Pathogenicity Requires TLR2 and the Oral Microbiome.

Abstract

Enrichment of the oral microorganismis strongly associated with the progression of periodontitis. However,is part of a complex dysbiotic microbial community, and the organism's direct pathogenic potential remains uncharacterized. Using the oral gavage model of experimental periodontitis, we revealed thatpromotes alveolar bone loss, as well as significant overexpression of proinflammatory markers associated with osteoclastogenesis and inflammation in oral tissues. Interestingly, despite colonizing in low abundance,infection promoted the perturbation of the homeostatic oral microbial community toward a dysbiotic state. Systemically, high levels of proinflammatory cytokines, chemokines, and antibody titers againstwere detected in the sera of infected animals. Germ-free mice or TLR2-deficient mice did not develop alveolar bone loss when infected with, demonstrating that the commensal microbial community and the presence of TLR2 are required forto display its pathogenic potential. These findings identifyas an oral pathogen that can disrupt the homeostatic relationship between the host and the oral microbiome, causing inflammation and alveolar bone resorption. Our findings provide novel insights into the pathogenic potential ofin periodontitis.