Calcium Hydroxide Removal in Curved Root Canals with Apical Transportation In Vitro

Calcium hydroxide（CH） is applied to improve disinfection of root canals in most root canal retreatment. This study aimed to analyze the CH removal efficacy using 7 different root preparing files（K file, pre-curved K file, EndoActivator, Ultrasonic file, pre-curved ultrasonic file, F file and needle irrigation alone） with apical transportation. Standardized models of curved canal with such apical transportation or not were set up before applying CH to root canal for 7 days. Seven techniques described above were used for its removal. Then the roots were disassembled and digital photos were taken. The ratio of residual CH in the overall canal surface was calculated using the image analyzer image pro plus 6.0. The data were analyzed using one-way ANOVA with post hoc Tukey test. Results revealed that CH was effectively removed（P〈0.05） by using all 6 mechanical methods except irrigation alone. In curved root canals with apical transportation, EndoActivator, pre-curved ultrasonic file and F file were found to be more effective in removing CH than the other four file（P〈0.001）, while there was no significant difference among EndoActivator, pre-curved ultrasonic file and F file groups（P〉0.05）. The percentage of residual CH in the canal with apical transportation was higher than that in the canal without apical transportation（P〈0.05）. In conclusion, CH can be hardly removed completely. Canal with apical transportation will result in insufficient CH removal. EndoActivator, pre-curved ultrasonic file and F file are more effective in the curved root canal with apical transportation.

Effects of apical sodium-bile acid transporter inhibitor and obeticholic acid co-treatment in experimental non-alcoholic steatohepatitis

Background and aims:Several bile acids-based monotherapies have been developed for non-alcoholic steatohepatitis(NASH)treatment but clinical trial findings suggest that they do not satisfactorily improve NASH and liver fibrosis in many patients.Recently,we have shown that combining a gut-restricted apical sodium-bile acid transporter(ASBT)inhibitor GSK2330672(GSK)with adeno-associated virus(AAV)-mediated liver fibroblast growth factor 15(FGF15)overexpression provides significantly improved efficacy than either single treatment against NASH and liver fibrosis in a high fat,cholesterol,and fructose(HFCFr)diet-induced NASH mouse model.The beneficial effects of the com-bined treatment can be attributed to the markedly reduced bile acid pool that reduces liver bile acid burden and intestinal lipid absorption.The aim of this study is to further investigate if combining GSK treatment with the orally bioavailable obeticholic acid(OCA),which induces endogenous FGF15 and inhibits hepatic bile acid synthesis,can achieve similar anti-NASH effect as the GSKþAAV-FGF15 co-treatment in HFCFr-diet-fed mice.Materials and methods:Male C57BL/6J mice were fed HFCFr diet to induce NASH and liver fibrosis.The effect of GSK,OCA,and GSKþOCA treatments on NASH development was compared and contrasted among all groups.Results:Findings from this study showed that the GSKþOCA co-treatment did not cause persistent reduction of obesity over a 12-week treatment period.Neither single treatment nor the GSKþOCA co-treatment reduce hepatic steatosis,but all three treatments reduced hepatic inflammatory cytokines and fibrosis by a similar magnitude.The GSKþOCA co-treatment caused a higher degree of total bile acid pool reduction(~55%)than either GSK or OCA treatment alone.However,such bile acid pool reduction was insufficient to cause increased fecal lipid loss.The GSKþOCA co-treatment prevented GSK-mediated induction of hepatic cholesterol 7alpha-hydroxylase but failed to induce ileal FGF15 expression.GSK did not reduce gallbladder OCA amount in the GSKþOCA group compared to the OCA group,suggesting that ASBT inhibition does not reduce hepatic OCA distribution.Conclusions:Unlike the GSKþAAV-FGF15 co-treatment,the GSKþOCA co-treatment does not provide improved efficacy against NASH and liver fibrosis than either single treatment in mice.The lack of synergistic effect may be partly attributed to the moderate reduction of total bile acid pool and the lack of high level of FGF15 exposure as seen in the GSKþAAV-FGF15 co-treatment.