IL 1 gene polymorphisms in relation to external apical root resorption concurrent with orthodontia

Objective External apical root resorption ( EARR ) is permanent shortening of the end of the tooth root. It is a common clinical complication of orthodontic treatment. Polymorphisms in the interleukin 1 ( IL 1 ) gene cluster have been related to an increased EARR risk. The aim of this study was to a...

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Bibliographic Details
Published inOral diseases Vol. 19; no. 3; pp. 262 - 270
Main Authors Linhartova, P, Cernochova, P, Izakovicova Holla, L
Format Journal Article
LanguageEnglish
Published 01.04.2013
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Summary:Objective External apical root resorption ( EARR ) is permanent shortening of the end of the tooth root. It is a common clinical complication of orthodontic treatment. Polymorphisms in the interleukin 1 ( IL 1 ) gene cluster have been related to an increased EARR risk. The aim of this study was to analyze possible associations of IL 1 gene variants with EARR in Czech population. Subjects and Methods In this case–control study, 32 patients with EARR (age 15.0 ± 4.1 years) and 74 controls (age 15.2 ± 5.3 years) were genotyped using PCR ‐based methods for IL 1A (−889C/T), IL 1B (+3953C/T), and IL 1 RN [ IL 1 receptor antagonist, variable number tandem repeat ( VNTR )] gene polymorphisms. Results While no statistical significant differences in the IL 1A and IL 1B genotype, allele and reconstructed IL 1 haplotype frequencies between patients with EARR and controls were found, marginally significant differences were observed in the frequencies of IL 1 RN variant ( P  = 0.05 for *22 genotype and P  = 0.06 for a short (2) allele). In addition, significant associations between IL 1 RN *12, *22 genotypes and the short (2) allele and EARR were identified in the subgroup of girls ( P  = 0.04 and P  = 0.02, P  = 0.02). Conclusions Although no significant role of IL 1A (−889C/T) and IL 1B (+3953C/T) variants in EARR was confirmed, IL 1 RN VNTR may be associated with EARR , especially in girls.
ISSN:1354-523X
1601-0825
DOI:10.1111/j.1601-0825.2012.01973.x