Effects of Green Tea Application Time on Bond Strength after Enamel Bleaching

This study evaluated the effect of green tea application time on the bond strength of enamel after enamel bleaching. Enamel samples were obtained from 80 third molars and randomly divided into 7 experimental groups (G1-G7) and 1 group without treatment (G8): G1, bleached with 10% carbamide peroxide (CP); G2, CP + 10% sodium ascorbate gel (SA) for 15 min; G3, CP + SA for 30 min; G4, CP + SA for 60 min; G5, CP + 10% green tea gel (GT) for 15 min; G6, CP + GT for 30 min; G7, CP + GT for 60 min. The CP was applied onto the enamel surface for 8 h for 14 days. The SA was applied in groups 2, 3 and 4, and the GT was applied in groups 5-8 according to the above described application times. Immediately after treatment, the specimens were bonded with Adper Single Bond 2 and Filtek Z350XT. The specimens were prepared to microtensile bond strength analysis. Fracture mode analysis was performed using a stereoscopic loupe. The data were statistically analyzed by two-way analysis of variance, the Tukey's and Dunnett's tests (=5%). The means (standard deviation) were: G1, 23.3 (3.2); G2, 25.2 (3.9); G3, 26.4 (5.4); G4, 30.2 (4.5); G5, 26.6 (3.4); G6, 22.0 (5.4); G7, 31.4 (3.3); G8, 31.4 (3.2). All groups had a high percentage of adhesive failures. In conclusion, the bond strength values were higher than the value in the bleached group only when the antioxidants were applied for 60 min.

Este estudo avaliou o efeito do tempo de aplicação do chá verde na resistência de união do esmalte após o clareamento. Amostras de esmalte foram obtidas a partir de 70 terceiros molares e aleatoriamente divididas em 7 grupos experimentais (G1-G7) e um grupo sem tratamento (G8). Os 7 grupos experimentais foram tratados como segue: G1, clareado com peróxido de carbamida a 10% (PC); G2, PC + gel de ascorbato de sódio a 10% (AS) por 15 min; G3, PC + AS por 30 min; G4, PC + AS por 60 min; G5, PC + gel de chá verde a 10% (CV) por 15 min; G6, PC + CV por 30 min; G7, PC + CV por 60 min. O PC foi aplicado na superfície do esmalte por 8 h, durante 14 dias. O AS foi aplicado nos grupos 2, 3 e 4 e o CV foi aplicado nos grupos 5, 6 e 7 de acordo com os tempos de aplicação descritos acima. Imediatamente após o tratamento, foi realizado o procedimento adesivo utilizando Adper Single Bond 2 e Filtek Z350XT. Em seguida, as amostras foram preparadas para o teste de microtração. A análise do padrão de fratura foi realizada em lupa estereoscópica. Os dados foram analisados através de ANOVA (2 fatores), testes de Tukey e Dunnett (α=5%). As médias (desvio padrão) foram: G1: 23,29 (3,20); G2: 25,18 (3,95); G3: 26,41 (5,40); G4: 30,17 (4,46); G5: 26,63 (3,43); G6: 22,02 (5,41); G7: 31,40 (3,35); G8: 31,4 (3,2). Todos os grupos apresentaram maior porcentagem de falhas adesivas. Em conclusão, os valores de resistência de união foram maiores que os dos grupos clareados somente quando os antioxidantes foram aplicados por 60 min.

Hfe mutations add iron overload in patients with alcoholic liver disease

Context Alcoholic liver disease (ALD) is generally associated with iron overload, which may contribute to its pathogenesis, through increased oxidative stress and cellular damage. There are conflicting reports in literature about hemochromatosis (HFE) gene mutations and the severity of liver disease in alcoholic patients. Objectives To compare the prevalence of mutations in the hemochromatosis (HFE) gene between patients with ALD and healthy controls; to assess the relation of HFE mutations with liver iron stores and liver disease severity. Methods Liver biopsy specimens were obtained from 63 ALD patients (during routine treatment) and 52 healthy controls (during elective cholecystectomy). All individuals underwent routine liver function tests and HFE genotyping (to detect wild-type sequences and C282Y, H63D, S65C, E168Q, E168X, V59M, H63H, P160delC, Q127H, Q283P, V53M and W164X mutations). Associations between HFE mutations and risk of excessive liver iron stores, abnormal serum ferritin, liver fibrosis, or necroinflammatory activity were assessed by multivariate logistic regression analysis. Results ALD patients had significantly higher serum ferritin and transferrin saturation than controls (both P<0.05), but the distribution of HFE mutations was similar between the two groups. For ALD patients, the odds ratio for having at least one HFE mutation and excessive liver iron stores was 17.23 (95% confidence interval (CI): 2.09-142.34, P = 0.008). However, the presence of at least one HFE mutation was not associated with an increased risk of liver fibrosis or necroinflammatory activity. Active alcohol ingestion showed the strongest association to increased serum ferritin (OR = 8.87, 95% CI: 2.11-34.78, P = 0.003). Conclusions ALD patients do not present with a differential profile of HFE mutations from healthy controls. In ALD patients, however, ...

Contexto A doença hepática alcoólica (DHA) está geralmente associada à sobrecarga de ferro, que pode contribuir para a sua patogênese, através do aumento do estresse oxidativo e dano celular. As descrições existentes na literatura sobre a associação entre mutações HFE e a gravidade da DHA nem sempre são concordantes. Objetivos Comparar a prevalência de mutações HFE entre um grupo de pacientes com DHA e uma população de controle. Avaliar a relação entre mutações HFE e os depósitos de ferro hepático. Avaliar se a presença dessas mutações está associada com a gravidade da DHA. Métodos Compararam-se 63 pacientes com DHA que efetuaram biopsia hepática com 52 controles saudáveis. A genotipagem HFE (wild type, C282Y, H63D, S65C, E168Q, E168X, V59M, H63H, P160delC, Q127H, Q283P, V53M, W164X) e uma avaliação laboratorial de rotina (incluindo cinética do ferro) foram feitos em todos os indivíduos. Realizou-se regressão logística multivariada nos casos para avaliar se a presença de mutações HFE estava relacionada com risco aumentado de depósitos de ferro hepático aumentados, ferritina sérica anormal, fibrose hepática significativa ou atividade necroinflamatória. Resultados Os pacientes apresentaram ferritina sérica e saturação da transferrina mais elevadas que os controles, mas não existiram diferenças significativas na distribuição de mutações HFE entre pacientes e controles. Considerando apenas os pacientes, o risco relativo de estes apresentarem pelo menos uma mutação HFE e depósitos de ferro hepático significativos foi de 17.23 (CI 95% 2.09-142.34, P = 0.008). Contudo, a presença ...

Alcohol induced liver disease: from molecular damage to treatment

Although the interaction between alcohol and the liver has been the subject of intensive investigation since many years, several uncertainties remain to be solved. Good examples of what we need to learn are: The real number of patients with alcohol-induced liver disease (AILD), the dose of alcohol "safe" for the liver, the genetic predisposition to the damage or, on the other side of the coin, protecting from the damage. Rather recently, however, part of these questions started to be clarified, thus permitting a better definition of the role of each of these factors in AILD. In parallel to the clinical approach to AILD, the unveiling of the molecular and biochemical mechanisms involved in AILD has progressed and proved to be important in both a better understanding of the disease and, more important, in a more rational treatment of these disorders. This review will focus on what we currently know of AILD in clinical, biochemical and molecular terms and what we need to address in the future