Tang Jianfei, Liu Junjie, Zhou Zekun, Cui Xinyan, Tu Hua, Jia Jia, Chen Baike, Dai Xiaohan, Liu Ousheng
Hunan Key Laboratory of Oral Health Research & Hunan 3D Printing Engineering Research Center of Oral Care & Hunan Clinical Research Center of Oral Major Diseases and Oral Health & Academician Workstation for Oral-Maxilofacial and Regenerative Medicine & Xiangya Stomatological Hospital & Xiangya School of Stomatology, Central South University, Changsha, China.
Int J Oral Sci. 2025 Feb 1;17(1):8. doi: 10.1038/s41368-024-00344-6.
Oral submucous fibrosis (OSF), characterized by excessive deposition of extracellular matrix (ECM) that causes oral mucosal tissue sclerosis, and even cancer transformation, is a chronic, progressive fibrosis disease. However, despite some advancements in recent years, no targeted antifibrotic strategies for OSF have been approved; likely because the complicated mechanisms that initiate and drive fibrosis remain to be determined. In this review, we briefly introduce the epidemiology and etiology of OSF. Then, we highlight how cell-intrinsic changes in significant structural cells can drive fibrotic response by regulating biological behaviors, secretion function, and activation of ECM-producing myofibroblasts. In addition, we also discuss the role of innate and adaptive immune cells and how they contribute to the pathogenesis of OSF. Finally, we summarize strategies to interrupt key mechanisms that cause OSF, including modulation of the ECM, inhibition of inflammation, improvement of vascular disturbance. This review will provide potential routes for developing novel anti-OSF therapeutics.
口腔黏膜下纤维化（OSF）是一种慢性进行性纤维化疾病，其特征是细胞外基质（ECM）过度沉积，导致口腔黏膜组织硬化，甚至癌变。然而，尽管近年来取得了一些进展，但尚未有针对OSF的靶向抗纤维化策略获得批准；这可能是因为引发和驱动纤维化的复杂机制仍有待确定。在本综述中，我们简要介绍了OSF的流行病学和病因。然后，我们重点阐述了重要结构细胞的细胞内在变化如何通过调节生物学行为、分泌功能以及产生ECM的肌成纤维细胞的激活来驱动纤维化反应。此外，我们还讨论了固有免疫细胞和适应性免疫细胞的作用以及它们如何促成OSF的发病机制。最后，我们总结了中断导致OSF的关键机制的策略，包括调节ECM、抑制炎症、改善血管紊乱。本综述将为开发新型抗OSF治疗方法提供潜在途径。
