Igor Bassi Ferreira Petean1, Erika Calvano Küchler2, Isadora Mello Vilarinho Soares1, Raquel Assed Bezerra Segato2, Léa Assed Bezerra da Silva2, Lívia Azeredo Alves Antunes3, Alessandro Guimarães Salles3, Leonardo Santos Antunes3, Manoel Damião de Sousa-Neto4. 1. Department of Restorative Dentistry School of Dentistry of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil. 2. Department of Pediatric Dentistry, School of Dentistry of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil. 3. Clinical Research Unit, Fluminense Federal University, Niterói, Rio de Janeiro, Brazil; Department of Specific Formation, School of Dentistry of Nova Friburgo, Fluminense Federal University, Nova Friburgo, Rio de Janeiro, Brazil. 4. Department of Restorative Dentistry School of Dentistry of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil. Electronic address: sousanet@forp.usp.br.
Abstract
INTRODUCTION: The outcome of root canal treatment has been reported as intimately related to the host response. Genetic polymorphisms might be associated with apical periodontitis repair. The aim of this study was to evaluate the association between receptor activator of nuclear factor kappa B (RANK), receptor activator of nuclear factor kappa B ligand (RANKL), and osteoprotegerin (OPG) genetic polymorphisms with persistent apical periodontitis (PAP) in Brazilian subjects. METHODS: Subjects with at least 1 year of follow-up after nonsurgical root canal therapy were recalled. Sixty-four subjects with signs/symptoms of PAP and 86 subjects with root canal-treated teeth exhibiting healthy periradicular tissues (healed) were included. Genomic DNA was extracted from saliva and used for RANK (rs3826620), RANKL (rs9594738), and OPG (rs2073618) genotyping by real-time exact tests, and odds ratio were implemented using Epi Info 3.5.2 (Centers for Disease Control and Prevention, Atlanta, GA). A logistic regression analysis was also performed using the time of follow-up as the covariate. All tests were performed with an established alpha of 0.05 (P = .05). RESULTS: An association between allele distribution and the polymorphism in RANK was observed. Subjects who carry the T allele had a lower risk of having PAP (P < .05). In RANKL polymorphism, the genotype distribution was statistically significant different between the PAP and healed groups (P = .05). The time of follow-up was associated with PAP (P < .05). In the logistic regression analysis using time as a covariant, RANK (P < .05) and RANKL (P < .05) were associated with PAP. The polymorphism rs2073618 in OPG was not associated with PAP (P > .05). CONCLUSIONS: These findings suggest that polymorphisms in RANK and RANKL genes are associated with PAP.
INTRODUCTION: The outcome of root canal treatment has been reported as intimately related to the host response. Genetic polymorphisms might be associated with apical periodontitis repair. The aim of this study was to evaluate the association between receptor activator of nuclear factor kappa B (RANK), receptor activator of nuclear factor kappa B ligand (RANKL), and osteoprotegerin (OPG) genetic polymorphisms with persistent apical periodontitis (PAP) in Brazilian subjects. METHODS: Subjects with at least 1 year of follow-up after nonsurgical root canal therapy were recalled. Sixty-four subjects with signs/symptoms of PAP and 86 subjects with root canal-treated teeth exhibiting healthy periradicular tissues (healed) were included. Genomic DNA was extracted from saliva and used for RANK (rs3826620), RANKL (rs9594738), and OPG (rs2073618) genotyping by real-time exact tests, and odds ratio were implemented using Epi Info 3.5.2 (Centers for Disease Control and Prevention, Atlanta, GA). A logistic regression analysis was also performed using the time of follow-up as the covariate. All tests were performed with an established alpha of 0.05 (P = .05). RESULTS: An association between allele distribution and the polymorphism in RANK was observed. Subjects who carry the T allele had a lower risk of having PAP (P < .05). In RANKL polymorphism, the genotype distribution was statistically significant different between the PAP and healed groups (P = .05). The time of follow-up was associated with PAP (P < .05). In the logistic regression analysis using time as a covariant, RANK (P < .05) and RANKL (P < .05) were associated with PAP. The polymorphism rs2073618 in OPG was not associated with PAP (P > .05). CONCLUSIONS: These findings suggest that polymorphisms in RANK and RANKL genes are associated with PAP.