Genetic variation may explain why females are less susceptible to dental erosion

Uhlen, Marte-Mari Nordsetmoen; Stenhagen, Kjersti Refsholt; Dizak, Piper M.; Holme, Børge; Mulic, Aida; Tveit, Anne Bjørg; Vieira, Alexandre R.

doi:10.1111/eos.12297

Cited by 27 publications

(21 citation statements)

References 33 publications

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“…Regarding statistical analysis, similarly to the family-based study also using the TDT reported by Vieira et al [2004], we decided not to apply the Bonferroni correction to our results since it would reduce the α-value to 0.004 (0.05/11 SNPs). This would increase the type II error [Uhlen et al, 2016;Vieira et al, 2017], which would lead us to reject a hypothesis of a true biological association. The use of these corrections may prevent the identification of discrete biological effects.…”

Section: Discussionmentioning

confidence: 99%

Genes Regulating Immune Response and Amelogenesis Interact in Increasing the Susceptibility to Molar-Incisor Hypomineralization

et al. 2018

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Ameloblasts are sensitive cells whose metabolism and function may be affected by inflammatory stimuli. The aim of this study was to evaluate the possible association between polymorphisms in immune response-related genes and molar-incisor hypomineralization (MIH), and their interaction with polymorphisms in amelogenesis-related genes. DNA samples were obtained from 101 nuclear families that had at least 1 MIH-affected child. Eleven single-nucleotide polymorphisms (SNPs) were investigated in immune response genes using TaqMan® technology allele-specific probes. A transmission disequilibrium test was performed to verify overtransmission of alleles in all MIH families, as well as in families only with mild or severe MIH-affected children. Gene-gene interactions between the immune-related and amelogenesis-related polymorphisms were analyzed by determining whether alleles of those genes were transmitted from heterozygous parents more often in association than individually with MIH-affected children. In severe cases of MIH, significant results were observed for rs10733708 (TGFBR1, OR = 3.5, 95% CI = 1.1–10.6). Statistical evidence for gene-gene interactions between rs6654939 (AMELX) and the SNPs rs2070874 (IL4), rs2275913 (IL17A), rs1800872 (IL10), rs1800587 (IL1A), and rs3771300 (STAT1) was observed. The rs2070874 SNP (IL4) was also significantly overtransmitted from heterozygous parents with the rs7526319 (TUFT1) and the rs2355767 (BMP2) SNPs, suggesting a synergistic effect of the transmission of these alleles with susceptibility to MIH. This family-based study demonstrated an association between variation in TGFBR1 and MIH. Moreover, the polymorphisms in immune response and amelogenesis genes may have an additive effect on the risk of developing MIH.

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Section: Discussionmentioning

confidence: 99%

Genes Regulating Immune Response and Amelogenesis Interact in Increasing the Susceptibility to Molar-Incisor Hypomineralization

et al. 2018

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“…Previous studies have shown a genetic association between dental caries and polymorphisms in genes associated with the mineralization of bone, formation of enamel, microbial colonization and the degradation of amelogenin, which is an essential step in enamel formation [1][2][3][4][5]. Other studies have shown that the formation of dental enamel is influenced by genetic variation and can impact the prevalence of dental caries [6]. Further, it has also been shown that mouse dental enamel with less amelogenin is "weaker" than enamel with normal levels of amelogenin [7].…”

Section: Introductionmentioning

confidence: 99%

Measuring the Microscopic Structures of Human Dental Enamel Can Predict Caries Experience

Kelly

Kallistová

Küchler

et al. 2020

JPM

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Objectives: The hierarchical structure of enamel gives insight on the properties of enamel and can influence its strength and ultimately caries experience. Currently, past caries experience is quantified using the decayed, missing, filled teeth/decayed, missing, filled surface (DMFT/DMFS for permanent teeth; dmft/dmfs for primary teeth), or international caries detection and assessment system (ICDAS) scores. By analyzing the structure of enamel, a new measurement can be utilized clinically to predict susceptibility to future caries experience based on a patient’s individual’s biomarkers. The purpose of this study was to test the hypothesis that number of prisms by square millimeter in enamel and average gap distance between prisms and interprismatic areas, influence caries experience through genetic variation of the genes involved in enamel formation. Materials and Methods: Scanning electron microscopy (SEM) images of enamel from primary teeth were used to measure (i) number of prisms by square millimeter and interprismatic spaces, (ii) prism density, and (iii) gap distances between prisms in the enamel samples. The measurements were tested to explore a genetic association with variants of selected genes and correlations with caries experience based on the individual’s DMFT+ dmft score and enamel microhardness at baseline, after an artificial lesion was created and after the artificial lesion was treated with fluoride. Results: Associations were found between variants of genes including ameloblastin, amelogenin, enamelin, tuftelin, tuftelin interactive protein 11, beta defensin 1, matrix metallopeptidase 20 and enamel structure variables measured (number of prisms by square millimeter in enamel and average gap distance between prisms and interprismatic areas). Significant correlations were found between caries experience and microhardness and enamel structure. Negative correlations were found between number of prisms by square millimeter and high caries experience (r value= −0.71), gap distance between prisms and the enamel microhardness after an artificial lesion was created (r value= −0.70), and gap distance between prisms and the enamel microhardness after an artificial lesion was created and then treated with fluoride (r value= −0.81). There was a positive correlation between number of prisms by square millimeter and prism density of the enamel (r value = 0.82). Conclusions: Our data support that genetic variation may impact enamel formation, and therefore influence susceptibility to dental caries and future caries experience. Clinical Relevance: The evaluation of enamel structure that may impact caries experience allows for hypothesizing that the identification of individuals at higher risk for dental caries and implementation of personalized preventative treatments may one day become a reality.

