Our data demonstrate that mice infected with P. gingivalis displayed increased Th17-driven responses in the serum via IL-17 and IFNγ, reactivated splenocytes via IL-1β, IL-6, TNFα, transforming growth factor beta (TGF-β), and IL-23, increased osteoclast numbers in the joints, and enhanced arthritis progression and development. The gene discussed is IL17A; the disease is arthritic joint disease.