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

It has been demonstrated that periodontitis can induce systemic inflammation. In this study we evaluated whether periodontitis can modulate the inflammatory response at a site distant to oral cavity. Wistar rats were subjected to ligature-induced experimental periodontitis. Fourteen days after procedure, paw edema was induced by carrageenan or by different receptor-specific inflammatory mediators. Blood and tissue of the paws were obtained for TNF-α and IL-1β 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 was also potentiated in periodontitis animals. Periodontitis increased plasma levels of TNF-α, tissue IL-1β and also up-regulated kinin B1 receptor expression in paw tissue. Treatment with anti-TNF-α, etanercept, abolished the edema induced by des-Arg9-BK. 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.