牙源性角化囊肿分子机制研究进展——从病理发生到复发风险的多层次解析

Molecular Mechanism Research Progress of Odontogenic Keratocyst—A Multilevel Analysis from Pathogenesis to Recurrence Risk

摘要: 牙源性角化囊肿(odontogenic keratocyst, OKC)是一类源自牙板上皮残余或口腔黏膜上皮的颌骨囊性病变，具有高复发率和局部侵袭性，其分子机制研究已成为近年关注的热点。最新研究表明，OKC的发生发展可能与Hedgehog (SHH/PTCH)信号通路异常激活、DNA甲基化失衡、AP-1家族转录因子上调、PKM2介导的糖酵解、RANKL介导的骨破坏及角化相关蛋白异常定位等密切相关；单细胞测序进一步揭示了具有高干性或高侵袭性的上皮细胞亚群，以及成纤维细胞与免疫细胞的表型转变在病程中的潜在作用。多种分子机制协同作用，赋予OKC显著的局部侵袭性与高复发风险。本文系统梳理了近年来OKC分子病理机制的研究进展，旨在为深入阐明其发病机制和风险评估提供参考。

Abstract: Odontogenic keratocyst (OKC) is a type of jaw cystic lesion originating from remnants of the dental lamina epithelium or oral mucosal epithelium. It is characterized by a high recurrence rate and local aggressiveness, making its molecular mechanisms a research focus in recent years. Latest studies have revealed that the occurrence and progression of OKC are closely associated with abnormal activation of the Hedgehog (SHH/PTCH) signaling pathway, imbalance in DNA methylation, upregulation of AP-1 family transcription factors, PKM2-driven glycolysis, RANKL-mediated bone resorption, and aberrant localization of keratin-associated proteins. Single-cell sequencing has further identified epithelial cell subpopulations with high stemness or invasiveness, as well as potential roles of phenotypic transformation in fibroblasts and immune cells during disease progression. Multiple molecular mechanisms act synergistically to confer significant local aggressiveness and a high recurrence risk to OKC. This paper systematically reviews recent advances in the study of OKC’s molecular pathological mechanisms, aiming to provide a reference for deeper understanding of its pathogenesis and risk assessment.