Objectives To test the hypothesis that there is no difference in the in vivo maximum wear of enamel opposing monolithic zirconia crowns, enamel opposing porcelain fused to metal crowns and enamel opposing enamel. Methods Thirty patients needing single crowns were randomized to receive either a monolithic zirconia or metal-ceramic crown. Two non-restored opposing teeth in the same quadrants were identified to serve as enamel controls. After cementation, quadrants were scanned for baseline data. Polyvinylsiloxane impressions were obtained and poured in white stone. Patients were recalled at six-months and one-year for re-impression. Stone models were scanned using a tabletop laserscanner to determine maximum wear. Statistical analysis was performed using Mann-Whitney U to determine any significant differences between the wear of enamel against zirconia and metal-ceramic crowns. Results Sixteen zirconia and 14 metal-ceramic crowns were delivered. There were no statistical differences in mean wear of crown types (p = 0.165); enamel antagonists (p = 0.235) and enamel controls (p = 0.843) after one year. Conclusion Monolithic zirconia exhibited comparable wear of enamel compared with metal-ceramic crowns and control enamel after one year. Significance This study is clinically significant because the use of polished monolithic zirconia demonstrated comparable wear of opposing enamel to metal-ceramic and enamel antagonists.

Caries lesions develop when acid production from bacterial metabolism of dietary carbohydrates outweighs the various mechanisms that promote pH homeostasis, including bacterial alkali production. Therapies that provide arginine as a substrate for alkali production in supragingival oral biofilms have strong anticaries potential. The objective of this study was to investigate the metabolic profile of site-specific supragingival plaque in response to the use of arginine (Arg: 1.5% arginine, fluoride-free) or fluoride (F: 1,100 ppm F/NaF) toothpastes. Eighty-three adults of different caries status were recruited and assigned to treatment with Arg or F for 12 wk. Caries lesions were diagnosed using International Caries Detection and Assessment System II, and plaque samples were collected from caries-free and carious tooth surfaces. Taxonomic profiles were obtained by HOMINGS (Human Oral Microbe Identification using Next Generation Sequencing), and plaque metabolism was assessed by the levels of arginine catabolism via the arginine deiminase pathway (ADS), acidogenicity, and global metabolomics. Principal component analysis (PCA), partial least squares–discriminant analysis, analysis of variance, and random forest tests were used to distinguish metabolic profiles. Of the 509 active lesions diagnosed at baseline, 70 (14%) were inactive after 12 wk. Generalized linear model showed that enamel lesions were significantly more likely to become inactive compared to dentin lesions ( P < 0.0001), but no difference was found when treatment with Arg was compared to F ( P = 0.46). Arg significantly increased plaque ADS activity ( P = 0.031) and plaque pH values after incubation with glucose ( P = 0.001). F reduced plaque lactate production from endogenous sources ( P = 0.02). PCA revealed differences between the metabolic profiles of plaque treated with Arg or F. Arg significantly affected the concentrations of 16 metabolites, including phenethylamine, agmatine, and glucosamine-6-phosphate ( P < 0.05), while F affected the concentrations of 9 metabolites, including phenethylamine, N-methyl-glutamate, and agmatine ( P < 0.05). The anticaries mechanisms of action of arginine and fluoride are distinct. Arginine metabolism promotes biofilm pH homeostasis, whereas fluoride is thought to enhance resistance of tooth minerals to low pH and reduce acid production by supragingival oral biofilms.

Titanium (Ti) corrodes clinically in the presence of bacteria. We investigated this phenomenon as a function of Ti particles found in biopsied tissues around peri-implantitis sites and surface roughness of failed Ti implants. Tissue biopsies were surgically collected from peri-implantitis sites, processed, and embedded in resin. The resin-embedded samples were hand trimmed to the region of interest and semi-thick (500 nm) sections were collected onto coverslips. One section was toluidine blue post-stained as a reference. The remainder sections were left unstained for energy-dispersive X-ray spectroscopy (EDX) analysis. Processed samples were examined under scanning electron microscopy (SEM) and EDX. Corresponding failed implants were also removed and examined under SEM and EDX. Five out of eight biopsied samples demonstrated the presence of Ti particles in the soft tissue, suggesting the true rate among all failures was between 24.5% and 91.5% (the lower bound of a 95% confidence interval for the true rate of Ti presence). SEM analysis of failed implant bodies also indicated changes in surface morphology and appeared less detailed with decreased weight percent of Ti on the surface of the failed implants. In conclusion, Ti particles were noted in 5/8 biopsied samples. Surface morphologies were smoother in failed implants compared with the reference implant.

Background Subgingival microbiome in disease-associated subgingival sites is known to be dysbiotic and significantly altered. In patients with rheumatoid arthritis (RA), the extent of dysbiosis in disease- and health-associated subgingival sites is not clear. Methods 8 RA and 10 non-RA subjects were recruited for this pilot study. All subjects received full oral examination and underwent collection of subgingival plaque samples from both shallow (periodontal health-associated, probing depth ≤ 3mm) and deep subgingival sites (periodontal disease-associated, probing depth ≥ 4 mm). RA subjects also had rheumatological evaluation. Plaque community profiles were analyzed using 16 S rRNA sequencing. Results The phylogenetic diversity of microbial communities in both RA and non-RA controls was significantly higher in deep subgingival sites compared to shallow sites (p = 0.022), and the overall subgingival microbiome clustered primarily according to probing depth (i.e. shallow versus deep sites), and not separated by RA status. While a large number of differentially abundant taxa and gene functions was observed between deep and shallow sites as expected in non-RA controls, we found very few differentially abundant taxa and gene functions between deep and shallow sites in RA subjects. In addition, compared to non-RA controls, the UniFrac distances between deep and shallow sites in RA subjects were smaller, suggesting increased similarity between deep and shallow subgingival microbiome in RA. Streptococcus parasanguinis and Actinomyces meyeri were overabundant in RA subjects, while Gemella morbillorum, Kingella denitrificans, Prevotella melaninogenica and Leptotrichia spp. were more abundant in non-RA subjects. Conclusions The aggregate subgingival microbiome was not significantly different between individuals with and without rheumatoid arthritis. Although the differences in the overall subgingival microbiome was driven primarily by probing depth, in contrast to the substantial microbiome differences typically seen between deep and shallow sites in non-RA patients, the microbiome of deep and shallow sites in RA patients were more similar to each other. These results suggest that factors associated with RA may modulate the ecology of subgingival microbiome and its relationship to periodontal disease, the basis of which remains unknown but warrants further investigation.