It is thought that externally applied bleaching agents may penetrate into the pulp chamber. This study was conducted to evaluate the diffusion of peroxide bleaching agents into the pulp chamber of teeth restored with various restorative materials. Sixty-five human extracted anterior maxillary teeth were separated into the 13 groups containing 5 teeth. Five teeth (control group) were not subjected to any cavity preparation and restoration. Standardized class V cavities were prepared in the other 60 teeth and restored using composite resin (Charisma), polyacid modified composite resin (Dyract), or resin-modified glass ionomer cement (Vitremer). All teeth were sectioned 3 mm apical to the cementoenamel junction to remove the intracoronal pulp tissue, and the pulp chamber was filled with acetate buffer to absorb and stabilize any peroxide that might penetrate. Vestibular crown surfaces of teeth in the experimental groups were subjected to four different bleaching agents for 30 min at 37 degrees C, whereas the teeth in the control groups were exposed only to distilled water. Then the acetate buffer solution in the pulp chamber of each tooth was removed, and the pulp chamber of each tooth was rinsed with 100 ml of distilled water twice. Leukocrystal violet and enzyme horseradish peroxidase were added to the mixture of the acetate buffer and rinse water. The optical density of the resulting blue solution was determined spectrophotometrically and converted into microgram equivalents of hydrogen peroxide. Higher hydrogen peroxide concentrations resulted in a higher pulpal peroxide penetration. The highest pulpal peroxide penetration was found in resin-modified glass ionomer cement groups, whereas composite resin groups showed the lowest pulpal peroxide penetration.

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This in vitro study was performed to evaluate the effect of various concentrations of carbamide peroxide bleaching agents on the pulp chambers of teeth restored by a composite resin. Forty-nine human extracted anterior teeth were used. All the teeth were sectioned 3 mm apical of the cemento-enamel junction and the intracoronal tissue removed. The teeth were separated into the seven groups each containing seven teeth. Twenty-eight teeth were used as controls (groups I-IV), standardized cavities were prepared with the remaining 21 teeth (groups V, VI, VII), and restored with a hybrid composite resin (XR Herculite). Acetate buffer was placed in the pulp chamber to absorb and stabilize any peroxide that might penetrate. Group I was exposed only to distilled water. Groups II and V were applied with 10% CP (Contrast PM), groups III and VI were applied with 15% CP (Contrast PM), groups IV and VII were applied with 35% CP (Quik Start) and left for 30 min at 37 degrees C. Then, the acetate buffer solution in the pulp chamber of each tooth was removed and the chamber was then rinsed twice with 100 ml of distilled water. The contents then had leucocryctal violet and enzyme horseradish peroxidase added. The optical density of the resulting blue solution was determined spectrophotometrically, and was converted into microgram equivalents of hydrogen peroxide. A higher level of bleaching agent penetrated into the pulp chamber in the restored teeth than in the sound teeth.

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Novel purine ribonucleoside analogues (9-13) containing a 4-substituted piperazine in the substituent at N(6) were synthesized and evaluated for their cytotoxicity on Huh7, HepG2, FOCUS, Mahlavu liver, MCF7 breast, and HCT116 colon carcinoma cell lines. The purine nucleoside analogues were analyzed initially by an anticancer drug-screening method based on a sulforhodamine B assay. Two nucleoside derivatives with promising cytotoxic activities (11 and 12) were further analyzed on the hepatoma cells. The N(6)-(4-Trifluoromethylphenyl)piperazine analogue 11 displayed the best antitumor activity, with IC(50) values between 5.2 and 9.2 μM. Similar to previously described nucleoside analogues, compound 11 also interferes with cellular ATP reserves, possibly through influencing cellular kinase activities. Furthermore, the novel nucleoside analogue 11 was shown to induce senescence-associated cell death, as demonstrated by the SAβ-gal assay. The senescence-dependent cytotoxic effect of 11 was also confirmed through phosphorylation of the Rb protein by p15(INK4b) overexpression in the presence of this compound.