Impact of infected and noninfected human dentine debris on bone healing in rats.

AIM: To evaluate in vivo the bone tissue response of rats to varying amounts of infected and noninfected dentine debris. METHODOLOGY: Bone tissue reactions were evaluated histologically in 42 Wistar rats after 7, 30 and 60 days. For each animal, three surgical cavities were prepared on the femur and filled with varying amounts (5, 10 or 20 mg) of infected or noninfected dentine debris pellets. In the negative control group, the surgical cavities were not filled. At the end of each experimental period, the animals were euthanized. The samples were processed histologically and analysed using a light microscope. The presence and the severity of inflammatory reaction, as well as hard tissue deposition were evaluated. Data were subjected to statistical analysis and the effects of the dependent variables calculated using nonparametric tests Kruskal-Wallis and Mann-Whitney U with due Bonferroni corrections at P = 0.05. RESULTS: At 7 days, the presence of infected debris significantly increased the histopathological scores for neutrophils (P < 0.05), and abscess formation (P < 0.05). Noninfected debris scored significantly higher for lymphocyte infiltrate compared with the control group and infected debris (P < 0.05). Both infected and noninfected debris equally triggered eosinophil cells compared with no-dentine (P < 0.05). As for giant cells and macrophages, no difference was detected amongst the dentine groups (P > 0.05). Hard tissue deposition was similar regardless of the presence or the bacteriological status of the dentine (P = 1.00). None of the above histopathological parameters was significantly influenced by the amount of debris (P > 0.05). For all parameters evaluated, at 7 days of analysis, the inflammatory response was significantly more intense compared with 30 and 60 days (P < 0.05). Inflammatory parameters were scored similarly for the evaluated groups after 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. CONCLUSION: The assumption that the amount of extruded debris may negatively affect the inflammatory response of bone tissue was not validated in the present in vivo animal study. Infected dentine may trigger acute inflammatory parameters especially during the first 7 days of contact with the tissue; however, in the long term, these negative effects are mitigated.

First phylogenetic analysis of dengue virus serotype 4 circulating in Espírito Santo state, Brazil, in 2013 and 2014.

The purpose of the present study was to reconstruct the phylogeny of dengue virus serotype 4 (DENV-4) that was circulating in Espírito Santo state, Brazil, in 2013 and 2014, and to discuss the epidemiological implications associated with this evolutionary hypothesis. Partial envelope gene of eight DENV-4 samples from Espírito Santo state were sequenced and aligned with 72 worldwide DENV-4 reference sequences from GenBank. A phylogenetic tree was reconstructed through Bayesian Inference and the Time of the Most Recent Common Ancestor was estimated. The study detected the circulation of DENV-4 genotype II in Espírito Santo state, which was closely related to strains from the states of Mato Grosso collected in 2012 and of São Paulo sampled in 2015. This cluster emerged around 2011, approximately 4 years after the entry of the genotype II in Brazil through its northern states, possibly imported from Venezuela and Colombia. This is so far the first phylogenetic study of the DENV-4 circulating in Espírito Santo state and shows the importance of an internal route of dengue viral circulation in Brazil to the introduction of the virus into this state.