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磨牙切牙矿化不全(MIH)患者颊黏膜上皮细胞中 、 、 、 、 和 基因的表达——一项初步研究

Expression of , , , , and Genes in Buccal Epithelial Cells from Patients with Molar Incisor Hypomineralization (MIH)-A Pilot Study.

作者信息

Tynior Wojciech, Hudy Dorota, Gołąbek Karolina, Raczkowska-Siostrzonek Agnieszka, Strzelczyk Joanna Katarzyna

机构信息

Department of Medical and Molecular Biology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, 19 Jordana St., 41-808 Zabrze, Poland.

Department of Dental Surgery, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, 17 Plac Akademicki, 41-902 Bytom, Poland.

出版信息

Int J Mol Sci. 2025 Jan 17;26(2):766. doi: 10.3390/ijms26020766.


DOI:10.3390/ijms26020766
PMID:39859478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11766068/
Abstract

Molar incisor hypomineralization (MIH) is a developmental defect that affects the enamel tissue of permanent teeth. Clinicians may observe a range of opacities in the affected teeth, varying from white to creamy, yellow, and brown. Of particular interest is an etiology of MIH that has not been rigorously elucidated. Researchers believe that there are many potential etiological factors with strong genetic and/or epigenetic influence. The primary factors contributing to the risk of MIH development include specific medical conditions and circumstances. These encompass prematurity, cesarean delivery, perinatal hypoxia, and various health issues such as measles, urinary tract infections, otitis media, gastrointestinal disorders, bronchitis, kidney diseases, pneumonia, and asthma. Although genetic research in this area has received substantial attention, the investigation of epigenetic factors remains comparatively underexplored. Special attention is given to genes and their protein products involved in amelogenesis. Examples of such genes are , , , , , and . The median relative gene expression in the control group was 0.038 (0.031-0.061) and 0.045 (0.032-0.087) in the study group in buccal swabs. The median relative gene expression in the control group was 0.328 (0.247-0.456) and 0.704 (0.334-1.183) in the study group in buccal swabs. Furthermore, children with MIH had significantly higher expression levels compared to the control group (-value = 0.0043). Alterations in the expression of the and genes could be contributing factors to MIH pathogenesis. Nonetheless, further investigation is essential to comprehensively elucidate the roles of all analyzed genes in the pathogenesis of MIH.

摘要

磨牙切牙矿化不全(MIH)是一种影响恒牙牙釉质组织的发育缺陷。临床医生可能会观察到患牙出现一系列不同程度的色泽改变,从白色到乳黄色、黄色和棕色不等。特别值得关注的是,MIH的病因尚未得到严格阐明。研究人员认为,有许多潜在的病因因素具有强大的遗传和/或表观遗传影响。导致MIH发生风险的主要因素包括特定的医疗状况和情况。这些包括早产、剖宫产、围产期缺氧以及各种健康问题,如麻疹、尿路感染、中耳炎、胃肠道疾病、支气管炎、肾脏疾病、肺炎和哮喘。尽管该领域的基因研究受到了广泛关注,但对表观遗传因素的研究仍相对不足。特别关注参与釉质形成的基因及其蛋白质产物。此类基因的例子有 、 、 、 、 和 。在颊拭子中,对照组中 基因的相对表达中位数为0.038(0.031 - 0.061),研究组为0.045(0.032 - 0.087)。在颊拭子中,对照组中 基因的相对表达中位数为0.328(0.247 - 0.456),研究组为0.704(0.334 - 1.183)。此外,与对照组相比,患有MIH的儿童 表达水平显著更高( -值 = 0.0043)。 和 基因表达的改变可能是MIH发病机制的促成因素。尽管如此,进一步的研究对于全面阐明所有分析基因在MIH发病机制中的作用至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bd/11766068/a0141c303e6d/ijms-26-00766-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bd/11766068/bb15dff52fc3/ijms-26-00766-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bd/11766068/a0141c303e6d/ijms-26-00766-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bd/11766068/bb15dff52fc3/ijms-26-00766-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bd/11766068/a0141c303e6d/ijms-26-00766-g002.jpg

相似文献

[1]
Expression of , , , , and Genes in Buccal Epithelial Cells from Patients with Molar Incisor Hypomineralization (MIH)-A Pilot Study.

Int J Mol Sci. 2025-1-17

[2]
Genes expressed in dental enamel development are associated with molar-incisor hypomineralization.

Arch Oral Biol. 2013-6-19

[3]
Family-Based Genetic Association for Molar-Incisor Hypomineralization.

Caries Res. 2016

[4]
Dataset on amelogenesis-related genes variants ( and interacting genes) and on human leukocyte antigen alleles (DQ2 and DQ8) distribution in children with and without molar-incisor hypomineralisation (MIH).

Data Brief. 2020-8-25

[5]
Interactions with the aquaporin 5 gene increase the susceptibility to molar-incisor hypomineralization.

Arch Oral Biol. 2019-12-23

[6]
Human and mouse enamel phenotypes resulting from mutation or altered expression of AMEL, ENAM, MMP20 and KLK4.

Cells Tissues Organs. 2009

[7]
Exclusion of candidate genes in seven Turkish families with autosomal recessive amelogenesis imperfecta.

Am J Med Genet A. 2009-7

[8]
Significance of genetic variations in developmental enamel defects of primary dentition in Polish children.

Clin Oral Investig. 2017-4-5

[9]
Metagenomic Analysis of the Buccal Microbiome by Nanopore Sequencing Reveals Structural Differences in the Microbiome of a Patient with Molar Incisor Hypomineralization (MIH) Compared to a Healthy Child-Case Study.

Int J Mol Sci. 2024-12-6

[10]
Genes Regulating Immune Response and Amelogenesis Interact in Increasing the Susceptibility to Molar-Incisor Hypomineralization.

Caries Res. 2018-8-21

本文引用的文献

[1]
Mutations and Genotype-Phenotype Correlation in X-Linked Amelogenesis Imperfecta.

Int J Mol Sci. 2024-6-1

[2]
Small Molecules Promote the Rapid Generation of Dental Epithelial Cells from Human-Induced Pluripotent Stem Cells.

Int J Mol Sci. 2024-4-9

[3]
Overexpression of ameloblastin in secretory ameloblasts results in demarcated, hypomineralized opacities in enamel.

Front Physiol. 2024-1-11

[4]
CRISPR/Cas9-Induced Fam83h Knock-out Leads to Impaired Wnt/β-Catenin Pathway and Altered Expression of Tooth Mineralization Genes in Mice.

Iran J Biotechnol. 2023-10-1

[5]
Splicing mutations in AMELX and ENAM cause amelogenesis imperfecta.

BMC Oral Health. 2023-11-20

[6]
Mobility gene expression differences among wild-type, Mmp20 null and Mmp20 over-expresser mice plus visualization of 3D mouse ameloblast directional movement.

Sci Rep. 2023-11-1

[7]
In silico screening of non-synonymous SNPs in human TUFT1 gene.

J Genet Eng Biotechnol. 2023-10-6

[8]
Relationship between the TGFBR1 Gene and Molar Incisor Hypomineralization.

J Pers Med. 2023-4-30

[9]
Association between genetic factors and molar-incisor hypomineralisation or hypomineralised second primary molar: A systematic review.

Arch Oral Biol. 2023-8

[10]
Enam expression is regulated by Msx2.

Dev Dyn. 2023-10

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