This study examined the surface staining mechanism of a photopolymerized composite by coffee, oolong tea, and red wine.Dental composite was subjected to an experimental 24-hour staining cycle: 17-hour immersion in artificial saliva solution containing 0.3％ mucin followed by 7-hour immersion in coffee, tea, or wine. After one, two, and four weeks, digital images of the composite surface were analyzed in grayscale mode with an imaging analyzer. Specimens polished but not immersed were used as a baseline measurement for color change. Additionally, the effects of mechanical brushing and chlorhexidine on drink-induced staining were examined.Wine caused the most severe staining, followed by tea and coffee. After four weeks of immersion, brushing reduced surface staining by wine. On the contrary, chlorhexidine increased the staining effect of tea and coffee（p＜0.05）when compared to the control specimens. In conclusion, we showed that common drinks stained the dental composite, but each by a specific mechanism that depended on external conditions such as the presence of chlorhexidine.

Thioredoxin reductase (TrxR) reduces thioredoxin (Trx), thereby contributing to cellular redox balance, facilitating the synthesis of deoxy-ribose sugars for DNA synthesis, and regulating redox-sensitive gene expression. Auranofin is a gold compound that potently inhibits TrxR. This inhibition is one suspected mechanism of auranofin's therapeutic benefit in the treatment of rheumatoid arthritis. The use of other gold compounds to treat cancer or inflammatory disease may rely on their ability to inhibit TrxR. In the current study, we tested the hypothesis that a variety of gold compounds may inhibit TrxR.Methods: We exposed rat-TrxR1 to auranofin, gold sodium thiomalate, sodium aurothiosulfate, triphenyl phosphine gold chloride, or gold acetate, and measured TrxR activity ex-vivo. We then compared TrxR1 inhibitory levels of gold compounds to those that inhibited mitochondrial activity of THP1 monocytes and OSC2 epithelial cells, estimated by succinate dedhydrogenase activity.Results: All gold compounds inhibited TrxR1 at concentrations ranging from 5-4000 nM (50% inhibitory concentration). The oxidation state of gold did not correlate with inhibitory potency, but ligand configuration was important. Au(I)-phosphine compounds (triphenyl phosphine gold chloride and auranofin) were the most potent inhibitors of TrxR. All TrxR1 inhibitory concentrations were sublethal to mitochondrial activity in both THP1 and OSC2 cells. AbstractThioredoxin reductase (TrxR) reduces thioredoxin (Trx), thereby contributing to cellular redox balance, facilitating the synthesis of deoxy-ribose sugars for DNA synthesis, and regulating redox-sensitive gene expression. Auranofin is a gold compound that potently inhibits TrxR. This inhibition is one suspected mechanism of auranofin's therapeutic benefit in the treatment of rheumatoid arthritis. The use of other gold compounds to treat cancer or inflammatory disease may rely on their ability to inhibit TrxR. In the current study, we tested the hypothesis that a variety of gold compounds may inhibit TrxR.Methods: We exposed rat-TrxR1 to auranofin, gold sodium thiomalate, sodium aurothiosulfate, triphenyl phosphine gold chloride, or gold acetate, and measured TrxR activity ex-vivo. We then compared TrxR1 inhibitory levels of gold compounds to those that inhibited mitochondrial activity of THP1 monocytes and OSC2 epithelial cells, estimated by succinate dedhydrogenase activity.Results: All gold compounds inhibited TrxR1 at concentrations ranging from 5-4000 nM (50% inhibitory concentration). The oxidation state of gold did not correlate with inhibitory potency, but ligand configuration was important. Au(I)-phosphine compounds (triphenyl phosphine gold chloride and auranofin) were the most potent inhibitors of TrxR. All TrxR1 inhibitory concentrations were sublethal to mitochondrial activity in both THP1 and OSC2 cells.Conclusions: Diverse types of gold compounds may be effective inhibitors of TrxR1 at concentrations that do not suppress cellular mitochondrial function. Inhibition may ...

