Role of experimental periodontitis in inducing pulmonary inflammation in mice.

Abstract

The aim of the study was to explore the potential role of experimental periodontitis in pulmonary inflammation in mice. Mice were divided into control, ligature-induced periodontitis (L) and ligature plus Porphyromonas gingivalis (P. gingivalis)-induced periodontitis (LPG) groups. Alveolar bone resorption, pulmonary function, lung tissue histology and cytokine expression were examined at 2, 4 and 8weeks. Then cytokines and neutrophils in the peripheral blood and lung tissue were further assessed at 8weeks to determine the role of cytokines induced by LPG periodontitis, and the effect of P. gingivalis was evaluated using P. gingivalis-IgG and P. gingivalis gingipain. Alveolar bone resorption was more severe in the L and LPG groups. However, pulmonary inflammation was observed only in the LPG group at 8weeks when cytokines and neutrophils in the peripheral blood and lung tissue were the most significant elevation, along with higher levels of P. gingivalis-IgG and P. gingivalis gingipain. Cytokine levels were also increased in the gingival tissue, peripheral blood and lung tissue in the L group, accompanied by elevated peripheral blood neutrophils, but not as significantly as that in the LPG group. LPG periodontitis can trigger pulmonary inflammation over the long term, in which cytokines and P. gingivalis play an important role.