State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, Sichuan, China.
Clin Oral Investig. 2023 Nov;27(11):6689-6700. doi: 10.1007/s00784-023-05278-7. Epub 2023 Sep 29.
Cytokines that mediate the immune responses are important in the pathogenesis of periodontitis. The genetic polymorphisms of IL-10, TNFAIP3 (A20), and NF-κB1 (p105/p50) and their association with the risk of periodontitis were investigated.
Venous blood from 102 clinical periodontal healthy participants and 100 patients with periodontitis was collected to genotype the IL-10 (rs1800872), A20 (rs2230926, rs5029937, rs6927127), and NF-κB1 (rs28362491) SNP loci by Sanger technology. Univariable and multivariable logic regression and path analysis model was used to analyze the genotypes and alleles.
Single-gene mutations in the A20 (rs2230926, rs5029937, rs6927127) and IL-10 (rs1800872) genes were not associated with the risk of periodontitis. NF-κΒ1 (rs28362491) gene influenced periodontitis susceptibility by affecting CAL. The combined effect of A20 and IL-10 was related to the risk of periodontitis (OR = 0.123-0.151). One site mutated in the A20 (rs2230926, rs5029937, rs6927127) gene or IL-10 (rs1800872) gene reduced the risk of periodontitis.
Single gene polymorphisms in A20 and IL-10 genes were not associated with the risk of periodontitis. NF-κB1 gene polymorphism indirectly affects susceptibility to periodontitis. The combined effect of anti-inflammatory gene polymorphisms (A20 and IL-10) correlated with the decreased risk of periodontitis.
This study helps to explore the potential mechanisms underlying the role of anti-inflammatory genes in the progression of periodontal disease and provides a basis for the selection and development of appropriate periodontal treatment strategies based on the genetic profile of the patient.
细胞因子在调节免疫应答中发挥重要作用，其在牙周炎的发病机制中也具有重要意义。本研究旨在探讨白细胞介素 10（IL-10）、肿瘤坏死因子诱导蛋白 3（TNFAIP3，也称为 A20）和核因子-κB1（NF-κB1）的遗传多态性及其与牙周炎发病风险的相关性。
采集 102 例临床牙周健康参与者和 100 例牙周炎患者的静脉血，采用 Sanger 技术对白细胞介素 10（rs1800872）、A20（rs2230926、rs5029937、rs6927127）和 NF-κB1（rs28362491）SNP 位点进行基因分型。采用单变量和多变量逻辑回归及路径分析模型分析基因型和等位基因。
A20（rs2230926、rs5029937、rs6927127）和白细胞介素 10（rs1800872）基因的单基因突变与牙周炎的发病风险无关。NF-κB1（rs28362491）基因通过影响 CAL 影响牙周炎易感性。A20 和白细胞介素 10 的联合作用与牙周炎的发病风险相关（OR=0.123-0.151）。A20（rs2230926、rs5029937、rs6927127）或白细胞介素 10（rs1800872）基因的一个位点发生突变会降低牙周炎的发病风险。
A20 和白细胞介素 10 基因的单基因多态性与牙周炎的发病风险无关。NF-κB1 基因多态性间接影响牙周炎的易感性。抗炎基因多态性（A20 和白细胞介素 10）的联合作用与牙周炎发病风险降低相关。
本研究有助于探讨抗炎基因在牙周病进展中的作用机制，并为基于患者的遗传特征选择和制定适当的牙周治疗策略提供依据。
