44 research outputs found

    Prevention of Early Childhood Caries with Prenatal Oral Health Care

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    Dental caries is perhaps the most common bacterial infection in humans. Mutans streptococci are the principal bacteria responsible for dental caries. Infants are thought to acquire these organisms by vertical transmission from an infected individual, primarily the mother within a discrete period called the “window of infectivity”. Recent investigations showed that colonization of S. mutans can occur in pre-dentate infants. If an infant acquires MS from the mother before or after the emergence of the primary teeth, preventive interventions aimed at reducing the mother’s burden of MS could prevent or reduce the vertical transmission of these organism to infants and hence reduce subsequent caries experience

    Prevention of Early Childhood Caries with Prenatal Oral Health Care

    Get PDF
    Dental caries is perhaps the most common bacterial infection in humans. Mutans streptococci are the principal bacteria responsible for dental caries. Infants are thought to acquire these organisms by vertical transmission from an infected individual, primarily the mother within a discrete period called the “window of infectivity”. Recent investigations showed that colonization of S. mutans can occur in pre-dentate infants. If an infant acquires MS from the mother before or after the emergence of the primary teeth, preventive interventions aimed at reducing the mother’s burden of MS could prevent or reduce the vertical transmission of these organism to infants and hence reduce subsequent caries experience

    Evidence of gene-environment interaction for two genes on chromosome 4 and environmental tobacco smoke in controlling the risk of nonsyndromic cleft palate

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    Nonsyndromic cleft palate (CP) is one of the most common human birth defects and both genetic and environmental risk factors contribute to its etiology. We conducted a genome-wide association study (GWAS) using 550 CP case-parent trios ascertained in an international consortium. Stratified analysis among trios with different ancestries was performed to test for GxE interactions with common maternal exposures using conditional logistic regression models. While no single nucleotide polymorphism (SNP) achieved genome-wide significance when considered alone, markers in SLC2A9 and the neighboring WDR1 on chromosome 4p16.1 gave suggestive evidence of gene-environment interaction with environmental tobacco smoke (ETS) among 259 Asian trios when the models included a term for GxE interaction. Multiple SNPs in these two genes were associated with increased risk of nonsyndromic CP if the mother was exposed to ETS during the peri-conceptual period (3 months prior to conception through the first trimester). When maternal ETS was considered, fifteen of 135 SNPs mapping to SLC2A9 and 9 of 59 SNPs in WDR1 gave P values approaching genome-wide significance (10-6<P<10-4) in a test for GxETS interaction. SNPs rs3733585 and rs12508991 in SLC2A9 yielded P = 2.26×10-7 in a test for GxETS interaction. SNPs rs6820756 and rs7699512 in WDR1 also yielded P = 1.79×10-7 and P = 1.98×10-7 in a 1 df test for GxE interaction. Although further replication studies are critical to confirming these findings, these results illustrate how genetic associations for nonsyndromic CP can be missed if potential GxE interaction is not taken into account, and this study suggest SLC2A9 and WDR1 should be considered as candidate genes for CP. © 2014 Wu et al

    Mutations in Exons 1 and 2 of PAX9 Gene and Hypodontia

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    Hypodontia is one of the most common dental anomalies that result in aesthetic and functional problems. A wide range of prevalence values for missing teeth has been reported ranging from 1.6% to 25.4% in adult population. Our understanding of the genetic basis of tooth agenesis is still limited. Several genes have been explored, including, but not limited to PAX9 and MSX1. The normal function of the PAX9 gene, a transcription factor that plays an important role in signaling between epithelial and mesenchymal cells during tooth development, seems to be critical during development of dental lamina

    Mutations in Exons 1 and 2 of PAX9 Gene and Hypodontia

    No full text
    Hypodontia is one of the most common dental anomalies that result in aesthetic and functional problems. A wide range of prevalence values for missing teeth has been reported ranging from 1.6% to 25.4% in adult population. Our understanding of the genetic basis of tooth agenesis is still limited. Several genes have been explored, including, but not limited to PAX9 and MSX1. The normal function of the PAX9 gene, a transcription factor that plays an important role in signaling between epithelial and mesenchymal cells during tooth development, seems to be critical during development of dental lamina

