Brilliant white teeth is a desire for most Americans today. Currently there is different whitening products to bring this shine, however the stains themselves do not have structured origins. Throughout their life, a tooth’s shade can change due to age, unrelated impacts, a number of oral cavity diseases, and by the products which we consume. Exploring the consumption of our food products, the chemistry of the oral cavity, and the associating microbial communities in relation to tooth staining is the focus of this study. In hopes of determining the chemical compounds that are causing the staining to occur extrinsically (in the enamel) and intrinsically (in the dentin) within the coronal portion of the tooth. In addition to this goal the study aims to assess the differences between teeth that have been stained significantly over time, versus teeth that have normal natural stain occurrences throughout time. The teeth that have been stained significantly over time were artificially stained with common staining solutions. Those staining solutions include: coffee, tobacco, tea, and wine. These solutions have been index and annotated for comparison to normal naturally stained teeth. 1000 human teeth were used in this study, which were analyzed using HPLC-MS/MS. Based on the metabolomics analysis, microbial communities will be analyzed in correlation to the various staining measurements
Clinical parameters for dental whitening such as peroxide concentration and treatment time have been empirically derived. However, limited quantitative analyses examine reactivity of hydrogen peroxide on in vivo tooth stains under various catalytic settings. The wide range of possible activators and stains are challenging in creating a standardized tooth model to isolate various effects for clinical applications. This study uses three model systems to determine the effects of heat, light, metal catalysts, and pH on peroxide bleaching. By first using a model chemical stain, alkaline pH levels (7.4), 35°C heat treatment, and 490nm light activation were optimal for increasing overall bleaching efficacy. When the same conditions were applied to bleaching stained bovine teeth using liquid peroxide, only 35°C heat treatment showed catalytic effect, increasing overall luminosity and decreasing yellowness. A final evaluation of the activation parameters on teeth treated with commercially used gel peroxides revealed positive catalytic activity for heat alone. These results, in conjunction with future clinical studies, can provide the basis for optimizing clinical whitening parameters and ultimately control peroxide reactivity to enhance bleaching efficacy while minimizing undesired side-effects.
Alagille Syndrome is a multisystem genetic disorder characterized by chronic cholestasis,cardiovascular anomalies, ocular abnormalities, skeletal defects, and characteristic facial features. Mutations in Jagged1 (Jag1), a key ligand in the Notch signaling pathway, are associated with the majority of cases. The Notch signaling pathway plays important roles in the development and homeostasis of most, if not all tissues. However, the roles of Jag1 and the Notch signaling pathway in craniofacial and dental development remain unclear. This study aimed to elucidate the roles of Notch signaling pathway in craniofacial and dental development using a mouse model of Alagille Syndrome (Jag1Ndr/Ndr mice, which possess a missense mutation (H268Q) in Jag1). Embryonic and postnatal mouse specimens were collected at various stages from Jag1Ndr/Ndr mice. Micro-computed tomography (microCT) and three-dimensional (3D) Geometric Morphometric Analysis (GMA) were performed on adult skulls to analyze changes in craniofacial morphology. Hematoxylin and eosin (H&E) staining on histological sections was performed on control and Jag1Ndr/Ndr mice at embryonic day (E)14.5, E16.5, postnatal (P)0, and P7 to analyze tooth development. 3D GMA showed variations in the coronoid process, zygomatic process, and the area where parietal, occipital, and squamosal bones intersect in Jag1Ndr/Ndr mutant mice. In addition, mutants had more convex crania from both frontal and lateral views and a longer snout. Our histological analysis of tooth development showed defects in cell-matrix adhesion (ameloblast-enamel matrix) and cell-cell adhesion (ameloblast-stratum intermedium) at P7. MicroCT analysis of P7 and adult molars supported our histological findings and revealed changes in tooth morphology. Disruption in Notch signaling due to a missense mutation (H268Q) in Jag1 led to: 1) specific changes in craniofacial morphology; 2) defective cell-matrix and cell-cell attachments during tooth development; 3) possible changes in tooth structures due to abnormal tooth development and mineralization. Our study demonstrates for the first time that Notch signaling is essential for specific changes in craniofacial morphology and proper dental development.
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