Experimental periodontitis in rats potentiates inflammation at a distant site: Role of B1 kinin receptor

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-alpha and IL-1 beta 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-Arg(9)-BK (B-1 agonist) was also potentiated in periodontitis animals and blocked by a B-1 antagonist. Ligature-induced periodontitis increased plasma levels of TNF-alpha and tissue IL-1 beta. Periodontitis also up-regulated kinin B-1 receptor expression in paw tissue. Additionally, the treatment of ligature animals with anti-TNF-alpha, etanercept, completely abolished the potentiation of edema induced by des-Arg(9)-BK. Taken together, these results show that experimental periodontitis in rats can induce systemic inflammation through the up-regulation of kinin B-1 receptors at a site distant from the oral cavity, modifying the inflammatory response.