外根尖吸收和正畸牙齿移动的遗传多态性:系统评价。
Genetic polymorphisms in external apical root resorption and orthodontic tooth movements: A systematic review.
发表日期:2024 Aug 20
作者:
Ana Luiza Cabral de Ávila Andrade, Yasmin Dias de Almeida Pinto, Bernardo Emerenciano Barros Maia, Joice Dias Corrêa, Diogo de Azevedo Miranda, Flávio Ricardo Manzi, Izabella Lucas de Abreu Lima
来源:
GENES & DEVELOPMENT
摘要:
根尖外吸收(EARR)的特点是根尖处的牙齿结构永久丧失。本研究旨在系统评价正畸患者中与 EARR 相关的基因多态性。在多个数据库中进行了电子数据库检索。该系统评价包括 21 项研究。结果测量基于治疗前后获得的射线照片上观察到的牙齿尺寸。使用聚合酶链反应-限制性片段长度多态性分析对以下基因的多态性进行基因分型:嘌呤受体-P2X、配体门控离子通道7 (P2RX7)、caspase-1/白细胞介素转换酶(CASP1/ICE)、caspase- 5 (CASP5)、IL-1beta (IL1B)、IL-1alpha (IL1A)、白介素 1 受体拮抗剂基因 (IL1RN)、组织非特异性碱性磷酸酶 (TNSALP)、肿瘤坏死因子-α (TNFα)、肿瘤坏死因子受体超家族基因成员 11a (TNFRSF11A)、分泌型磷蛋白 1 (SPP1)、肿瘤坏死因子受体超家族基因成员 11b (TNFRSF11B)、白细胞介素 17A (IL17)、白细胞介素 6 (IL6)、核因子 kappa B 受体激活剂 ( RANK)、骨保护素 (OPG)、基质抗原 2 (STAG2)、维生素 D 受体 (VDR)、细胞色素 P450 家族 24 亚家族 A 成员 1 (CYP24A1)、细胞色素 P450 家族 27 亚家族 B (CYP27B1)、组特异性成分 (GC) ) 和白细胞介素-1 受体相关激酶 1 (IRAK1)。几乎所有研究都表明 IL1 基因与 EARR 相关。此外,P2RX7可能是导致EARR发病机制的重要因素。 TNFRSF11A、SPP1、IL1RN、IL6、TNFRSF11B、STAG2、VDR、IRAK1、IL-17、CASP1/ICE 和 CASP5 已在单独的研究中得到鉴定。需要进一步的观察性研究来更好地解释这些基因与 EARR 之间的关联。
External apical root resorption (EARR) is characterized by permanent loss of dental structure at the root apex. This study aimed to systematically review gene polymorphisms associated with EARR in orthodontic patients.Electronic database searches were performed across several databases.This systematic review included 21 studies. Outcome measures were based on tooth dimensions observed on radiographs obtained before and after treatment. Polymorphisms in the following genes were genotyped using polymerase chain reaction-restriction fragment length polymorphism analysis: purinergic-receptor-P2X, ligand-gated ion channel 7 (P2RX7), caspase-1/interleukin-converting enzyme (CASP1/ICE), caspase-5 (CASP5), IL-1beta (IL1B), IL-1alpha (IL1A), interleukin-1 receptor antagonist gene (IL1RN), tissue non-specific alkaline phosphatase (TNSALP), tumor necrosis factor-alpha (TNFα), tumor necrosis factor receptor superfamily gene member 11a (TNFRSF11A), secreted phosphoprotein 1 (SPP1), tumor necrosis factor receptor superfamily gene member 11b (TNFRSF11B), interleukin 17A (IL17), interleukin 6 (IL6), receptor activator of nuclear factor-kappa B (RANK), osteoprotegerin (OPG), stromal antigen 2 (STAG2), vitamin D receptor (VDR), cytochrome P450 family 24 subfamily A member 1 (CYP24A1), cytochrome P450 family 27 subfamily B (CYP27B1), group-specific component (GC), and interleukin-1 receptor-associated kinases 1 (IRAK1).Almost all studies suggested that IL1 gene is associated with EARR. Additionally, P2RX7 may be an important factor contributing to the etiopathogenesis of EARR. TNFRSF11A, SPP1, IL1RN, IL6, TNFRSF11B, STAG2, VDR, IRAK1, IL-17, CASP1/ICE and CASP5 have been identified in isolated studies. Further observational studies are needed to better explain the association between these genes and EARR.