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“…To avoid the influences of these potentially confounding factors on our results, only one surface of one type of tooth was used in the present study (the buccal surface of sound premolars that were extracted for orthodontic reasons), and 150–200 μm of the surface enamel was removed in a controlled manner using a Vernier caliper. Previous studies of the correlations between changes in acid-induced enamel microhardness or demineralization-associated lesions and genetic variations in enamel formation genes included small samples of 28 and 90 subjects (Shimizu et al, 2012 ; Uhlen et al, 2016 ). The present study included 213 individuals.…”

Section: Discussionmentioning

confidence: 99%

“…Genetic association studies of dental caries have suggested that caries may be influenced by variations in enamel formation genes, such as ameloblastin ( AMBN ), amelogenin ( AMELX ), enamelin ( ENAM ), matrix metalloproteinase 20 ( MMP20 ), tuftelin ( TUFT1 ), and tuftelin-interacting protein 11 ( TFIP11 ) (Shimizu et al, 2012 ; Wang et al, 2012 ; Gasse et al, 2013 ; Shaffer et al, 2015 ; Gerreth et al, 2016 ). Previous studies have sought to explain how enamel formation genes influence caries susceptibility (Shimizu et al, 2012 ; Daubert et al, 2016 ; Uhlen et al, 2016 ). One hypothesis is that variation in these genes results in the formation of enamel that is more susceptible to cariogenic challenge (Shimizu et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Variation in Enamel Formation Genes Influences Enamel Demineralization In Vitro in a Streptococcus mutans Biofilm Model

et al. 2017

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Genetic studies have shown that variations in enamel formation genes are associated with caries susceptibility. The aim of this study was to test in vitro whether variants in these genes are associated with dental enamel demineralization in a Streptococcus mutans biofilm model. DNA and enamel samples were obtained from 213 individuals. DNA was extracted from saliva, and 16 single nucleotide polymorphisms were analyzed. The physical and chemical properties of sound enamel samples and the mineral loss and the lesion depth of the demineralized enamel samples under cariogenic challenge were analyzed. Microhardness, enamel chemicals, mineral loss and demineralization depth were compared between different genotypes at each single nucleotide polymorphism. The GG genotype of TUFT1 (rs17640579) and the GT genotype of MMP20 (rs1612069) exhibited increased microhardness (p = 0.044 and 0.016, respectively). The GG genotype of AMBN (rs7694409) had a higher magnesium level, while the CT genotype of TFIP11 (rs2097470) had a lower magnesium level (p = 0.044 and 0.046, respectively). The GT genotype of MMP20 (rs1612069) had a higher calcium level (p = 0.034). The GG genotype of AMBN (rs13115627), the AG genotype of ENAM (rs12640848) and the AA genotype of MMP20 (rs2292730) had a lower phosphorus level (p = 0.012, 0.006, and 0.023, respectively). The GG genotype of AMBN (rs13115627) was also associated with a higher calcium-phosphorus ratio (p = 0.034). Individuals with the CC genotype of TFIP11 (rs134143) exhibited significantly more mineral loss (p = 0.011) and a deeper lesions (p = 0.042). Individuals with the TT genotype of TFIP11 (rs2097470) had more mineral loss (p = 0.018). Individuals with the GG genotype of TUFT1 (rs17640579) exhibited a shallower demineralization depth (p = 0.047). Individuals with the GT genotype of MMP20 (rs1612069) exhibited a shallower demineralization depth (p = 0.042). Individuals with the GG genotype of ENAM (rs12640848) exhibited less mineral loss (p = 0.01) and a shallower demineralization depth (p = 0.03). Genetic variations in TFIP11, TUFT1, MMP20, and ENAM influenced enamel demineralization in a Streptococcus mutans biofilm model.

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Genetic variation may explain why females are less susceptible to dental erosion

Cited by 27 publications

References 33 publications

Genes Regulating Immune Response and Amelogenesis Interact in Increasing the Susceptibility to Molar-Incisor Hypomineralization

Genes Regulating Immune Response and Amelogenesis Interact in Increasing the Susceptibility to Molar-Incisor Hypomineralization

Measuring the Microscopic Structures of Human Dental Enamel Can Predict Caries Experience

Variation in Enamel Formation Genes Influences Enamel Demineralization In Vitro in a Streptococcus mutans Biofilm Model

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