在巴西受试者中，TNF-⍺和 RANKL 基因多态性之间的相互作用与持续性根尖牙周炎的发展有关。

IF 2.2 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology Pub Date : 2024-10-10 DOI:10.1016/j.archoralbio.2024.106106

Igor Bassi Ferreira Petean , Alice Corrêa Silva-Sousa , Guido Artemio Marañón-Vásquez , Francisco Wanderley Garcia de Paula-Silva , Erika Calvano Küchler , Leonardo Santos Antunes , Raquel Assed Bezerra Segato , Lea Assed Bezerra da Silva , Jardel Francisco Mazzi-Chaves , Fabiane Carneiro Lopes-Olhê , Manoel Damião Sousa-Neto

{"title":"在巴西受试者中，TNF-⍺和 RANKL 基因多态性之间的相互作用与持续性根尖牙周炎的发展有关。","authors":"Igor Bassi Ferreira Petean , Alice Corrêa Silva-Sousa , Guido Artemio Marañón-Vásquez , Francisco Wanderley Garcia de Paula-Silva , Erika Calvano Küchler , Leonardo Santos Antunes , Raquel Assed Bezerra Segato , Lea Assed Bezerra da Silva , Jardel Francisco Mazzi-Chaves , Fabiane Carneiro Lopes-Olhê , Manoel Damião Sousa-Neto","doi":"10.1016/j.archoralbio.2024.106106","DOIUrl":null,"url":null,"abstract":"<div><h3>Objectives</h3><div>To investigate the association between genetic polymorphisms in suppressor of cytokine signaling-1 (<em>SOCS-1</em>)<em>,</em> tumor necrosis factor-⍺ (<em>TNF-α</em>) and its receptors 1 and 2 (<em>TNFRSF1A</em> and <em>TNFRSF1B</em>), receptor activator of nuclear factor kappa-b (<em>RANK</em>), receptor activator of nuclear factor-kappa B ligand (<em>RANKL</em>) and osteoprotegerin (<em>OPG</em>), and persistent apical periodontitis (PAP).</div></div><div><h3>Methods</h3><div>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 <em>SOCS1</em> (rs243327 and rs33977706), <em>TNF-α</em> (rs1800629), <em>TNFRSF1A</em> (rs1800693), <em>TNFRSF1B</em> (rs1061622), <em>RANK</em> (rs1805034), <em>RANKL</em> (rs1054016) and <em>OPG</em> (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 (<em>α</em> = 5 %).</div></div><div><h3>Results</h3><div>In the polymorphism rs1800629 in <em>TNF-</em>α, carrying at least one A risk allele significantly decreased the risk to develop PAP (OR=0.47; 95 %CI: 0.28–0.79; <em>p</em>=0.004). For the polymorphism rs1054016 in <em>RANKL</em> carrying both T risk alleles significantly decreased the risk to develop PAP (OR=0.47; 95 %CI: 0.24–0.92; <em>p</em>=0.027). None of the other polymorphisms evaluated were associated with PAP (<em>p</em>>0.05). A strong interaction was observed among rs1800629, rs1061622 and rs1054016.</div></div><div><h3>Conclusions</h3><div>Genetic polymorphisms rs1800629 (<em>TNF-α)</em> and rs1054016 (<em>RANKL)</em> had a strong interaction and were associated with a lower risk to develop PAP.</div></div>","PeriodicalId":8288,"journal":{"name":"Archives of oral biology","volume":"169 ","pages":"Article 106106"},"PeriodicalIF":2.2000,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Interaction between polymorphisms in TNF-⍺ and RANKL genes is associated with the development of persistent apical periodontitis, in Brazilian subjects\",\"authors\":\"Igor Bassi Ferreira Petean , Alice Corrêa Silva-Sousa , Guido Artemio Marañón-Vásquez , Francisco Wanderley Garcia de Paula-Silva , Erika Calvano Küchler , Leonardo Santos Antunes , Raquel Assed Bezerra Segato , Lea Assed Bezerra da Silva , Jardel Francisco Mazzi-Chaves , Fabiane Carneiro Lopes-Olhê , Manoel Damião Sousa-Neto\",\"doi\":\"10.1016/j.archoralbio.2024.106106\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objectives</h3><div>To investigate the association between genetic polymorphisms in suppressor of cytokine signaling-1 (<em>SOCS-1</em>)<em>,</em> tumor necrosis factor-⍺ (<em>TNF-α</em>) and its receptors 1 and 2 (<em>TNFRSF1A</em> and <em>TNFRSF1B</em>), receptor activator of nuclear factor kappa-b (<em>RANK</em>), receptor activator of nuclear factor-kappa B ligand (<em>RANKL</em>) and osteoprotegerin (<em>OPG</em>), and persistent apical periodontitis (PAP).</div></div><div><h3>Methods</h3><div>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 <em>SOCS1</em> (rs243327 and rs33977706), <em>TNF-α</em> (rs1800629), <em>TNFRSF1A</em> (rs1800693), <em>TNFRSF1B</em> (rs1061622), <em>RANK</em> (rs1805034), <em>RANKL</em> (rs1054016) and <em>OPG</em> (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 (<em>α</em> = 5 %).</div></div><div><h3>Results</h3><div>In the polymorphism rs1800629 in <em>TNF-</em>α, carrying at least one A risk allele significantly decreased the risk to develop PAP (OR=0.47; 95 %CI: 0.28–0.79; <em>p</em>=0.004). For the polymorphism rs1054016 in <em>RANKL</em> carrying both T risk alleles significantly decreased the risk to develop PAP (OR=0.47; 95 %CI: 0.24–0.92; <em>p</em>=0.027). None of the other polymorphisms evaluated were associated with PAP (<em>p</em>>0.05). A strong interaction was observed among rs1800629, rs1061622 and rs1054016.</div></div><div><h3>Conclusions</h3><div>Genetic polymorphisms rs1800629 (<em>TNF-α)</em> and rs1054016 (<em>RANKL)</em> had a strong interaction and were associated with a lower risk to develop PAP.</div></div>\",\"PeriodicalId\":8288,\"journal\":{\"name\":\"Archives of oral biology\",\"volume\":\"169 \",\"pages\":\"Article 106106\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2024-10-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Archives of oral biology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0003996924002279\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"DENTISTRY, ORAL SURGERY & MEDICINE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of oral biology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0003996924002279","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}

