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The present study aimed to investigate the association between nutritional status with delayed tooth eruption (DTE). Oral examination was performed in schoolchildren (8-11 years old), and DTE was defined by absence of dental gingival emergence or when primary tooth was still present in the oral cavity after the expected time. BMI z-score of each child were collected and nutritional status was defined. Chi-square test and binary logistic regression adjusted by age and gender were performed. Odds ratio (OR) and 95% Confidence Interval (95% CI) were calculated. The established alpha was 5%. Among 353 included children, 247 were classified as eutrophic, 16 as underweight, 64 as overweight, and 26 as obese. Underweight was associated as a risk factor to DTE (P = .014; OR = 3.5; 95% CI = 1.3-9.8), and underweight girls had more chance to present DTE than eutrophic girls (P = .048; OR = 4.4; 95% CI = 1.1-17.2) in chi square test. In logistic regression, underweight was associated as a risk factor to DTE (OR = 4.21; CI 95% = 1.42-12.43; P = .009). Underweight children have a higher risk of DTE in permanents.

Objective. To evaluate if nutritional status is associated with caries and gingivitis in Brazilian schoolchildren. Material and methods. Children of both genders, age ranging from 8 to 11 years old, were included in this study. Caries was diagnosed using ICDAS (International System for Detection and Assessment of Carious Lesions) and gingivitis was diagnosed using the Community Periodontal Index. The nutritional status of each child was defined by BMI Z-score calculation. Data on oral health behavior and dietary habit were collected through parent’s questionnaires. Parametric analyzes were performed to compare the groups. The established alpha was 5%. Results. The sample consisted of 353 schoolchildren: 16 underweight children, 247 eutrophic children, 64 overweight children, and 26 were obese children. Overweight, Obese and Overweight + Obese children presented less cavitated caries lesion than Eutrophic children (P < .05). Gingivitis was not associated with nutritional status (P > .05). Conclusion. Caries was associated with overweight and obesity in Brazilian schoolchildren.

Bone morphogenetic proteins (BMPs) play an important role during the initial process of enamel development and therefore may play a role in caries susceptibility. The purpose of this study was to evaluate the association between the polymorphisms in the BMP2, BMP4 and BMP7 genes and their association with caries experience and primary enamel microhardness characteristics. DNA from buccal cells as well as clinical and demographic information from 1,731 subjects from three different data sets from Brazil were included. Polymorphisms in BMP2, BMP4 and BMP7 were analyzed by real-time polymerase chain reaction from genomic DNA. Association between caries experience, genotype, and allele distribution in both cohorts was evaluated using χ 2 and logistic regression analyses. In the family-based set, the association between caries experience and alleles was tested using the transmission disequilibrium test. In the Rio de Janeiro cohort, microhardness data on 108 exfoliated primary teeth before and after demineralization and remineralization challenges was included. Associations between microhardness values and genotype and allele distribution were evaluated using χ 2 and logistic regression analyses. Differences between caries experience and some risk factors were statistically significant. In the cohort from Nova Friburgo, BMP2 was associated with caries experience in primary dentition during logistic regression analysis (p = 0.023; OR = 2.58; 95% CI 1.13-5.86). There was no association between genotype and allele distribution for BMP polymorphisms and primary enamel microhardness alterations. Our result suggests that BMP2 may be involved in caries experience in primary dentition from a Nova Friburgo cohort.

Background There is evidence for a genetic contribution to chronic periodontitis. In this study, we conducted a genome wide association study among 866 participants of the University of Pittsburgh Dental Registry and DNA Repository, whose periodontal diagnosis ranged from healthy (N = 767) to severe chronic periodontitis (N = 99). Methods Genotyping i of over half-million single nucleotide polymorphisms was determined. Analyses were done twice, first in the complete dataset of all ethnicities, and second including only samples defined as self-reported Whites. From the top 100 results, twenty single nucleotide polymorphisms had consistent results in both analyses (borderline p-values ranging from 1E-05 to 1E-6) and were selected to be tested in two independent datasets derived from 1,460 individuals from Porto Alegre, and 359 from Rio de Janeiro, Brazil. Meta-analyses of the Single nucleotide polymorphisms showing a trend for association in the independent dataset were performed. Results The rs1477403 marker located on 16q22.3 showed suggestive association in the discovery phase and in the Porto Alegre dataset (p = 0.05). The meta-analysis suggested the less common allele decreases the risk of chronic periodontitis. Conclusions Our data offer a clear hypothesis to be independently tested regarding the contribution of the 16q22.3 locus to chronic periodontitis.