    VARIANTS OF FACIAL SHAPE GENES IN PATIENTS WITH CLASS II OR CLASS I MALOCCLUSION

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    Background and purpose: In recent years, questions regarding the genetic and environmental factors affecting variation in human craniofacial morphology have received increasing attention. Medical and clinical genetic research using family studies has proven foundational for our understanding of which genes affect craniofacial variation. On the other hand, cephalometricbased studies showed a relationship between the cranial base and midface characteristics among individuals with different skeletal pattern of malocclusion. The purpose of our pilot study was to analyze specific variants of facial genes that were suggested to be associated with cranial base width and depth in Class II and Class I malocclusions. Methods: Patient data (extraoral photographs, intraoral photographs, and iCAT CBCT images obtained as part of patients’ routine orthodontic examinations) was collected for patients who had come to the Orthodontic Clinic, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, CA, from July 2019 to July 2021. For 72 patients who met the inclusion criteria for Class I or Class II groups in our study, saliva samples were collected, and DNA was isolated and analyzed using rtPCR genotyping for the following single-nucleotide gene polymorphisms (SNPs): rs79272428 (A\u3eG), rs17106852 (A\u3eG), rs12786942 (A\u3eT) and rs6555969 (C\u3eT). Results: We observed differences between Class I and Class II malocclusions in genotype proportions and allele frequencies in gene variants rs6555969 (C\u3eT) and rs12786942. Genotype 4 CT (rs6555969) was found in a higher frequency in the Class I group generally and in the phenotypic Cluster 1. There were no differences observed for other gene variants studied. Regarding the cranial base characteristics, Asian patients had shorter and more acute cranial base. In Hispanic patients, there was a significant difference (P\u3c0.005) between Class I and Class II patients regarding the cranial base width. Conclusions: The aim of our study was to determine genotypic differences between Class I and Class II malocclusion groups and to study genotypic associations with phenotypic clusters. We showed genotypic and phenotypic cluster differences between Class I and Class II groups. These differences were not statistically significant, probably, due to a small size of the studied groups. However, in this pilot study, we found trends, on which we will focus in our future study using a larger sample

    Variants of PAX Gene Family in Patients with Class II or Class I Malocclusion

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    Background and Purpose. Orthodontic treatment helps to ensure proper function of teeth and to create healthy smiles. To this aim, the orthodontist’s goal is establishment of an esthetic harmony between soft and hard tissues of the face. Dimensions of facial width and height are crucial for accurate diagnosis and formulation of an efficient treatment plan. A knowledge of genetic determinants of these dimensions in Class II patients will deepen our understanding of etiology of skeletal Class II malocclusions and would make it possible to personalize a patient’s treatment plan. The purpose of our pilot study was to analyze, if specific variants of PAX 3, PAX 5, PAX 7 and PAX 9 genes are associated with Class II malocclusion but not with Class I malocclusion or vice versa. Methods. Patient data (extraoral photographs, intraoral photographs, and iCAT CBCT images obtained as part of patients’ routine orthodontic examinations) was collected for patients who had come to the Orthodontic Clinic, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, CA, from July 2019 to July 2021. For 72 patients who met the inclusion criteria for Class I or Class II groups in our study, saliva samples were collected, and DNA was isolated and analyzed using rtPCR genotyping for PAX 3 SNP: rs974448, PAX 5 SNP: rs7031673, PAX 7 SNP: rs4920520 and PAX 9 SNP: rs8004560. 4 Results. Genotype A5G5 (rs7031673, PAX5) was high in Class I generally, but also in phenotypic Cluster 1 and Cluster 9. Genotype G5G5 (rs7031673, PAX5) was high in Class II generally, but also in phenotypic Cluster 8 and Cluster 10. Allele G5 was more frequent in Class II than in Class I. Genotype A7A7 (rs4920520, PAX7) was high in Class II generally. It was absent in phenotypic Cluster 1 and Cluster 9, present in phenotypic Cluster 8 and Cluster 10. Genotype A9G9 (rs8004560, PAX9) was higher in Cluster 8 than in Cluster 10 (and also higher than in Clusters 1 and 9). Allele A9 was more frequent in Class II than in Class I. Conclusions. The aim of this study was to determine genotypic differences between Class I and Class II malocclusion groups and to study genotypic associations with phenotypic clusters. We showed genotypic and phenotypic cluster differences between Class I and Class II groups. We report several genotypes tentatively identified by genotypic analysis and found in association with certain phenotypic clusters. None of these differences proved to be statistically significant, probably, due to a small size of the studied groups. However, in this pilot study, we found trends, on which we will focus in our future study using a larger sample