引用次数: 0

摘要

目的研究细胞因子信号转导抑制因子-1（SOCS-1）、肿瘤坏死因子-237A(TNF-α)及其受体1和2（TNFRSF1A和TNFRSF1B）的遗传多态性之间的关联、核因子卡巴-b 受体激活剂（RANK）、核因子卡巴-B 受体激活剂配体（RANKL）和骨保护素（OPG）以及持续性根尖牙周炎（PAP）。研究方法对接受非手术根管治疗时出现牙髓坏死和根尖牙周炎的患者进行至少一年的随访。共纳入 423 名受试者，其中 172 人有牙髓坏死的迹象/症状，251 人的根尖牙周炎已痊愈。研究人员从唾液中提取 DNA，并通过实时 PCR 对 SOCS1（rs243327 和 rs33977706）、TNF-α（rs1800629）、TNFRSF1A（rs1800693）、TNFRSF1B（rs1061622）、RANK（rs1805034）、RANKL（rs1054016）和 OPG（rs1032128）的多态性进行基因分型。使用卡方检验或费雪精确检验和几率比验评估基因型和等位基因的频率。还使用多因素降维法（α = 5 %）对相互作用进行了测试：结果：在 TNF-α 的多态性 rs1800629 中，携带至少一个 A 风险等位基因可显著降低罹患 PAP 的风险（OR=0.47；95 %CI：0.28-0.79；p=0.004）。对于 RANKL 的多态性 rs1054016，携带两个 T 风险等位基因可明显降低罹患 PAP 的风险（OR=0.47；95 %CI：0.24-0.92；p=0.027）。所评估的其他多态性均与 PAP 无关（P>0.05）。在 rs1800629、rs1061622 和 rs1054016 之间观察到强烈的交互作用：结论：rs1800629（TNF-α）和rs1054016（RANKL）的基因多态性具有很强的交互作用，与较低的PAP发病风险相关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

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.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Archives of oral biology 医学-牙科与口腔外科

CiteScore

5.10

自引率

3.30%

发文量

177

审稿时长

26 days

期刊介绍： Archives of Oral Biology is an international journal which aims to publish papers of the highest scientific quality in the oral and craniofacial sciences. The journal is particularly interested in research which advances knowledge in the mechanisms of craniofacial development and disease, including: Cell and molecular biology Molecular genetics Immunology Pathogenesis Cellular microbiology Embryology Syndromology Forensic dentistry