Color and translucency of A2 shade resin composites after curing, polishing and thermocycling

This study determined the differences in values and changes of color and translucency of eight brands of A2 shade resin composites after curing, polishing and thermocycling (TC). The color of specimens 10-mm in diameter and 2-mm thick was measured on a reflection spectrophotometer with SCE geometry under D65 illumination over a white and black background. Measurements were obtained before curing, after curing, after polishing and after TC. The color change (deltaE*ab), translucency parameter (TP) and contrast ratio (CR) were then compared. The range of deltaE*ab after curing was 3.8 to 10.2 (average deltaE*ab for the eight composites = 6.4), which was deemed perceptible to the observer. Polishing caused deltaE*ab of 1.9 to 4.5, which was perceptible in five of the eight composites. After 2,000 TC, deltaE*ab was 0.4 to 1.3. TP values tended to increase after curing and decrease after TC (range before curing was 7.1 to 17.2). Changes in TP values after curing were statistically significant in all composites (p<0.05). Changes in CR values were similar to the translucency changes in TP. Though the composite shades were all designated as A2, color coordinates, TP and CR values, changes in color and translucency after curing, polishing and thermocycling varied by brand.     

Association between Second-hand Smoke Exposure and Urinary NNAL Level in Korean Adolescents

BackgroundThe 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) is a metabolite of tobacco-specific lung carcinogen that can be found in both smokers and non-smokers. Particularly, NNAL levels of children with a history of exposure to second-hand smoke (SHS) are higher than those of adults. Thus, we aimed to investigate the association between SHS exposure and urine NNAL levels in Korean adolescents.MethodsThis cross-sectional study used data from the Korea National Health and Nutrition Examination Survey VII. Overall, 648 never-smoking adolescents (425 boys and 223 girls) aged 12 to 18 were included in this study. Logistic regression analyses identified the relationship between SHS exposure and elevated urine NNAL levels.ResultsThe mean urine NNAL levels of the no exposure and exposure group in boys were 1.39 and 2.26 ng/mL, respectively, whereas they were 1.01 and 2.45 ng/mL in girls, respectively (P < 0.001). Among the adolescents exposed to SHS, the confounder-adjusted odds ratio (95% confidence intervals) for elevated urine NNAL levels according to exposure area as overall, home, and public area were 2.68 (1.58–4.53), 31.02 (9.46–101.74), and 1.89 (1.12–3.17) in boys; and 6.50 (3.22–13.11), 20.09 (7.08–57.04), and 3.94 (1.98–7.77) in girls, respectively.ConclusionSHS exposure was significantly associated with elevated urine NNAL levels in Korean adolescents, particularly in female adolescents and in those with home exposure. These findings remind us of the need to protect adolescents from SHS.     

Effects of N-acetylcysteine on TEGDMA- and HEMA-induced suppression of osteogenic differentiation of human osteosarcoma MG63 cells

Triethyleneglycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) are major resinous components of dental restorative materials and dentin bonding adhesives. Resin monomers are known to cause cytotoxicity in mammalian cells via oxidative stress and inhibit differentiation of dental pulp cells and osteoblasts. This study was aimed to investigate whether oxidative stress was involved in the inhibition of TEGDMA- and HEMA-induced differentiation. TEGDMA and HEMA reduced alkaline phosphatase (ALP) activity and the mRNA expression of the osteopontin (OPN) gene in MG63 cells at noncytotoxic concentrations. On the other hand, N-acetylcysteine (NAC) did not affect ALP activity at concentrations below 10 mM. Reduced ALP activity and OPN mRNA expression by TEGDMA were partially recovered via cotreatment with NAC. However, NAC did not exhibit significant effects in HEMA-treated cells. Glutathione (GSH) levels were also down-regulated by both TEGDMA and HEMA. The addition of NAC induced the partial recovery of GSH in cells treated with 0.5 mM TEGDMA. On the other hand, the levels of GSH in HEMA-treated cells were not affected by NAC. These results suggest that oxidative stress is involved in the suppression of differentiation by TEGDMA. Translocation of Nrf2 from the cytoplasm to the nucleus has been known to play a role in the suppression of osteogenic differentiation by oxidative stress. However, Nrf2 did not move into the nucleus in resin monomer-treated MG63 cells, suggesting the contribution of other signaling pathways to the suppressive effects of resin monomers.     

