LAUSR

&NA; It has been demonstrated that periodontitis, a chronic oral disease, can induce systemic inflammation which is associated with systemic diseases, including rheumatoid arthritis. Here, we evaluated whether periodontitis can modulate the inflammatory response at a site distant to the oral cavity. Wistar rats were subjected to ligature‐induced experimental periodontitis. Fourteen days after the procedure, paw edema was induced by carrageenan or by different receptor‐specific inflammatory mediators. Blood and the tissue of the paws were obtained for TNF‐&agr; and IL‐1&bgr; measurement. It was observed that carrageenan‐induced paw edema and leukocyte migration was potentiated in periodontitis animals. The edema induced by carrageenan, bradykinin and des‐Arg9‐BK (B1 agonist) was also potentiated in periodontitis animals and blocked by a B1 antagonist. Ligature‐induced periodontitis increased plasma levels of TNF‐&agr; and tissue IL‐1&bgr;. Periodontitis also up‐regulated kinin B1 receptor expression in paw tissue. Additionally, the treatment of ligature animals with anti‐TNF‐&agr;, etanercept, completely abolished the potentiation of edema induced by des‐Arg9‐BK. Taken together, these results show that experimental periodontitis in rats can induce systemic inflammation through the up‐regulation of kinin B1 receptors at a site distant from the oral cavity, modifying the inflammatory response. Graphical abstract: The experimental periodontitis in rats can induce systemic inflammation and up‐regulate B1 receptors in the rat paw, modifying the inflammatory response at a site distant from oral infection. Figure. No caption available.