<i>FGF10</i>and<i>FGF13</i>genetic variation and tooth-size discrepancies

Marañón‐Vásquez, Guido Artemio; Vieira, Alexandre R.; Santos, Luiza Vertuan dos; Cunha, Arthur S; Weiss, Suyany Gabriely; Araújo, Mônica Tirre de Souza; Bolognese, Ana Maria; Scariot, Rafaela; Küchler, Érika Calvano; Stuani, Maria Bernadete Sasso

doi:10.2319/060920-531.1

Cited by 5 publications

(5 citation statements)

References 42 publications

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“…Our data of reduced dental crown size in FGF10 +/− mutant mice is consistent with observations made in craniosynostosis and LADD syndromes 36–38 . Another FGF10 ‘single nucleotide polymorphisms’ mutation has also been linked to macrodontia, 39 and, although these polymorphisms are not directly related to our study, the collective observations reiterate the notion that the FGF10 gene is an important regulator of tooth size. The underlying mechanism of the dental developmental anomaly is likely to involve disrupted FGF10 function in the epithelial‐mesenchymal interactions (reciprocal signalling) during amelogenesis.…”

Section: Discussionsupporting

confidence: 92%

Craniofacial anomalies in a murine model of heterozygous fibroblast growth factor 10 gene mutation

Tan

Jones

Teague

et al. 2023

Orthod Craniofacial Res

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ObjectiveDysregulation of Fibroblast Growth Factor 10 (FGF10), a member of the family of Fibroblast Growth Factor (FGF) proteins, has been implicated in craniofacial and dental anomalies, including craniosynostosis, cleft palate, and Lacrimo‐Auriculo‐Dento‐Digital Syndrome. The aim of this murine study was to assess the craniofacial and dental phenotypes associated with a heterozygous FGF10 gene (FGF10+/−) mutation at skeletal maturity.MethodsSkulls of 40 skeletally mature mice, comprising two genotypes (heterozygous FGF10+/− mutation, n = 22; wildtype, n = 18) and two sexes (male, n = 23; female, n = 17), were subjected to micro‐computed tomography. Landmark‐based linear dimensions were measured for the cranial vault, maxilla, mandible, and first molar teeth. Multivariate analysis of variance was performed to assess whether there were significant differences in the craniofacial and dental structures between genotypes and sexes.ResultsThe craniomaxillary skeleton and the first molar teeth were smaller in the FGF10+/− mice (P < .05), but the mandible was unaffected. Sex did not have a significant effect on these structures (P > .05). Cranial sutural defects were noted in 5/22 (22.7%) mutant versus 2/18 (11.1%) wildtype mice, and cleft palate in only one (4.5%) mutant mouse. None of the mice displayed craniosynostosis, expansive bony lesions, bifid condyles, or impacted teeth.ConclusionThe FGF10+/− mutation was associated with craniomaxillary skeletal hypoplasia that probably arose from deficient (delayed) intramembranous ossification of the sutured bones. Overall, the skeletal and dental data suggest that the FGF10 gene plays an important role in the aetiology of craniofacial dysmorphology and malocclusion.

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Section: Discussionsupporting

confidence: 92%

Craniofacial anomalies in a murine model of heterozygous fibroblast growth factor 10 gene mutation

Tan

Jones

Teague

et al. 2023

Orthod Craniofacial Res

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“…Studies indicate that the morphogenesis of each type of tooth is differently regulated by different growth factors [30][31][32]. Thus, it is reasonable to hypothesize that testosterone suppression may affect a specific type or group of teeth [33][34][35].…”