The purpose of this study was to evaluate the optical properties--not only the translucency but also the colours--of opaque-shade resin composites. The CIELAB parameters (L*, a* and b*) of disks of A2 and opaque A2 (OA2) shades of Charisma (Heraeus-Kulzer), Solare (GC) and Filtek Supreme (3M) were evaluated on backings of black, white and the material itself to calculate the translucency parameter (TP) and the colour differences (delta E*) between A2 and OA2. A two-way analysis of variance (anova) for the TP indicated a less statistically significant TP value in the OA2 shade than the A2 shade for all products. As for the products, Charisma showed a statistically greater TP value than the other two products. Regarding the delta E* between A2 and OA2, all the products revealed clinically perceptible colour differences (delta E* > 3.3). Hence, we must take the colour differences of opaque-shade resin composites into consideration, as well as the translucency of the materials, for a clinically acceptable colour match of the restoration.

This study evaluated the microtensile bond strength and the interfacial morphology of newer adhesives. The occlusal surfaces of extracted teeth were ground flat for random allocation to four equal groups. Resin composite was bonded to each surface using either Clearfil SE Bond [SEB], Clearfil Protect Bond [PB], G-Bond [GB], or an experimental adhesive, SSB-200 [SSB]. After storage for 24 h in water at 37 degrees C, they were sectioned into beams (cross-sectional area 1 mm(2)) for microtensile bond strength testing (muTBS) at a crosshead speed of 1 mm/min. The load at failure of each was recorded; the data were analyzed by one-way ANOVA and Games Howell tests. The surfaces of the fractured specimens were observed using SEM. For the ultra-morphology of the interface, the occlusal surfaces of four more teeth were prepared as before and a thin layer of flowable resin composite was bonded to each surface using one of the four adhesives. The mean muTBS ranged from 39.68 MPa (GB) to 64.97 MPa (SEB). There were no statistical differences between SEB and SSB, or between PB and GB (p > 0.05). The muTBS of SEB and SSB were significantly greater than that of PB and GB (p < 0.05). SEMs of the fractured surfaces revealed a mixed (cohesive/interfacial) failure. TEM examination highlighted differences in the hybrid layer; SEB had a thicker layer than the others. In conclusion, the newer all-in-one adhesives produced a thin hybrid layer but varied in their bond strengths. The 2-step self-etching adhesives do not necessarily produce higher bond strengths than that of the all-in-one systems.

SUMMARYObjective. This study evaluated color and translucency changes caused by light curing resin composite materials. Methods. The CIELAB parameters (L*, a* and b*) of disks of A2 and opaque A2 shades of Charisma (Heraeus-Kulzer), Solare (GC) and Filtek Supreme (3M) were evaluated on the backings of black, white and the material itself both before and after light curing to evaluate color and translucency changes (by means of calculating ∆ ∆E* and the translucency parameter, respectively). Results. Solare and Filtek Supreme showed significantly smaller color changes during light curing than Charisma; however, the value of ∆ ∆E* of all the products/shades was still in the clinically unacceptable range. Regarding translucency changes during light curing, the A2 and opaque A2 shades of Charisma showed a statistically significant increase, although no difference was observed in the other products. Conclusions. Solare and Filtek Supreme tended to show less changes in translucency and color during light curing compared to Charisma. Nevertheless, the changes in color during light curing were still in the range of unacceptable color change. Therefore, direct shade matching of these materials for a precise shade match should be performed by using the cured material.

