Tynior Wojciech, Hudy Dorota, Gołąbek Karolina, Raczkowska-Siostrzonek Agnieszka, Strzelczyk Joanna Katarzyna
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.
Int J Mol Sci. 2025 Jan 17;26(2):766. doi: 10.3390/ijms26020766.
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.
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。
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