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Cellular regulation of inflammatory processes in periodontal disease controlled by the ανβ6 integrin, a junctional epithelium cell receptor Nica, Daniela

Abstract

Periodontitis is an inflammatory disease caused by a combination of specific bacteria, host susceptibility and environmental factors. The sulcular and junctional epithelia act as the barrier for the plaque biofilm. Increased anaerobic pathogens are potent virulent factors that interact with the gingival epithelium inducing inflammatory cytokines including TGFβ. As an immunosuppressive cytokine, TGFβ acts as a growth inhibitor of the junctional epithelium. The latent form of TGFβ can be activated by άvβ6 integrin, a keratinocyte cell receptor found in the junctional epithelium (JE). In this study we have used a rat model of periodontitis induced by LPS and blocking antibodies for άcvβ6 integrin to manipulate the function of this integrin in order to observe its role in inflammation. Pocket epithelium formation was also investigated in a knock out (KO) mouse models for β6, TSP-1 and for both β6 and TSP-1. In the rat model, 24 animals were divided in four groups that were treated for 8 weeks. The experimental groups (n=6) were treated with blocking (6.3G9) or non-blocking (7.8B3) anti-β6 antibody and LPS. The control group was treated with pyrogen free water and one group was treated with LPS alone. Measurements of the junctional epithelium migration for area and length below the cementum enamel junction (CEJ) were quantified and compared statistically. Our findings showed that there was significant differences in JE migration between all rat treatment groups (ANOVA and Tukey test, p

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