Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology

By G. Hajishengallis, R. J. Lamont. Molecular Oral Microbiology, 2012

1,157 citations recorded by the source corpus.

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, polymicrobial synergy and dysbiosis, we term it the PSD model.

Subfields: Molecular Biology, Periodontics, Physiology

View Paper: https://www.semanticscholar.org/paper/7682a4e6bd010b3fc06d8f0bebd619f2232e0195

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In Molecular Biology

1. Sweta Paliwal
2. S. Ivanovski
3. S. Hienz

In Periodontics

1. Sweta Paliwal
2. S. Ivanovski
3. S. Hienz

Citations in the corpus

• Mechanisms of Bone Resorption in Periodontitis (2015, background): “Recent developments in the area of biological processes and mediators of osteoclast differentiation and activity have expanded our knowledge of resorption processes and set the stage for new diagnostic and therapeutic modalities to treat situations of localized bone loss as seen in periodontal disea”