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DNA甲基化与口腔扁平苔藓的发病机制OA

DNA methylation and the pathogenesis of oral lichen planus

中文摘要英文摘要

口腔扁平苔藓(oral lichen planus,OLP)是一种高发病率的口腔黏膜慢性炎症性疾病,以T细胞介导的免疫异常为主要特征,具有潜在恶变风险.DNA甲基化作为一种重要的表观遗传调控机制,通过影响免疫相关基因的表达参与OLP的发病过程.环境因素和遗传多态性可导致DNA甲基化模式异常,进而影响T细胞功能、细胞因子分泌及炎症反应调控.在OLP患者中,已发现多种免疫相关基因、微RNA及转录因子存在特征性甲基化改变.其不仅参与了疾病的发生和发展,还与疾病活动度及恶性转化密切相关.DNA甲基化通过调控基因表达,在OLP的发病机制、病情评估及恶变预测等方面的研究逐渐深入,为OLP开发新型诊断标志物和靶向治疗策略提供了重要理论依据.

Oral lichen planus(OLP)is a chronic inflammatory disease of the oral mucosa with a high incidence,characterized primarily by T-cell-mediated immune dysregulation and carrying a potential risk of malignant transformation.DNA methylation,as an important epigenetic regulatory mechanism,participates in the pathogenesis of OLP by influencing the expression of immune-related genes.Environmental factors and genetic polymorphisms can lead to abnormal DNA methylation patterns,thereby affecting T cell function,cytokine secretion,and the regulation of inflammatory responses.In patients with OLP,characteristic methylation alterations have been identified in various immune-related genes,microRNAs,and transcription factors.These changes not only participate in the occurrence and development of the disease but are also closely associated with disease activity and malignant transformation.DNA methylation,through the regulation of gene expression,has been increasingly studied in relation to pathogenesis,disease assessment,and prediction of malignant transformation in OLP,providing important theoretical support for the development of novel diagnostic biomarkers and targeted therapeutic strategies.

李凯;邓睿恒;朱慧敏;常瑜;成志勇

定州市人民医院口腔科,定州 073000暨南大学口腔医学院,广州 510632河北北方学院研究生学院,张家口 075000||保定市第一医院血液内科,保定 071000保定市第一医院口腔科,保定 071000保定市第一医院血液内科,保定 071000

医药卫生

口腔扁平苔藓DNA甲基化发病机制甲基化标志物微RNA

oral lichen planusDNA methylationpathogenesismethylation markersmicroRNA

《临床与病理杂志》 2026 (1)

89-98,10

河北省重点研发计划(223777105D).This work was supported by the Key Research and Development Project of Hebei Province,China(223777105D).

10.11817/j.issn.2095-6959.2026.250880

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