口腔扁平苔藓的分子标记及其发病机制。

IF 3.2 Q2 PATHOLOGY
Maria Zaharieva Mutafchieva, Milena Nenkova Draganova, Georgi Tomchev Tomov
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引用次数: 0

摘要

目的:口腔扁平苔藓(OLP)是一种以免疫介导的基底角化细胞凋亡为特征的慢性炎症性疾病。近年来,程序性细胞死亡对OLP组织破坏的重要性一直存在争议,而与此同时,这些病变的上皮细胞增殖指数增加。OLP被认为是一种癌前病变。本研究通过研究促凋亡、抗凋亡和增殖标志物在OLP病变中的表达,试图进一步了解该疾病的发病机制和恶性潜能。方法:对20例经组织学证实的OLP患者与10例健康对照进行p53、p63、bcl-2、Ki-67、COX-2水平的免疫组化分析。结果:与正常口腔黏膜相比,p63在OLP病变中的表达明显降低。p53、bcl-2、Ki-67、COX-2水平与对照组比较无显著差异。p63和Ki-67之间存在显著相关性(p = 0.001), p63和p53之间存在显著相关性(p = 0.016)。炎性COX-2和凋亡性p53的表达似乎相互独立(p = 0.44)。五种分析标记物的表达强度与临床表现的严重程度无关。结论:细胞凋亡可能不是本病发病的主要机制。另一方面,p63的表达降低似乎起着重要作用。这种蛋白质缺乏的可能影响包括程序性细胞死亡的激活、细胞周期阻滞、细胞衰老或衰老;抑制细胞增殖或改变细胞分化观察到p63、Ki67和bcl-2水平的降低易导致上皮变薄、侵蚀和/或溃疡。对于提出的OLP队列,没有分子证据表明病变的恶性潜能增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular Markers in Oral Lichen Planus - Insight into Pathogenesis.

Purpose: Oral lichen planus (OLP) is a chronic inflammatory disease, characterized by immune-mediated basal keratinocyte apoptosis. In recent years the importance of programmed cell death for the tissue destruction in OLP has been disputed, while at the same time an increased proliferative index has been reported in the epithelium of these lesions. OLP is considered as a precancerous condition. This study investigated the expression of pro-apoptotic, anti-apoptotic and proliferative markers in OLP lesions in an attempt to understand more about the pathogenesis and malignant potential of the disease.

Methods: Twenty patients with histologically confirmed OLP were compared to ten healthy controls through immunohistochemical analysis of the levels of p53, p63, bcl-2, Ki-67 and COX-2.

Results: The results demonstrated significantly decreased expression of p63 in OLP lesions compared to normal oral mucosa. The levels of p53, bcl-2, Ki-67, and COX-2 were not significantly different from those in the control group. A significant association was found between p63 and Ki-67 (p = 0.001), as well as between p63 and p53 (p = 0.016). Expression of the inflammatory COX-2 and the apoptotic p53 appeared to be independent of each other (p = 0.44). The intensity of expression of any of the five analyzed markers was not related to the severity of the clinical manifestation.

Conclusions: The obtained results suggest that apoptosis may not be the dominant mechanism in the disease's pathogenesis. Decreased expression of p63 on the other hand appears to play an important role. Among the possible effects of this protein deficiency are activation of programmed cell death, cell cycle arrest, cellular senescence, or anoikis; suppression of cell proliferation or changes in cell differentiation. The observed reduction in p63, Ki67 and bcl-2 levels predisposes to epithelial thinning, erosions and/or ulcers. For the presented OLP cohort, there was no molecular evidence of increased malignant potential of the lesions.

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来源期刊
CiteScore
5.70
自引率
9.50%
发文量
99
期刊介绍: Head & Neck Pathology presents scholarly papers, reviews and symposia that cover the spectrum of human surgical pathology within the anatomic zones of the oral cavity, sinonasal tract, larynx, hypopharynx, salivary gland, ear and temporal bone, and neck. The journal publishes rapid developments in new diagnostic criteria, intraoperative consultation, immunohistochemical studies, molecular techniques, genetic analyses, diagnostic aids, experimental pathology, cytology, radiographic imaging, and application of uniform terminology to allow practitioners to continue to maintain and expand their knowledge in the subspecialty of head and neck pathology. Coverage of practical application to daily clinical practice is supported with proceedings and symposia from international societies and academies devoted to this field. Single-blind peer review The journal follows a single-blind review procedure, where the reviewers are aware of the names and affiliations of the authors, but the reviewer reports provided to authors are anonymous. Single-blind peer review is the traditional model of peer review that many reviewers are comfortable with, and it facilitates a dispassionate critique of a manuscript.
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