Dysbiosis of the Oral Microbiota: Host Gene and Pathogen Effects

Objective: Previously, using the mouse model of periodontal disease, we demonstrated that oral gavage with Porphyromonas gingivalis leads to an increase in the oral microbial load and a qualitative change in the commensal microbiota. The resultant dysbiotic microbiota leads to accelerated alveolar bone loss. Similarly, we demonstrated that the oral microbiota is elevated in CXCR2^-/- mice defective in neutrophil homing. These mice also demonstrate accelerated bone loss. In this work we aimed to determine whether transfer of these dysbiotic microbiota into germ free mice would reproduce the disease phenotype in the recipient animals.

Method: P. gingivalis oral gavage was performed in 10 week old C3H mice. Transfer of the resultant dysbiotic microbiota was performed by co-caging with germ free C3H mice for 14days. Transfer of the dysbiotic microbiota of CXCR2^-/- mice into germ free mice was performed in an identical manner. The oral microbiota was assessed by culture and 16S rRNA cloning and sequencing. Bone loss was determined microscopically.

Results: Gavage with P. gingivalis caused an increase in the total microbial counts and a qualitative shift in composition. This dysbiotic microbiota was effectively transferred into germ free animals to a similar level and with a similar pattern of predominant species. Bone loss in these animals was accelerated to a similar degree as the original P. gingivalis-challenged mice. In contrast, only partial transfer of the oral microbiota of CXCR2^-/- mice into germ free wild type mice was observed and the recipient animals did not develop increased bone loss.   

Conclusions: Transfer of a dysbiotic microbiota caused by the introduction of a periodontal pathogen is accompanied by transfer of the disease phenotype. However, the dysbiotic microbiota present in the oral cavity of mice deficient in the innate response is not able to establish in wild type mice and does not cause periodontal bone loss.