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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: Mol Oral Microbiol. 2012 Sep 3;27(6):409–419. doi: 10.1111/j.2041-1014.2012.00663.x

Figure 1.

Figure 1

The polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology. The gingival crevice is colonized by a diverse microbiota, and compatible organisms assemble into heterotypic communities. These communities are in equilibrium with the host. Although they are proinflammatory and can produce toxic products such as proteases, overgrowth and overt pathogenicity are controlled by the host. The microbial constituents of the communities can vary over time, and from person to person and site to site. Colonization by keystone pathogens such as Porphyromonas gingivalis elevates the virulence of the entire community following interactive communication with accessory pathogens such as mitis group streptococci. Host immune surveillance is impaired and the dysbiotic community increases in number eventually disrupting tissue homeostasis and causing destruction of periodontal tissues.