Changes of optical properties of dental nano-filled resin composites after curing and thermocycling

The objective was to evaluate the color changes after curing, polishing, and thermocycling of a nano-filled resin composite. A nano-filled composite was grouped into two shades of enamel (EN) and translucent (TL). One hybrid composite was used as a control (CL). Color of specimens of 10 mm in diameter and 2 mm in thickness was measured on a reflection spectrophotometer with SCE geometry under the D65 illumination over white and black backgrounds. Color before curing and after curing, polishing and thermocycling was measured. Color change (DeltaE(*) (ab)), translucency parameter (TP), and contrast ratio (CR) were compared. Average DeltaE(*) (ab) after curing was 4.6 in the EN group and 10.4 in the TL group compare to 2.9 in CL. Polishing caused average DeltaE(*) (ab) of 3.3-3.6, which was not different by the shade group (p > 0.05). After 2000 cycles of thermocycling, average DeltaE(*) (ab) was 1.4-1.8, which was not different by the shade group (p > 0.05). TP values increased after curing in the EN group, but decreased in the TL group (p < 0.05). TP values after thermocycling decreased in the EN group but did not change in TL (p = 0.05). TP values of TL shades were higher than those of EN regardless of specimen conditions (p < 0.05). Changes in CR values showed similar trends to those of TP values in translucency. Changes of color and translucency after curing, polishing, and thermocycling varied by the shade group.     

Effects of the iron-chelating agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity

Triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxylethyl methacrylate (HEMA) are known to deplete glutathione in mammalian cells, generate reactive oxygen species (ROS), and cause oxidative stress. In this study, we investigated whether hydroxyl radicals (·OH), the most lethal and genotoxic ROS, and the Fenton reaction are involved in the cytotoxicity of resin monomers to four different cell types, namely MC3T3-E1 preosteoblasts, human dental pulp cells (HDPCs), human gingival fibroblasts, and L929 mouse fibroblasts. Deferoxamine (DFO), an iron chelating agent, effectively protected MC3T3-E1 cells from resin monomer-induced cytotoxicity, indicating that cytotoxicity was caused primarily by hydroxyl radicals. However, DFO only had a protective effect against relatively high concentrations of TEGDMA and HEMA in HDPCs and human gingival fibroblasts, and resin monomer-induced cytotoxicity in L929 was not attenuated by DFO. A labile iron pool (LIP) was detectable only in MC3T3-E1 cells among the four cell types. This indicates that the generation of hydroxyl radicals induced by resin monomers is likely dependent on LIP levels. In contrast to resin monomers, hydrogen peroxide (H(2)O(2))-induced cytotoxicity was not prevented by DFO in any of the cell types examined, although hydroxyl radicals were detected in MC3T3-E1 cells and HDPCs on exposure to exogenous H(2)O(2). This result suggests that generation of hydroxyl radicals is not always the primary cause of cytotoxicity in H(2)O(2)-treated cells.     

Mechanisms of root canal sealers cytotoxicity on osteoblastic cell line MC3T3-E1.

OBJECTIVE: The cytotoxic mechanisms of root canal sealers (Sealapex, AH26, and N2 Universal) were studied in vitro with MC3T3-E1 osteoblastic cells. STUDY DESIGN: MC3T3-E1 cells were cotreated with root canal sealers and antioxidants, and concentrations of intracellular glutathione (GSH) and reactive oxygen species (ROS) were measured. DNA fragmentation was observed after treatment with the sealers. RESULTS: N-Acetylcysteine (NAC) prevented N2 Universal- and AH26-induced cytotoxicities. However, ascorbic acid and Trolox did not affect the cytotoxicity of the sealers. N2 Universal and AH26 significantly decreased the GSH pool within a 3-hour treatment period. Unlike GSH levels, the ROS levels were not altered by the sealers. Cytotoxicity of Sealapex was not affected by NAC, and there were no changes of GSH/glutathione disulfide levels in cells treated with Sealapex. CONCLUSION: Cytotoxicities of N2 Universal and AH26 are caused by an intracellular GSH depletion without a burst of ROS. Sealapex may cause cytotoxicity in a way different from N2 Universal and AH26.