The aim of this study is to evaluate if single nucleotide polymorphisms (SNPs) in WNT6 and WNT10A are associated with the risk of dental pulp calcification in orthodontic patients. This cross-sectional study followed the “Strengthening the Reporting of Genetic Association Studies” (STREGA) guidelines. Panoramic radiographs (pre- and post-orthodontic treatment) and genomic DNA from 132 orthodontic patients were studied. Dental pulp calcification (pulp stones and/or pulp space narrowing) was recorded in upper and lower first molars. The SNPs in WNT6 and WNT10A ( rs7349332 , rs3806557 , rs10177996 , and rs6754599 ) were assessed through genotyping analysis using DNA extracted from buccal epithelial cells. The association between pulp calcification and SNPs were analyzed using allelic and genotypic distributions and haplotype frequencies (p<0.05). Prevalence of dental pulp calcification was 42.4% in the 490 studied molars. In the genotypic analysis, the SNPs in WNT10A showed a statistically significant value for molar calcification (p = 0.027 for rs1017799 ), upper molar calcification (p = 0.040 for rs1017799 ) (recessive model), and molar calcification (p = 0.046 for rs3806557 ) (recessive model). In the allelic distribution, the allele C of the SNP rs10177996 in WNT10A was associated with molar calcifications (p = 0.042) and with upper first molar calcification (p = 0.035). Nine combinations of haplotypes showed statistically significant value (p<0.05). The findings of this study indicates that SNPs in WNT10A and WNT6 are associated with dental pulp calcification in molars after orthodontic treatment and may be considered as biomarkers for dental pulp calcification.

[This corrects the article DOI: 10.1371/journal.pone.0288782.].

Bruxism is a masticatory muscle activity characterized by grinding of the teeth and clenching of the jaw that causes tooth wear and breakage, temporomandibular joint disorders, muscle pain, and headache. Bruxism occurs in both adults and children. Clinical characteristics and habits were evaluated in an adult sample. Moreover, we used DNA samples from 349 adults and 151 children to determine the presence of association with specific genes. Genomic DNA was obtained from saliva. The markers rs2241145 and rs243832 (metalloproteinase 2 (MMP2)), rs13925 and rs2236416 (metalloproteinase 9 (MMP9)), and rs6269 (cathecol-o-methyltransferase (COMT)) were genotyped. Data were submitted to statistical analysis with a significance level of 0.05. In adults, in univariate logistic regression, presence of caries, attrition, and use of alcohol were increased in bruxism individuals (p < 0.05). In addition, in adults, there was an association between bruxism and MMP9 (rs13925, p = 0.0001) and bruxism and COMT (rs6269, p = 0.003). In children, a borderline association was observed for MMP9 (rs2236416, p = 0.08). When we performed multivariate logistic regression analyses in adults, the same clinical characteristics remained associated with bruxism, and orthodontic treatment was also associated, besides rs13925, in the AG genotype (p = 0.015, ORa: 3.40 (1.27–9.07)). For the first time, we provide statistical evidence that these genes are associate with bruxism.

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.

BackgroundBisphenol A (BPA) is released from orthodontic composites used for bracket bonding. Genetic variations could modify the metabolism of this chemical within the organism. Considering that free BPA binds to estrogen receptors causing harmful effects to health, the present in vivo study aimed to evaluate the association between genetic polymorphisms in genes encoding estrogen receptors (ESR1 and ESR2) and excreted BPA levels in orthodontic patients.MethodsQuantification of BPA levels in the urine of 16 patients was performed in a gas chromatograph mass spectrometer before (T0), at 24 h (T1), and 1 week (T2) after bracket bonding. DNA was extracted from saliva, and one genetic polymorphism in ESR1 (rs2234693) and two in ESR2 (rs4986938 and rs1256049) were analyzed by real-time PCR. Increases in BPA levels in the urine at T1 and T2 were grouped according to the genotype, and mean differences were compared by unpaired T test or Mann-Whitney test according to the normality of the data. The established alpha was 5%.ResultsBPA levels increased significantly at T1 and T2. There were no statistically significant differences in the increases in BPA levels according to the genotype for any genetic polymorphism (P > 0.05), at neither 24 h nor 1 week after bracket bonding.ConclusionsThe results suggested that there are no association between excreted BPA levels after bracket bonding and the evaluated genetic polymorphisms in ESR1 and ESR2. Further research should be performed in order to confirm these results.

Introduction: Skeletal abnormalities and malocclusions have varied features that impact populations globally, impairing aesthetics and lowering life quality. The prevalence of the Skeletal Class III disease is the lowest among all angle malocclusions, with varied prevalence across nations. Environmental, genetic, and societal factors play a role in its numerous etiologies. In this study, we conducted a thorough search across the published data relating to quantitative trait loci (QTL) and the genes associated with Class III progression in humans, discussed these findings and their limitations, and proposed future directions and strategies for studying this phenotype. Methods: An inclusive search of published papers in the PubMed and Google Scholar search engines using the following terms: 1. Human skeletal Class III; 2. Genetics of Human skeletal Class III; 3. QTL mapping and gene associated with human skeletal Class III; 4. enriched skeletal Class-III-malocclusion-associated pathways. Results: Our search has found 53 genes linked with skeletal Class III malocclusion reported in humans, genes associated with epigenetics and phenomena, and the top 20 enriched pathways associated with skeletal Class III malocclusion. Conclusions: The human investigations yielded some contentious conclusions. We conducted a genome-wide association study (GWAS), an epigenetics-wide association study (EWAS), RNA-seq analysis, integrating GWAS and expression quantitative trait loci (eQTL), micro- and small-RNA, and long non-coding RNA analysis in tissues connected to skeletal Class III malocclusion phenotype in tissues connected with the skeletal phenotype. Finally, we invite regional, national, and international orthodontists and surgeons to join this effort by contributing human samples with skeletal Class III malocclusion following the accepted Helsinki ethical protocol to challenge these phenomena jointly.