No abstract

SUMMARYThis study evaluated the repair bond strengths of light-cured resins to provisional restoration materials with different chemical compositions and polymerization techniques. Fifty discs (10 mm in diameter and 1.5 mm thick) were fabricated for each provisional resin base material, including a self-cured methacrylate (Alike), selfcured bis-acrylate (Protemp 3 Garant), lightcured bis-acrylate (Revotek LC) and a heat-cured methacrylate (Namilon). All specimens were stored in distilled water at 37°C for seven days before undergoing repair with one of four lightcured resins, including AddOn, Revotek LC, Dyractflow and Unifast LC and a self-cured resin (Alike), according to the manufacturers' instructions, for a total of 200 specimens. After 24 hours of storage in 37°C water, the shear bond strengths were measured with a universal testing machine and fracture surfaces were examined under a stereomicroscope. Two-way ANOVA revealed that provisional resin-base material (p<0.001), repair material (p<0.001) and their interactions (p<0.001) significantly affected the repair strength. Tukey's multiple comparisons showed that the lowest bonding strengths were found in specimens of heat-cured methacrylate resin materials repaired with bis-acryl resins, with their failure modes primarily being of the adhe- Clinical RelevanceSpecific repair resins should be chosen for certain provisional materials, since optimal bond strength can be achieved only when the repair resin has similar chemical components to those of the resin matrix (either methacrylate or bis-acryl) for the provisional restoration.sive type. The highest bond strengths were recorded when the provisional resin-base materials and repairing resins had similar chemical components and the failure modes tended to be of the cohesive type.

No abstract

In modern times, potent dietary carcinogens are key contributors for neoplastic development. For oral squamous cell carcinoma (OSCC), one of the leading cancer types in developing countries, main oncogenic inducers/enhancers, including areca nut chewing, tobacco smoking, and alcohol consumption, were shown to promote cancer initiation/progression. Over decades, studies from different laboratories have identified underlying cellular and molecular mechanisms for carcinogen-induced OSCC. In this review, we will give an overview of where we are in understanding potential oral carcinogenic factors stimulated OSCC tumorigenesis, especially those associated with areca nut chewing in Asians, aiming to provide future scope of possible interception.