DIAN AGUSTIN WAHJUNINGRUM, 090810073 D (2013) PATOGENESIS MOLEKULAR RESORBSI TULANGALVEOLARIS PADA PERIODONTITIS APIKALIS AKIBAT INDUKSI LPS DALAM SALURAN AKAR GIGI TIKUS WISTAR. Disertasi thesis, UNIVERSITAS AIRLANGGA.

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Abstract

Background : Apical Periodontitis is a group of inflammatory diseases caused by microorganism/s (mainly bacteria) infecting the root canal system. Apical Periodontitis represent a local immune response to the progression of microorganisms from the dental pulp to the apical foramen that results in bone resorption. Porphyromonas gingivalis, an important endo-periodontal pathogen, is closely associated with inflammatory alveolar bone resorption. Several component of the organism such as lipopolysaccharide have an ability to stimulate production of cytokines such as IL-1, TNFα, TGF-β1 and MMP8 that promote in both inflammatory bone destruction or remodeling. TGF-β1 has been shown to play a critical role in anti-inflamation. MMP8 has been shown to play a critical role in pro-inflamation; however, the role of TGF-β1 and MMP8 in alveolaris bone resorbtion remains unclear. Pg LPS 1435/1450 induces cell activation via a TLR4 and TLR2. In which each of these, have a different capacity signaling in either apical and marginal periodontal. Evidence exist that Toll-like receptor (TLR) signaling regulates both inflammation and bone remodeling induced NFkB activation in Apical Periodontitis remains unclear. We investigate the expression and interaction of TLR2, TLR4, NFkB, IL-1, TNFα, TGF-β1and MMP8 in Apical Periodontitis. Method : True Experimental Design on 21 male Rat Wistar were conducted. Apical Periodontitis induced by intrapulpal injection LPS on first upper molar. Rats were randomized into three groups, 7 subject each. The first group (P1) received LPS 1μg, the second group (P2) received only aquades solution, the last group (P0) served as control group. Periapical tissue samples were taken after three week for each group. Analysis of cytokines expression using immunohistochemical method. Results : The data was analysis by Anova (SPSS 13.0), Tukey HSD and Regresion. Degree of confidence 95%. The results by statistic analysis were showed expressions TLR2, TLR4, NFkB, TNFα, IL-1β, TGFβ1 and MMP8 in group P1 were significantly different between group P2 p = 0,001*(p<0,05). Conclusion : These results suggest that macrophages are involved in both progression and resolution of Apical Periodontitis. Macrophage expressing MMP8 may play an important role in increasing the destructive mediators in periapical lesions. Macrophage expressing TGFβ1 may play an important role in reducing the destructive mediators in periapical lesions and in the activation of new bone formation during the healing process of apical periodontitis.This new fact may open new opportunity to treat root canal treatment with TGF-β1 to achieve better bone remodeling in alveolar bone resorbtion with Apical Periodontitis. Our finding reveal novel aspect of interactions between MMP8 and TGF-β1 and provide a new model for understanding the mechanism underlying the pathogenesis of bacteria-mediated bone loss.

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