Periodontitis is a polymicrobial oral
infection characterized by the destruction of tooth-supporting structures that can be linked to systemic diseases such as
cardiovascular disease, diabetes or
rheumatoid arthritis. Porphyromonas gingivalis, a bacterium implicated in the etiology of
periodontitis, has shown variation in inducing T-cell responses among different strains. Therefore, in this study we investigated the strain-specific immune response using a murine experimental model of
periodontitis.
Periodontitis was induced by P. gingivalis strains A7A1-28, W83 and W50, and later confirmed by the presence of P. gingivalis in the oral microflora and by alveolar
bone resorption. Splenocytes were evaluated for gene expression, cellular
proteins and
cytokine expression. Dendritic cells were stimulated in vitro for T helper cell-
cytokine profiling. Results showed that P. gingivalis had the ability to alter the systemic immune response after bacterial exposure. Strains W50 and W83 were shown to induce
alveolar bone loss, whereas the A7A1-28 strain did not significantly promote
bone resorption in mice. Splenocytes derived from mice infected with strains W50 and W83 induced expression of high levels of
interleukin-4 (IL-4) but A7A1-28 stimulated increased
IL-10. Stimulation of dendritic cells in vitro showed a similar pattern of
cytokine expression of
IL-12p40,
IL-6 and
transforming growth factor-β among strains. A distinct systemic response in vivo was observed among different strains of P. gingivalis, with
IL-10 associated with the least amount of
alveolar bone loss. Evaluation of pathogen-driven systemic immune responses associated with
periodontal disease pathogenesis may assist in defining how
periodontitis may impact other diseases.