Resposta do tecido ósseo a debris de dentina infectados e não infectados

Abstract

In spite of the large number of in vitro studies demonstrating and quantifying the occurrence of apical extrusion with different endodontic preparation systems, there is no biological scientific evidence to confirm the influence of the amount and the infection of extruded debris on bone tissue response. Therefore, the objective of this study is to evaluate in vivo the bone tissue response to different amounts of infected and non-infected dentin debris. Bone tissue reactions were evaluated in 42 Wista rats after 7, 30, and 60 days For each animal, three surgical cavities were prepared on the right femur and filled with different amounts (5mg, 10mg or 20mg) of infected or non-infected dentin debris. In negative control group, the surgical cavities were kept unfilled. By the end of each experimental period, animals were randomly euthanized. The samples were histologically processed and analyzed using a light microscope. The presence and the severity of inflammatory reaction, as well as hard tissue deposition were evaluated. Data was analyzed statistically and effects of the dependent variables calculated using SPSS statistical software (version 20.0, SPSS, Inc., Chicago, USA) using non-parametric tests Kruskal Wallis and Mann-Whitney U with due Bonferroni correction at p=0.05. The presence of infected debris significantly raised the histopathological scores for neutrophils (P<0.05), and abscess formation (P<0.05). Non-infected debris scored significantly higher for the lymphocyte infiltrate compared to control group, and infected debris (P<0.05). Both infected and noninfected debris equally triggered eosinophil cells compared to no-dentine (P<0.05). As for giant cells and macrophages no difference was detected among the dentine groups (P>0.05). Initially, hard tissue deposition was similar regardless of the presence or the bacteriological status of the debris (P=1.00). None of the above histopathological parameters was significantly influenced by the amount of debris (P>0.05). For all parameters evaluated, after 7 days of analysis, the inflammatory response was significantly more intense compared to 30 and 60 days (P<0.05). However, hard tissue deposition has significantly increased after 30 days (P<0.05). No difference was seen between 30 and 60 days of analysis (P=1.00) for all histological parameters evaluated. In conclusion, the assumption that the amount of extruded debris may negatively affect the inflammatory response of bone tissue is not validated in the present in vivo animal study. Infected dentine debris may trigger acute inflammatory parameters especially along the first 7 days of contact with the tissue; however, in the long run these negative effects are mitigated.