IADR Abstract Archives
Genetic Polymorphisms in Promoter Region of DEFB1 Associated Persistent Apical Periodontitis
Objectives: Compromised innate immune systems and/or genetic alterations of the host's defense could play an important role on the development, progression, and healing of apical periodontitis (AP). The aim of this study was to evaluate the association between the promoter region of Defensin Beta 1 (DEFB1) genetic polymorphisms with persistente AP in Brazilian patients.
Methods: Seventy-three patients with post-treatment AP and 89 patients with root canal–treated teeth exhibiting healed/healing healthy periradicular tissues (controls) were included. All teeth had AP lesions at the time of treatment. Patients with at least 1 year of follow-up after nonsurgical root canal therapy were recalled. Genomic DNA was extracted from saliva. DEFB1 at position g. -52G>A (rs1799946), and g. -20G>A (rs11362) were analyzed by by real-time exact tests from genomic DNA. Odds ratio were implemented using Epi Info 3.5.2 (Centers for Disease Control and Prevention, Atlanta, GA). A logistic regression analysis in the co-domonant model, using time of follow up as a variable, was performed and was also used to evaluate the SNP-SNP interaction. All tests were performed with an established alpha of 0.05 (P = .05).
Results: An association between genetic polymorphism in DEFB1 and persistente AP was observed. In DEFB1 gene (rs11362) in the co-dominant and recessive model, patients who carried 2 copies of the T allele had a lower risk of having persistente AP (P=0.040 and P =0.031, respectively). For the polymorphism rs1799946 in DEFB1, in the co-dominant model and recessive model, carrying 1 copies of the T allele increases the risk of having PAP (P =0.007 and P =0.031, respectively). In the logistic regression analysis using time as a covariant, DEFB1 (P<0.0001) were associated with persistente AP.
Conclusions: These findings suggest that polymorphisms in DEFB1 genes are associated with the occurrence of post-treatment AP.
Methods: Seventy-three patients with post-treatment AP and 89 patients with root canal–treated teeth exhibiting healed/healing healthy periradicular tissues (controls) were included. All teeth had AP lesions at the time of treatment. Patients with at least 1 year of follow-up after nonsurgical root canal therapy were recalled. Genomic DNA was extracted from saliva. DEFB1 at position g. -52G>A (rs1799946), and g. -20G>A (rs11362) were analyzed by by real-time exact tests from genomic DNA. Odds ratio were implemented using Epi Info 3.5.2 (Centers for Disease Control and Prevention, Atlanta, GA). A logistic regression analysis in the co-domonant model, using time of follow up as a variable, was performed and was also used to evaluate the SNP-SNP interaction. All tests were performed with an established alpha of 0.05 (P = .05).
Results: An association between genetic polymorphism in DEFB1 and persistente AP was observed. In DEFB1 gene (rs11362) in the co-dominant and recessive model, patients who carried 2 copies of the T allele had a lower risk of having persistente AP (P=0.040 and P =0.031, respectively). For the polymorphism rs1799946 in DEFB1, in the co-dominant model and recessive model, carrying 1 copies of the T allele increases the risk of having PAP (P =0.007 and P =0.031, respectively). In the logistic regression analysis using time as a covariant, DEFB1 (P<0.0001) were associated with persistente AP.
Conclusions: These findings suggest that polymorphisms in DEFB1 genes are associated with the occurrence of post-treatment AP.