyright Information:
© 2012 John Wiley & Sons A/S.
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MeSH Terms
Descriptor/Qualifier:
Bacteria / immunology,  pathogenicity
Host-Pathogen Interactions / physiology
Humans
Immune Evasion / immunology,  physiology
Inflammation Mediators / immunology
Microbial Consortia / physiology*
Periodontitis / immunology,  microbiology*
Symbiosis / physiology*
Virulence / physiology
Grant Support
ID/Acronym/Agency:
DE11111/DE/NIDCR NIH HHS; DE12505/DE/NIDCR NIH HHS; DE15254/DE/NIDCR NIH HHS; DE16690/DE/NIDCR NIH HHS; DE17138/DE/NIDCR NIH HHS; DE17921/DE/NIDCR NIH HHS; DE18292/DE/NIDCR NIH HHS; DE21580/DE/NIDCR NIH HHS; DE21685/DE/NIDCR NIH HHS; DE22867/DE/NIDCR NIH HHS; R01 DE011111/DE/NIDCR NIH HHS; R01 DE012505/DE/NIDCR NIH HHS; R01 DE015254/DE/NIDCR NIH HHS; R01 DE016690/DE/NIDCR NIH HHS; R01 DE017138/DE/NIDCR NIH HHS; R01 DE017921/DE/NIDCR NIH HHS; R01 DE018292/DE/NIDCR NIH HHS; R01 DE021685/DE/NIDCR NIH HHS; R21 DE022867/DE/NIDCR NIH HHS; R37 DE011111/DE/NIDCR NIH HHS; RC4 DE021580/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Inflammation Mediators
Comments/Corrections

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