Acknowledgement of Financial AssistanceThe authors thank the Medical College of Georgia and Ministry of Funding in Japan for seed funds to do this work. 2 SYNOPSISBlue light from dental photopolymerization devices has significant biological effects on cells.These effects may alter normal cell function of tissues exposed during placement of oral restorations, but, recent data suggest that some light-induced effects also may be therapeutically useful, for example in the treatment of epithelial cancers. Reactive oxygen species (ROS) appear to mediate blue light effects in cells, but the sources of ROS (intra-vs. extra-cellular) and their respective roles in the cellular response to blue light are not known. In the current study, we tested the hypothesis that intra-and extra-cellular sources of blue lightgenerated ROS synergize to depress mitochondrial function. Methods: Normal human epidermal keratinocytes (NHEK) and oral squamous cell carcinoma (OSC2) cells were exposed to blue light (380-500 nm; 5-60 J/cm 2 ) from a dental photopolymerization source (quartztungsten-halogen, 550 mW/cm 2 ). Light was applied in cell-culture media or balanced salt solutions with or without cells present. Intracellular ROS levels were estimated using the dihydrofluorescein diacetate (DFDA) assay; extracellular ROS levels were estimated using the leucocrystal violet assay. Cell response was estimated using the MTT mitochondrial activity assay. Results: Blue light increased intracellular ROS equally in both NHEK and OSC2. Blue light also increased ROS levels in cell-free MEM or salt solutions, and riboflavin supplements increased ROS formation. Extracellularly applied ROS rapidly (50-400 μM, < 1 min) increased intracellular ROS levels, which were higher and longer-lived in NHEK than OSC2. The type of cell-culture medium significantly affected the ability of blue light to suppress cellular mitochondrial activity; the greatest suppression was observed in DMEM-containing or NHEK media. Collectively, the data support our hypothesis that intra-and extracellularly generated ROS synergize to affect cellular mitochondrial suppression of tumor cells in response to blue light. However, the identity of blue light targets that mediate these changes remain unclear.These data support additional investigations into the risks of coincident exposure of tissues to blue light during material polymerization of restorative materials, and possible therapeutic 14,27,28 These data support a hypothesis that blue light induced-ROS mediate, at least in part, the suppression of mitochondrial function. However, the roles of intra-and extracellular sources of the ROS in causing blue light effects, a possible role for riboflavin or flavins in vitro in generating ROS, and the degree to which these two sources interact to cause cellular responses are unclear. In the current study, we show that both intra-and extra-cellular ROS are generated by blue light in epithelial cultures, and that both mediate blue light induced-mitochondrial responses. Our data support furthe...

The radical-scavenging antioxidants play an important role against oxidative stress in the defense system in vivo. The beneficial effects of antioxidants contained in foods and beverages have been well-accepted, and their antioxidant capacity has been assessed by various methods. In the present study, a simple method is proposed in which the total radical scavenging capacity is assessed from the bleaching of pyranine and pyrogallol red induced by free radicals generated from azo initiator. The total content of antioxidants contained in red wine, green tea, and cassis drink and their reactivities toward peroxyl radicals were measured from the lag phase and rate of bleaching using pyranine and pyrogallol red as a probe, respectively. It was found that this method to follow the bleaching of two probes by visible light spectrophotometer is convenient and applicable for assessment of total radical scavenging capacity of both content and activity of the antioxidants contained in beverages.

The role of radical scavenging antioxidants against oxidative stress has received much attention, and the antioxidant capacity has been assessed by various methods. Among them, a method that measures the effect of antioxidant on decay of the probe is one of the most widely used methods. The present study was performed to compare the two methods to assess the antioxidant capacity, one to follow the decay of the probe and the other to measure lipid peroxidation products in human plasma. It was shown that the method following probe decay was suitable for assessment of radical scavenging capacity of antioxidant, but not for the capacity to inhibit lipid peroxidation in plasma. This is true whether a hydrophilic or lipophilic probe is used. Such different results arise from the fact that the efficacy of inhibition of lipid peroxidation by antioxidants depends on the fate of antioxidant-derived radical and interaction between antioxidants as well as the capacity of free radical scavenging. Thus, the capacity of antioxidants for inhibition of lipid peroxidation should be assessed from the effect on the extent of oxidation, not from the effect on probe decay.