Skull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Periodontics, School of Dentistry, Hamadan University of Medical Sciences, Hamadan, Iran.
Hum Antibodies. 2022;30(1):47-55. doi: 10.3233/HAB-211507.
Periodontal diseases are common conditions in almost all age groups and a public health problem. Numerous risk factors have been demonstrated for this condition. The main mechanism of tissue destruction in the periodontitis is the functional interactions between microbial pathogens and host immune responses, thus cytokines have crucial roles in the pathogenesis periodontitis. Our previous study has demonstrated the susceptibility role of HLA-DRB104 allele in development of this disease. So, the individuals who were positive for HLA-DRB104 allele were excluded. We aimed to appraise the function of cytokines in the pathogenesis of periodontitis via assessment of tissue and blood levels of a number of cytokine coding genes, namely IL-1B, CXCL8, IL-17, IFNG, TGFB and TNFA1. Expressions of IFNG, IL-17, TGFB and TNFA1 were significantly higher in the peripheral blood of individuals with periodontitis compared with unaffected persons (Posterior beta = 1.91, P value = 0.043; Posterior beta = 1.84, P value = 0.033; Posterior beta = 0.713, P value = 0.009 and Posterior beta = 2.85, P value = 0.001, respectively). Moreover, expression of IL-17 was higher in females compared with males (Posterior beta = 1.47, P value = 0.036). As the interaction effect between gender and group was remarkable for IL-17 expression, we further conducted subgroup analysis within gender group. Expression of IL-17 was higher in male patients compared with unaffected males (Posterior beta = 1.9, P value = 0.048). We did not detect any significant difference in the expression of these cytokines in tissues obtained from affected individuals and unaffected controls. Therefore, our results imply dysregulation of cytokine coding genes in patients with periodontitis and warrant further mechanistical studies.
牙周病是几乎所有年龄段人群的常见疾病,也是一个公共卫生问题。已经证明了许多与这种疾病相关的危险因素。牙周炎组织破坏的主要机制是微生物病原体和宿主免疫反应的功能相互作用,因此细胞因子在牙周炎发病机制中起着至关重要的作用。我们之前的研究表明 HLA-DRB104 等位基因在该疾病的发展中具有易感性作用。因此,排除了 HLA-DRB104 等位基因阳性的个体。我们旨在通过评估一些细胞因子编码基因(即 IL-1B、CXCL8、IL-17、IFNG、TGFB 和 TNFA1)的组织和血液水平,来评估细胞因子在牙周炎发病机制中的作用。与无病个体相比,牙周炎患者外周血中 IFNG、IL-17、TGFB 和 TNFA1 的表达明显更高(后验β=1.91,P 值=0.043;后验β=1.84,P 值=0.033;后验β=0.713,P 值=0.009 和后验β=2.85,P 值=0.001)。此外,女性的 IL-17 表达高于男性(后验β=1.47,P 值=0.036)。由于性别和组之间的相互作用对 IL-17 的表达有显著影响,因此我们进一步在性别组内进行了亚组分析。与无病男性相比,男性患者的 IL-17 表达更高(后验β=1.9,P 值=0.048)。我们没有发现这些细胞因子在受影响个体和无病对照的组织中表达有任何显著差异。因此,我们的结果表明牙周炎患者的细胞因子编码基因失调,需要进一步进行机制研究。