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Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology
Author(s) -
Hajishengallis G.,
Lamont R.J.
Publication year - 2012
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/j.2041-1014.2012.00663.x
Subject(s) - dysbiosis , porphyromonas gingivalis , virulence , biology , bacterial adhesin , proinflammatory cytokine , pathogenesis , immune system , immunology , microbiology and biotechnology , periodontitis , computational biology , gut flora , genetics , gene , inflammation , medicine , bacteria
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.