Orofacial clefts (OFCs) have multiple etiologies and likely result from an interplay between genetic and environmental factors. Within the last decade, studies have implicated specific epigenetic modifications and noncoding RNAs as additional facets of OFC etiology. Altered gene expression through DNA methylation and histone modification offer novel insights into how specific genes contribute to distinct OFC subtypes. Epigenetics research has also provided further evidence that cleft lip only (CLO) is a cleft subtype with distinct etiology. Polymorphisms or misexpression of genes encoding microRNAs, as well as their targets, contribute to OFC risk. The ability to experimentally manipulate epigenetic changes and noncoding RNAs in animal models, such as zebrafish, Xenopus, mice, and rats, has offered novel insights into the mechanisms of various OFC subtypes. Although much remains to be understood, recent advancements in our understanding of OFC etiology may advise future strategies of research and preventive care.

中文翻译：

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表观遗传学和 miRNA 在口面部裂隙中的作用。

口面部裂隙 (OFC) 有多种病因，可能是遗传和环境因素相互作用的结果。在过去十年中，研究表明特定的表观遗传修饰和非编码 RNA 是 OFC 病因学的其他方面。通过 DNA 甲基化和组蛋白修饰改变的基因表达为特定基因如何促成不同的 OFC 亚型提供了新的见解。表观遗传学研究还提供了进一步的证据，证明仅唇裂 (CLO) 是一种具有不同病因的唇裂亚型。编码 microRNA 的基因及其靶标的多态性或错误表达会导致 OFC 风险。在动物模型（如斑马鱼、非洲爪蟾）中通过实验操作表观遗传变化和非编码 RNA 的能力、小鼠和大鼠提供了对各种 OFC 亚型机制的新见解。尽管还有很多需要了解，但我们对 OFC 病因学的理解的最新进展可能会为未来的研究和预防保健策略提供建议。