Influence of adhesive system on quartz fiber post dislocation resistance in endodontically treated teeth

Aim: To evaluate the dislocation resistance of the quartz fiber post/cement/dentin interface after different adhesion strategies. Methods: Forty bovine lower central incisors were selected and prepared with K-files using the step-back technique, and irrigated with 3 mL of distilled water preceding the use of each instrument. Prepared teeth were stored at 37ºC and 100% humidity for 7 days. The roots were prepared and randomized into 4 groups. The quartz fiber post was cemented with an adhesion strategy according to the following groups: GBisCem- BISCEM; GOneStep±C&B- One Step ± C&B; GAllBond±C&B- AllBond3 ± C&B; GAllBondSE±C&B- AllBondSE ±C&B with a quartz fiber post. Cross-sectional root slices of 0.7 mm were produced and stored for 24 h at 37° C before being submitted to push-out bond strength. Results: The mean and standard deviation values of dislocation resistance were GBisCem: 1.12 (± 0.23) MPa, GOneStep±C&B: 0.81 (± 0.31) MPa, GAllBond±C&B: 0.98 (± 0.14) MPa, and GAllBondSE±C&B: 1.57 (± 0.04) MPa. GAllBondSE±C&B showed significantly higher values of dislocation resistance than the other groups. Conclusions: Based on this study design, it may be concluded that adhesion strategies showed different results of quartz post dislocation resistance. Simplified adhesive system with sodium benzene sulphinate incorporation provided superior dislocation resistance.

Sodium hypochlorite effects on dentin bond strength and acid-base resistant zone formation by adhesive systems

Aim: To evaluate the effects of 10% NaOCl gel application on the dentin bond strengths and morphology of resin-dentin interfaces formed by three adhesives. Methods: Two etch-and-rinse adhesives (One-Step Plus, Bisco Inc. and Clearfil Photo Bond, Kuraray Noritake Dental) and one self-etch adhesive (Clearfil SE Bond, Kuraray Noritake Dental) were applied on dentin according to the manufacturers’ instructions or after the treatment with 10% NaOCl (ED-Gel, Kuraray Noritake Dental) for 60 s. For interfacial analysis, specimens were subjected to acid-base challenge and observed by SEM to identify the formation of the acid-base resistant zone (ABRZ). For microtensile bond strength, the same groups were investigated and the restored teeth were thermocycled (5,000 cycles) or not before testing. Bond strength data were subjected to two-way ANOVA and Tukey’s test (p<0.05). Results: NaOCl application affected the bond strengths for One-Step Plus and Clearfil Photo Bond. Thermocycling reduced the bond strengths for Clearfil Photo Bond and Clearfil SE Bond when used after NaOCl application and One-Step Plus when used as recommended by manufacturer. ABRZ was observed adjacent to the hybrid layer for self-etch primer. The etch-and-rinse systems showed external lesions after acid-base challenge and no ABRZ formation when applied according to manufacturer’s instructions. Conclusions: 10% NaOCl changed the morphology of the bonding interfaces and its use with etch-&-rinse adhesives reduced the dentin bond strength. Formation of ABRZ was material-dependent and the interface morphologies were different among the tested materials.

Analysis of contributions of herpes simplex virus type 1 UL43 protein to induction of cell-cell fusion

Purpose: To investigate whether UL43 protein, which is highly conserved in alpha- and gamma herpes viruses, and a non-glycosylated transmembrane protein, is involved in virus entry and virus-induced cell fusion. Methods: Mutagenesis was accomplished by a markerless two-step Red recombination mutagenesis system implemented on the Herpes simplex virus 1 (HSV-1) bacterial artificial chromosome (BAC). Growth properties of HSV-1 UL43 mutants were analyzed using plaque morphology and one-step growth kinetics. SDS-PAGE and Western blot was employed to assay the synthesis of the viral glycoproteins. Virus-penetration was assayed to determine if UL43 protein is required for efficient virus entry. Results: Lack of UL43 expression resulted in significantly reduced plaque sizes of syncytial mutant viruses and inhibited cell fusion induced by gBΔ28 or gKsyn20 (p < 0.05). Deletion of UL43 did not affect overall expression levels of viral glycoproteins gB, gC, gD, and gH on HSV-1(F) BAC infected cell surfaces. Moreover, mutant viruses lacking UL43 gene exhibited slower kinetics of entry into Vero cells than the parental HSV-1(F) BAC. Conclusion: Thus, these results suggest an important role for UL43 protein in mediating virus-induced membrane fusion and efficient entry of virion into target cells.