The effects of dentin wetness on the bond strength and adhesive interface morphology of universal adhesives have been investigated using micro-tensile bond strength (μTBS) testing and confocal laser scanning microscopy (CLSM). Seventy-two human third molars were wet ground to expose flat dentin surfaces. They were divided into three groups according to the air-drying time of the dentin surfaces: 0 (without air drying), 5, and 10 s. The dentin surfaces were then treated with three universal adhesives: G-Premio Bond, Single Bond Universal, and All-Bond Universal in self-etch or etch-and-rinse mode. After composite build up, a μTBS test was performed. One additional tooth was prepared for each group by staining the adhesives with 0.01 wt % of Rhodamine B fluorescent dye for CLSM analysis. The data were analyzed statistically using ANOVA and Tukey’s post hoc tests (α = 0.05). Two-way ANOVA showed significant differences among the adhesive systems and dentin moisture conditions. An interaction effect was also observed (p < 0.05). One-way ANOVA showed that All-Bond Universal was the only material influenced by the wetness of the dentin surfaces. Wetness of the dentin surface is a factor influencing the micro-tensile bond strength of universal adhesives.

Significance: Synaptotagmin 1 (Syt1) is widely considered to act as the fast Ca ²⁺ sensor for synchronous synaptic vesicle fusion through its tandem Ca ²⁺ -binding C2 domains. Here we demonstrate that Syt1’s C2 domains activate rapid synchronous fusion only if they are in the proper orientation and specifically tethered to the synaptic vesicle with an appropriate linker distance. Although expression of the cytoplasmic C2 domains of Syt1 alone did not support fast synchronous release, it did enhance the asynchronous component of exocytosis. These findings demonstrate that synaptic vesicle tethering of Syt1 positions the protein to allow its C2 domains to regulate the kinetics of vesicle fusion.

Chemotherapy is not a first-line therapy for oral squamous cell carcinoma (OSCC), which is the most common type of oral cancer, because most OSCC shows resistance to chemotherapeutic reagents. Inflammatory signals are suggested to be associated with chemoresistance as well as carcinogenesis in many different cancers, and thus chronic periodontitis, the most common chronic inflammatory disease of the oral cavity, could modulate responsiveness to chemotherapeutic agents used against oral cancer. This study was performed to define the role of chronic periodontitis in oral cancer progression and to determine the responsiveness of oral cancer to a chemotherapeutic reagent. First, we quantified the tumor growth rate and changes in serum cytokine profiles of mice administered Porphyromonas gingivalis, a major pathogen of chronic periodontitis. Compared with uninfected mice, the mice that were chronically administered P. gingivalis showed increased resistance to paclitaxel and a decreased tumor growth rate. In addition, P. gingivalis-treated mice exhibited higher serum levels of interleukin-6 (IL-6) than uninfected mice. Furthermore, the sensitivity of tumor xenografts to paclitaxel in mice administered P. gingivalis was dramatically increased when the mice were administered ibuprofen, an anti-inflammatory drug which supports the modulatory effect of periodontal pathogen-induced inflammation in chemoresistance.

Sang Mee Park, Hae Ryoun Park, and Ji Hye Lee. Mol. Cells 2017;40:151-61. https://doi.org/10.14348/molcells.2017.2307

Sang Mee Park, J. Troy Littleton, Hae Ryoun Park and Ji Hye Lee. Exp Neurobiol 2016;25:33-9. https://doi.org/10.5607/en.2016.25.1.33