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Background: It is common for dental technicians to adjust the proximal surface of adjacent teeth on casts when fabricating single crowns. However, whether the accuracy of the proximal contact is affected if this step is eliminated is unclear. Objective: To evaluate the accuracy of the proximal contact of single crowns for mandibular first molars fabricated from four different restorative materials, without adjustment of the proximal surface of the adjacent teeth by the laboratory/dental technician. Methods: This study was in vitro; all the clinical procedures were conducted on a dentoform. The mandibular first molar tooth on the dentoform was prepared using diamond burs and a high speed handpiece. Twenty single crowns were fabricated, five for each group (monolithic zirconia, lithium disilicate, metal ceramic, and cast gold). No proximal surface adjacent to the definitive crowns was adjusted for tight contact in the dental laboratory. Both the qualitative analyses, using dental floss and shimstock, and the quantitative analyses, using a stereo microscope, were performed to evaluate the accuracy of the proximal contact of the restoration with the adjacent teeth. In the quantitative analysis, one-way analysis of variance was used to compare mean values at a significance level of 0.05. Results: In quantitative analysis, the differences between the proximal contact tightness of the four groups was not statistically significant (P = 0.802 for mesial contacts, P = 0.354 for distal contacts). In qualitative analysis, in most crowns, dental floss passed through the contact with tight resistance and only one film of shimstock could be inserted between the adjacent teeth and the restoration. However, one specimen from the cast gold crown had open contact. Conclusions: Even without proximal surface adjustment of the adjacent teeth during the crown fabrication process, adequate proximal contact tightness between the restoration and adjacent teeth could be achieved.

Cardiovascular disease (CVD) is the leading cause of death in developed countries. Plasma cholesterol level is a key risk factor in CVD pathogenesis. Genetic and dietary variation both influence plasma cholesterol; however, little is known about dietary interactions with genetic variants influencing the absorption and transport of dietary cholesterol. We sought to determine whether gut expressed variants predicting plasma cholesterol differentially affected the relationship between dietary and plasma cholesterol levels in 1,128 subjects (772/356 in the discovery/replication cohorts, respectively). Four single nucleotide polymorphisms (SNPs) within three genes (APOB, CETP, and NPC1L1) were significantly associated with plasma cholesterol in the discovery cohort. These were subsequently evaluated for gene-by-environment (GxE) interactions with dietary cholesterol for the prediction of plasma cholesterol, with significant findings tested for replication. Novel GxE interactions were identified and replicated for two variants: rs1042034, an APOB Ser4338Asn missense SNP and rs2072183 (in males only), a synonymous NPC1L1 SNP in linkage disequilibrium with SNPs 5′ of NPC1L1. This study identifies the presence of novel GxE and gender interactions implying that differential gut absorption is the basis for the variant associations with plasma cholesterol. These GxE interactions may account for part of the “missing heritability” not accounted for by genetic associations.

HDL-associated paraoxonase 1 (PON1) activity is associated with cardiovascular and other human diseases. As the role of genetic variants outside of the PON gene cluster on PON1 activity is unknown, we sought to identify common and rare variants in such loci. We typed 33,057 variants on the CVD chip in 1,362 subjects to test for their effects on adjusted-PON1 activity. Three novel genes (FTO, ITGAL, and SERPINA12) and the PON gene cluster had SNPs associated with PON1 arylesterase (AREase) activity. These loci were carried forward for rare-variant analysis using Exome chip genotypes in an overlapping subset of 1,051 subjects using sequence kernel association testing. PON1 (P = 2.24 × 10−4), PON3 (P = 0.022), FTO (P = 0.019), and SERPINA12 (P = 0.039) had both common and rare variants associated with PON1 AREase. ITGAL variants were associated with PON1 activity when using weighted sequence kernel association testing (SKAT) analysis (P = 2.63 × 10−3). When adjusting for the initial common variants, SERPINA12 became marginally significant (P = 0.09), whereas all other findings remained significant (P < 0.05), suggesting independent rare-variant effects. We present novel findings that common and rare variants in FTO, SERPINA12, and ITGAL predict PON1 activity. These results further link PON1 to diabetes and inflammation and may inform the role of HDL in human disease.

HDL-associated paraoxonase 1 (PON1) activity has been consistently associated with cardiovascular and other diseases. Vitamins C and E intake have previously been positively associated with PON1 in a subset of the Carotid Lesion Epidemiology and Risk (CLEAR) cohort. The goal of this study was to replicate these findings and determine whether other nutrient intake affected PON1 activity. To predict nutrient and mineral intake values, 1,402 subjects completed a standardized food frequency survey of their dietary habits over the past year. Stepwise regression was used to evaluate dietary and covariate effects on PON1 arylesterase activity. Five dietary components, cholesterol (P < 2.0 × 10−16), alcohol (P = 8.51 × 10−8), vitamin C (P = 7.97 × 10−5), iron (P = 0.0026), and folic acid (0.037) were independently predictive of PON1 activity. Dietary cholesterol was positively associated and predicted 5.5% of PON1 activity, second in variance explained. This study presents a novel finding of dietary cholesterol, iron, and folic acid predicting PON1 activity in humans and confirms prior reported associations, including that with vitamin C. Identifying and understanding environmental factors that affect PON1 activity is necessary to understand its role and that of HDL in human disease.