Daniel Vitor de SOUZA, Wilton Mitsunari TAKESHITA, Glaucia Monteiro de CASTRO, Ana Claudia Muniz RENNO, Jean Nunes dos SANTOS, Daniel Araki RIBEIRO
{"title":"在接受固定正畸治疗的患者中使用微核测定脱落的口腔细胞:一项具有荟萃分析的系统综述","authors":"Daniel Vitor de SOUZA, Wilton Mitsunari TAKESHITA, Glaucia Monteiro de CASTRO, Ana Claudia Muniz RENNO, Jean Nunes dos SANTOS, Daniel Araki RIBEIRO","doi":"10.1590/1807-3107bor-2023.vol37.0116","DOIUrl":null,"url":null,"abstract":"The aim of this systematic review was to evaluate published papers regarding the micronucleus assay in oral mucosal cells of patients undergoing orthodontic therapy (OT). A search of the scientific literature was made in the PubMed, Scopus, and Web of Science databases for all data published until November, 2021 using the combination of the following keywords: “fixed orthodontic therapy,” “genetic damage”, “DNA damage,” “genotoxicity”, “mutagenicity”, “buccal cells”, “oral mucosa cells,” and “micronucleus assay”. The systematic review was designed according to the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines. Nine studies were retrieved. Some authors demonstrated that OT induces cytogenetic damage in oral mucosal cells. Out of the nine studies included, two were classified as strong, five as moderate, and two as weak, according to the quality assessment components of the Effective Public Health Practice Project (EPHPP). Meta-analysis data revealed no relationship between mutagenicity in oral cells and OT in different months of treatment. At one month, the SMD = 0.65 and p = 0.08; after three months of OT, the SMD = 1.21 and p = 0.07; and after six months of OT, the SMD = 0.56 and p = 0.11. In the analyzed months of OT, I2 values were >75%, indicating high heterogeneity. In summary, this review was not able to demonstrate that OT induces genetic damage in oral cells. 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引用次数: 0
摘要
本系统综述的目的是评价已发表的关于正畸治疗(OT)患者口腔黏膜细胞微核测定的论文。在PubMed、Scopus和Web of Science数据库中检索截至2021年11月发表的所有数据,使用以下关键词组合进行检索:“固定正畸治疗”、“遗传损伤”、“DNA损伤”、“遗传毒性”、“突变性”、“颊细胞”、“口腔黏膜细胞”和“微核测定”。系统评价按照系统评价和荟萃分析首选报告项目(PRISMA)指南设计。9项研究被检索。一些作者证实,OT可诱导口腔粘膜细胞的细胞遗传学损伤。在纳入的9项研究中,根据有效公共卫生实践项目(EPHPP)的质量评估组成部分,2项研究被分类为强,5项为中等,2项为弱。荟萃分析数据显示,在治疗的不同月份,口腔细胞的突变性与OT之间没有关系。1个月时,SMD = 0.65, p = 0.08;治疗3个月后,SMD = 1.21, p = 0.07;治疗6个月后,SMD = 0.56, p = 0.11。在OT的分析月份中,I2值>75%,异质性较高。总之,本综述无法证明OT诱导口腔细胞的遗传损伤。考虑到突变参与了多步骤的癌变过程,该研究对固定OT患者的保护具有重要意义。
The use of micronucleus assay in exfoliated oral cells in patients undergoing fixed orthodontic therapy: a systematic review with meta-analysis
The aim of this systematic review was to evaluate published papers regarding the micronucleus assay in oral mucosal cells of patients undergoing orthodontic therapy (OT). A search of the scientific literature was made in the PubMed, Scopus, and Web of Science databases for all data published until November, 2021 using the combination of the following keywords: “fixed orthodontic therapy,” “genetic damage”, “DNA damage,” “genotoxicity”, “mutagenicity”, “buccal cells”, “oral mucosa cells,” and “micronucleus assay”. The systematic review was designed according to the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines. Nine studies were retrieved. Some authors demonstrated that OT induces cytogenetic damage in oral mucosal cells. Out of the nine studies included, two were classified as strong, five as moderate, and two as weak, according to the quality assessment components of the Effective Public Health Practice Project (EPHPP). Meta-analysis data revealed no relationship between mutagenicity in oral cells and OT in different months of treatment. At one month, the SMD = 0.65 and p = 0.08; after three months of OT, the SMD = 1.21 and p = 0.07; and after six months of OT, the SMD = 0.56 and p = 0.11. In the analyzed months of OT, I2 values were >75%, indicating high heterogeneity. In summary, this review was not able to demonstrate that OT induces genetic damage in oral cells. The study is important for the protection of patients undergoing fixed OT, given that mutagenesis participates in the multi-step process of carcinogenesis.