Interaction between polymorphisms in TNF-⍺ and RANKL genes is associated with the development of persistent apical periodontitis, in Brazilian subjects.

Objectives: To investigate the association between genetic polymorphisms in suppressor of cytokine signaling-1 (SOCS-1), tumor necrosis factor-⍺ (TNF-α) and its receptors 1 and 2 (TNFRSF1A and TNFRSF1B), receptor activator of nuclear factor kappa-b (RANK), receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG), and persistent apical periodontitis (PAP).
Methods: Patients with pulp necrosis and apical periodontitis at the time of non-surgical root canal treatment were followed up for at least one year. A total of 423 subjects were included, 172 with signs/symptoms of PAP and 251 with apical periodontitis healed. DNA was extracted from saliva and used for genotyping polymorphisms in SOCS1 (rs243327 and rs33977706), TNF-α (rs1800629), TNFRSF1A (rs1800693), TNFRSF1B (rs1061622), RANK (rs1805034), RANKL (rs1054016) and OPG (rs1032128) by real-time PCR. The frequency of genotypes and alleles was assessed using chi-squared test or Fisher's exact test and odds ratio. Interactions were also tested using multifactor dimensionality reduction (α = 5 %).
Results: In the polymorphism rs1800629 in TNF-α, carrying at least one A risk allele significantly decreased the risk to develop PAP (OR=0.47; 95 %CI: 0.28-0.79; p=0.004). For the polymorphism rs1054016 in RANKL carrying both T risk alleles significantly decreased the risk to develop PAP (OR=0.47; 95 %CI: 0.24-0.92; p=0.027). None of the other polymorphisms evaluated were associated with PAP (p>0.05). A strong interaction was observed among rs1800629, rs1061622 and rs1054016.
Conclusions: Genetic polymorphisms rs1800629 (TNF-α) and rs1054016 (RANKL) had a strong interaction and were associated with a lower risk to develop PAP.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)