Genetic polymorphisms in external apical root resorption and orthodontic tooth movements:A systematic review
- Author:
Ana Luiza Cabral de Ávila ANDRADE
1
;
Yasmin Dias de Almeida PINTO
;
Bernardo Emerenciano Barros MAIA
;
Joice Dias CORRÊA
;
Diogo de Azevedo MIRANDA
;
Flávio Ricardo MANZI
;
Izabella Lucas de Abreu LIMA
Author Information
- Publication Type:Original Article
- From:The Korean Journal of Orthodontics 2024;54(5):284-302
- CountryRepublic of Korea
- Language:English
-
Abstract:
Objective: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.
Methods:Electronic database searches were performed across several databases.
Results: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 nonspecific 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 receptorassociated kinases 1 (IRAK1).
Conclusions: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.
