Keerthika R, Kamboj Mala, Girdhar Akhil, Narwal Anjali, Devi Anju, Anand Rahul, Juneja Manish
Department of Oral and Maxillofacial Pathology and Microbiology, Post Graduate Institute of Dental Sciences, Pandit Bhagwat Dayal Sharma University of Health Sciences, Rohtak, Haryana, India.
Department of Oral and Maxillofacial Pathology, Dr D Y Patil Dental College and Hospital, Dr D Y Patil Vidyapeeth, Pimpri, Pune, India.
J Oral Pathol Med. 2023 Oct;52(9):803-810. doi: 10.1111/jop.13472. Epub 2023 Aug 8.
Angiogenesis plays a vital role at the molecular level in various inflammatory lesions, that lead to their chronicity. Oral lichen planus is an immune-mediated chronic inflammatory disorder. The angiogenetic role and exact mechanisms in oral lichen planus are still unclear due to a dearth of studies. Its clinical significance with angiogenesis also requires further elucidation necessitating a thorough review of the studies that have been conducted so far. The present review was designed to identify the dependence of oral lichen planus progression on angiogenesis which could aid in devising metronomic treatments required to halt the progression of this disease.
A thorough search was made using MEDLINE by PubMed, Scopus, Google scholar, Cochrane library, and EMBASE databases. Original research articles, that immunohistochemically evaluated angiogenesis in oral lichen planus were included for review. Risk of bias was analysed for each study using Modified Newcastle-Ottawa scale and Review Manager 5.4 was used to output its result.
Twenty-nine published articles were included for data synthesis. The most commonly employed antibody was CD34, however, upregulated VEGF expression was the principal while ICAM-1, VCAM-1, and PECAM-1 were critical angiogenic factors to mediate angiogenesis in oral lichen planus.
The current evidence supports that angiogenesis, a fundamental pathogenetic mechanism of oral lichen planus, leads to its persistence and chronicity. However, studies with a larger sample size, standard evaluation criteria, different subtypes, and adequate follow-up are warranted.
血管生成在各种炎症性病变的分子水平上起着至关重要的作用，导致这些病变迁延不愈。口腔扁平苔藓是一种免疫介导的慢性炎症性疾病。由于研究匮乏，口腔扁平苔藓中血管生成的作用及确切机制仍不清楚。其与血管生成的临床意义也需要进一步阐明，因此有必要对迄今为止已开展的研究进行全面综述。本综述旨在确定口腔扁平苔藓进展对血管生成的依赖性，这有助于设计出阻止该疾病进展所需的节拍式治疗方案。
通过PubMed、Scopus、谷歌学术、Cochrane图书馆和EMBASE数据库使用MEDLINE进行全面检索。纳入通过免疫组织化学评估口腔扁平苔藓中血管生成的原始研究文章进行综述。使用改良的纽卡斯尔-渥太华量表对每项研究的偏倚风险进行分析，并使用Review Manager 5.4输出结果。
纳入29篇已发表文章进行数据综合分析。最常用的抗体是CD34，然而，VEGF表达上调是主要因素，而ICAM-1、VCAM-1和PECAM-1是介导口腔扁平苔藓血管生成的关键血管生成因子。
目前的证据支持血管生成作为口腔扁平苔藓的一种基本发病机制，导致其持续存在和慢性化。然而，需要开展样本量更大、评估标准规范、涵盖不同亚型且随访充分的研究。