Section: Discussionmentioning

confidence: 99%

The Impact of Testosterone Suppression on Dental Structures: An In vivo Study

Madureira,

Reis,

Ferreira

et al. 2024

J. Adv. Med. Med. Res.

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Aim: The aim of this study was to evaluate the impact of testosterone (T) suppression during puberty on the development of dental, periodontal and alveolar structures in rats. Materials and Methods: Thirty-six Wistar rats were selected for this study. Orchiectomy (ORX) was performed on the animals of the experimental group (n=18) and sham surgery on the animals of the control group (n=18) on the 23rd day of life. The animals were allocated into 4 groups: an ORX group (n=9) and a sham group (n=9) euthanized at 45 days of age, and the other ORX group (n=9) and the other sham (n=9) euthanized at 73 days of age. After the experimental period, the animals were euthanized and the mandibles and maxillas were removed, dissected and fixed in 10% formalin, decalcified, cut at 7 µm and stained with hematoxylin and eosin and picrosirius red. Qualitative analysis of slides stained with Hematoxylin and Eosin were performed, while collagen synthesis obtained from slides stained with Red Silver was quantitatively evaluated using ImageJ software. Collagen synthesis was compared between groups using the student's t test using the IBM SPSS software. Results: Histologically, the animals submitted to orchiectomy showed variations in the periodontal region, immature alveolar bone and periodontal ligament with the presence of atypical fat cells, in the dental structures, hyperemic pulp with calcification points (nodules) and variation in the arrangement and shape of the odontoblasts, with considerable significance when compared with the animals of the Sham group. Conclusion: In conclusion, the testosterone suppression induces changes in the differentiation of cells that form the tissues of dental and alveolar structures, through the incidence of pulp alterations, presence of atypical cells in the periodontal ligament and delay in the neoformation of alveolar bone in rats during puberty.

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“…Previous studies have indicated that the morphogenesis of each type of tooth is regulated by different growth factors and different sets of genes. 6,8,12 Therefore, it is reasonable to suggest that SNPs in growth factor decoder genes can influence the tooth size of only one type, one arch or one group of teeth, and impact the occlusal relationship, [13][14][15] depending on the group of genotypes and alleles that the patient carries. The investigated SNPs in BMP2 and BMP4 were not associated with tooth-size excess in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…Patients with a previous history of orthodontic treatment, congenital syndromes, tooth anomalies, interproximal caries, restorations or enamel reduction, occlusal dental wear, fractured or poorquality dental casts, and extreme tooth misalignment, were excluded. The sample was previously described by Marañón-Vásquez et al 13 Sixty-two patients were included in the current study.…”

Section: Methodsmentioning

confidence: 99%

“…Recent studies have investigated SNPs in odontogenesis-related genes and identified some as possible relevant factors related to tooth-size variability in humans. [13][14][15] Therefore, SNPs associated with growth factors that play an important role in odontogenesis could be a risk factor for TSD. Therefore, the current study aimed to investigate the association between SNPs in BMP4, BMP2, RUNX2 and SMAD6 genes and TSD.…”

Section: Introductionmentioning

confidence: 99%

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Single nucleotide polymorphisms in odontogenesis-related genes associated with tooth-size discrepancy

Reis

Marañón‐Vásquez

Matsumoto

et al. 2023

Australasian Orthodontic Journal

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Introduction: The present study aimed to determine the association between single nucleotide polymorphisms (SNPs) in RUNX2, SMAD6, BMP2, and BMP4 genes in relation to tooth-size discrepancy (TSD). Methods: A cross-sectional study of patients undergoing orthodontic treatment measured the mesiodistal width of permanent teeth from pretreatment dental casts. Sixty-two patients were included in the study and TSD was assessed according to the Bolton analysis. The patients were allocated into a control group (without a TSD), an anterior excess group and an overall excess group. Genomic DNA was extracted from saliva samples, and SNPs previously associated with tooth size were evaluated using a real-time polymerase chain reaction (PCR) system. The Fisher exact test was performed to compare genotype and allele frequencies at an α = 0.05. An Odds Ratio (OR) and 95% Confidence Interval (95% CI) were calculated. Results: The rs59983488 SNP in the RUNX2 gene was significantly related to the presence of anterior mandibular tooth-size excess in allele (T allele: p<0.001; OR = 11.74; 95% CI =2.61–55.80), and genotype models (GT genotype: p = 0.002; OR = 12.69; 95% CI = 2.47–64.83). The rs3934908 SNP in the SMAD6 gene was significantly associated with the presence of an overall maxillary tooth-size excess in allele (T allele: p < 0.001) and genotype models (TT genotype: p = 0.010). Conclusion: The present results suggest that SNPs in RUNX2 (rs59983488) and SMAD6 (rs3934908) genes may be associated with the presence of tooth-size excess.

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FGF10andFGF13genetic variation and tooth-size discrepancies

Cited by 5 publications

References 42 publications

Craniofacial anomalies in a murine model of heterozygous fibroblast growth factor 10 gene mutation

Craniofacial anomalies in a murine model of heterozygous fibroblast growth factor 10 gene mutation

The Impact of Testosterone Suppression on Dental Structures: An In vivo Study

Single nucleotide polymorphisms in odontogenesis-related genes associated with tooth-size discrepancy

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