MP produced the smoothest surface of denture base acrylic resin. The mean surface roughness values after MP and CP were not influenced by the type of acrylic resin.

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This laboratory study was assessing the nano-mechanical properties (NMP), surface roughness (Sa), and topographic changes caused by ethanol on the surface of heat-polymerized denture base polymers at different time past dough stage. Specimens of heat polymerizing acrylic resin (Interacryl Hot, Interdent, Celje, Slovenia) of size 10×10×3 mm were prepared, wet ground, and polished for uniform smoothness and treated with ethanol in concentrations of 40, 70, and 99.9% for 30, 60, and 120 s and statistical analysis was done. Some statistical significance for Sa were highest with 120 s exposure to 40% ethanol. NMP were the highest for specimens treated with 99.9% ethanol concentration for 120 s, on specimens prepared 30 min past the dough stage. This study suggested that heat-polymerized denture base polymers are prone for changes by ethanol which alters mechanical properties and surface topography. Dough time influenced the ethanol resistance.

BackgroundCigarette smoking is a major risk factor for lung cancer, asthma, and oral cancer, and is central to the altered innate immune responsiveness to infection. Many hypotheses have provided evidence that cigarette smoking induces more genetic changes in genes involved in the development of many cigarette-related diseases. This alteration may be from single-nucleotide polymorphisms (SNPs) in innate immunity genes, especially the toll-like receptors (TLRs).ObjectiveIn this study, the genotype frequencies of TLR2 and TLR6 in smoking and nonsmoking population were examined.MethodsSaliva samples were collected from 177 smokers and 126 nonsmokers. The SNPs used were rs3804100 (1350 T/C, Ser450Ser) and rs3804099 (597 T/C, Asn199Asn) for TLR2 and rs3796508 (979 G/A, Val327Met) and rs5743810 (745 T/C, Ser249Pro) for TLR6.ResultsResults showed that TLR2 rs3804100 has a significant effect in short-term smokers (OR =2.63; P=0.04), and this effect is not observed in long-term smokers (>5 years of smoking). Therefore, this early mutation may be repaired by the DNA repair system. For TLR2 rs3804099, the variation in genotype frequencies between the smokers and control patients was due to a late mutation, and its protective role appears only in long-term smokers (OR =0.40, P=0.018). In TLR6 rs5743810, the TT genotype is significantly higher in smokers than in nonsmokers (OR =6.90). The effect of this SNP is observed in long-term smokers, regardless of the smoking regime per day.ConclusionTLR2 (rs3804100 and rs3804099) and TLR6 (rs5743810) can be used as a potential index in the diagnosis and prevention of more diseases caused by smoking.