The parallel induction of arthritis and experimental periodontitis with periopathogens (A. actinomycetemcomitans and P. gingivalis) in the inflammation-prone AIRmax mice resulted in a more severe phenotype: higher leukocyte infiltration, higher local levels of IL-1β, TNF-α, RANKL, IFN-γ, and IL-17, skewed T cell polarization toward Th1 and Th17, and more periodontal destruction. The gene discussed is IL17A; the disease is periodontitis.