Genetic and other factors contributing to external apical root resorption in orthodontic patients

Abstract

Objective: External apical root resorption (EARR) is a multifactorial disorder with adverse clinical outcomes in orthodontic practices often resulting in significant root shortening. This study examined the effect that specific single nucleotide polymorphisms (SNPs) have on the risk of developing EARR in orthodontic patients in X. We also evaluated how other selected patient- and treatment-related factors may contribute to root resorption in these patients.

Setting/sample: Patients included in this case-control study were treated at the University of Alabama at Birmingham School of Dentistry, Department of Orthodontics.

Methods: Panoramic radiographs were used to measure root resorption of the maxillary incisors. EARR was recorded when at least 20% of the root length had been lost with orthodontic treatment. Factors evaluated for association with EARR included ethnicity, sex, age, dental and skeletal classifications, ANB, U1-SN, overjet, treatment type and time, and SNPs in IL-1A (rs1800587), IL-1B (rs1143634), IL-1RN (rs419598), P2RX7 (rs1718119 and rs2230912), IRAK1 (rs1059703) and CASP1 (rs530537, rs580253 and rs554344). Chi-square test, Student's t test, Wilcoxon test, Benjamin-Hochberg false discovery rate (FDR) adjustment and logistic regression were used to analyse the data. The significance level was defined as P < .05.

Results: We found that extraction treatment protocol and dental classification displayed significant association with root resorption. Furthermore, the GG genotype of IL-1A rs1800587 variant (in individuals with an increased overjet) predisposed Caucasians to EARR. While CASP1 (rs530537) variant may contribute to the risk of root resorption, it was not statistically significant after FDR adjustment (P = .09).

Conclusions: Both patient- and treatment-related factors contributed to EARR.

Keywords: caspase 1; external apical root resorption; orthodontic treatment; risk factors; single nucleotide polymorphism.