    Searching for association of GSK3β rs13314595, MSX1 rs3821949, TGFβ3 rs3917201, and BMP4 rs17563 with non-syndromic cleft lip and palate

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    Introduction: Non-syndromic cleft lip with or without cleft palate (NCL±P) is characterized by a multifactorial etiology with both genetic and environmental factors playing a role in its embryonic development. Recent genetic studies have identified susceptibility loci and genetic variations in several genes that were associated with the risk of developing NCL±P. The purpose of this study was to investigate the association of MSX1, BMP4, TGFβ3, and GSK3β gene variants with NCL±P in a casecontrol data set from Karaikal, India. Methods: The case sample consisted of 331 individuals who were diagnosed with CL (bi/unilateral cleft lip), CLP (bi/unilateral cleft lip and palate), or CP (cleft palate). The control sample consisted of 156 individuals from the same location who were not affected with an orofacial cleft and had a negative family history of NCL±P. Genotype proportions and allele frequencies were determined and compared. Results: We tested differences in proportions of genotypes and allele frequencies in four gene variants. No statistically significant differences were found in single nucleotide polymorphisms (SNPs) of MSX1 rs3821949 and BMP4 rs17563. However, when comparing frequencies of TGFβ3 alleles in bilateral NCL±P cases vs controls, there was a close-to-significant difference at p = 0.069165 found. When frequencies of GSK3β alleles in female NCL±P cases vs female controls were compared, the difference was marginally statistically significant at p = 0.058246. Conclusions: Out of four SNPs studied in this Indian population, a possible association with NCL±P was found for GSK-3β rs13314595 and for TGFβ3 rs3917201. It was previously observed that variants of susceptibility genes may occur only in some cleft populations. Therefore, it is important to perform genetic studies in local populations. Knowledge of the presence of certain SNPs is essential if risk calculations or prevention measures are considered

    Variants of PAX Gene Family in Patients with Class II or Class I Malocclusion

    No full text
    Background and Purpose. Orthodontic treatment helps to ensure proper function of teeth and to create healthy smiles. To this aim, the orthodontist’s goal is establishment of an esthetic harmony between soft and hard tissues of the face. Dimensions of facial width and height are crucial for accurate diagnosis and formulation of an efficient treatment plan. A knowledge of genetic determinants of these dimensions in Class II patients will deepen our understanding of etiology of skeletal Class II malocclusions and would make it possible to personalize a patient’s treatment plan. The purpose of our pilot study was to analyze, if specific variants of PAX 3, PAX 5, PAX 7 and PAX 9 genes are associated with Class II malocclusion but not with Class I malocclusion or vice versa. Methods. Patient data (extraoral photographs, intraoral photographs, and iCAT CBCT images obtained as part of patients’ routine orthodontic examinations) was collected for patients who had come to the Orthodontic Clinic, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, CA, from July 2019 to July 2021. For 72 patients who met the inclusion criteria for Class I or Class II groups in our study, saliva samples were collected, and DNA was isolated and analyzed using rtPCR genotyping for PAX 3 SNP: rs974448, PAX 5 SNP: rs7031673, PAX 7 SNP: rs4920520 and PAX 9 SNP: rs8004560. 4 Results. Genotype A5G5 (rs7031673, PAX5) was high in Class I generally, but also in phenotypic Cluster 1 and Cluster 9. Genotype G5G5 (rs7031673, PAX5) was high in Class II generally, but also in phenotypic Cluster 8 and Cluster 10. Allele G5 was more frequent in Class II than in Class I. Genotype A7A7 (rs4920520, PAX7) was high in Class II generally. It was absent in phenotypic Cluster 1 and Cluster 9, present in phenotypic Cluster 8 and Cluster 10. Genotype A9G9 (rs8004560, PAX9) was higher in Cluster 8 than in Cluster 10 (and also higher than in Clusters 1 and 9). Allele A9 was more frequent in Class II than in Class I. Conclusions. The aim of this study was to determine genotypic differences between Class I and Class II malocclusion groups and to study genotypic associations with phenotypic clusters. We showed genotypic and phenotypic cluster differences between Class I and Class II groups. We report several genotypes tentatively identified by genotypic analysis and found in association with certain phenotypic clusters. None of these differences proved to be statistically significant, probably, due to a small size of the studied groups. However, in this pilot study, we found trends, on which we will focus in our future study using a larger sample
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