Asymmetry in Class II subdivision malocclusion: Assessment based on 3D surface models.

INTRODUCTION: There is currently no consensus in the literature whether the aetiology of a Class II subdivision is dental, skeletal or both. The aim of this study was to identify and quantify skeletal and dental asymmetries in Class II subdivision malocclusions. METHODS: CBCTs from 33 Class II subdivision malocclusion patients were used to construct 3D volumetric label maps. Eighteen landmarks were identified. The original scan and associated 3D volumetric label map were mirrored. Registration of the original and mirrored images relative to the anterior cranial base, maxilla and mandible were performed. Surface models were generated, and 3D differences were quantified. Statistical analysis was performed. RESULTS: Anterior cranial base registration showed significant differences for fossa vertical difference, fossa roll, mandibular yaw, mandibular lateral displacement and lower midline displacement. Regional registrations showed significant differences for antero-posterior (A-P) mandibular length, maxillary roll, A-P maxillary first molar position, maxillary first molar yaw and maxillary first molar roll. Class II subdivision patients also show an asymmetric mandibular length as well as an asymmetric gonial angle. Moderate correlations were found between the A-P molar relationship and fossa A-P difference, mandibular first molar A-P difference, maxillary first molar A-P difference and maxillary first molar yaw. CONCLUSIONS: This study suggests that Class II subdivisions can result from both significant skeletal and dental factors. Skeletal factors include a shorter mandible as well as posterior and higher displacement of the fossa on the Class II side, resulting in mandibular yaw. Dental factors include maxillary and mandibular first molar antero-posterior asymmetry.

In Vitro Acid-Mediated Initial Dental Enamel Loss Is Associated with Genetic Variants Previously Linked to Caries Experience.

We have previously shown that AQP5 and BTF3 genetic variation and expression in whole saliva are associated with caries experience suggesting that these genes may have a functional role in protecting against caries. To further explore these results, we tested ex vivo if variants in these genes are associated with subclinical dental enamel mineral loss. DNA and enamel samples were obtained from 53 individuals. Enamel samples were analyzed for Knoop hardness of sound enamel, integrated mineral loss after subclinical carious lesion creation, and change in integrated mineral loss after remineralization. DNA samples were genotyped for single nucleotide polymorphisms using TaqMan chemistry. Chi-square and Fisher's exact tests were used to compare individuals above and below the mean sound enamel microhardness of the cohort with alpha of 0.05. The A allele of BTF3 rs6862039 appears to be associated with harder enamel at baseline (p = 0.09), enamel more resistant to demineralization (p = 0.01), and enamel that more efficiently regain mineral and remineralize (p = 0.04). Similarly, the G allele of AQP5 marker rs3759129 and A allele of AQP5 marker rs296763 are associated with enamel more resistant to demineralization (p = 0.03 and 0.05, respectively). AQP5 and BTF3 genetic variations influence the initial subclinical stages of caries lesion formation in the subsurface of enamel.

Genetic influences on dental enamel that impact caries differ between the primary and permanent dentitions.

Clinically, primary and permanent teeth are distinct anatomically and the presentation of caries lesions differs between the two dentitions. Hence, the possibility exists that genetic contributions to tooth formation of the two dentitions are different. The purpose of this study was to test the hypothesis that genetic associations with an artificial caries model will not be the same between primary and permanent dentitions. Enamel samples from primary and permanent teeth were tested for microhardness at baseline, after carious lesion creation, and after fluoride application to verify association with genetic variants of selected genes. Associations were found between genetic variants of ameloblastin, amelogenin, enamelin, tuftelin, tuftelin interactive protein 11, and matrix metallopeptidase 20 and enamel from permanent teeth but not with enamel from primary teeth. In conclusion, our data continue to support that genetic variation may impact enamel development and consequently individual caries susceptibility. These effects may be distinct between primary and permanent dentitions.

Role of estrogen related receptor beta (ESRRB) in DFN35B hearing impairment and dental decay.

BACKGROUND: Congenital forms of hearing impairment can be caused by mutations in the estrogen related receptor beta (ESRRB) gene. Our initial linkage studies suggested the ESRRB locus is linked to high caries experience in humans. METHODS: We tested for association between the ESRRB locus and dental caries in 1,731 subjects, if ESRRB was expressed in whole saliva, if ESRRB was associated with the microhardness of the dental enamel, and if ESRRB was expressed during enamel development of mice. RESULTS: Two families with recessive ESRRB mutations and DFNB35 hearing impairment showed more extensive dental destruction by caries. Expression levels of ESRRB in whole saliva samples showed differences depending on sex and dental caries experience. CONCLUSIONS: The common etiology of dental caries and hearing impairment provides a venue to assist in the identification of individuals at risk to either condition and provides options for the development of new caries prevention strategies, if the associated ESRRB genetic variants are correlated with efficacy.