Bioinformatics analysis reveals shared gene signatures and molecular mechanisms between periodontitis and rheumatoid arthritis in the context of aging.

IF 1.7 4区医学 Q3 DENTISTRY, ORAL SURGERY & MEDICINE

Acta Odontologica Scandinavica Pub Date : 2026-08-21 DOI:10.2340/aos.v85.46622

Hanlu Xiao, Yajun Zhao, Yishu Wang, Yuhan Wang, Dingxin Zhang, Rongzeng Huang, Chengwu Song, Shan Cao, Shuna Jin

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Abstract

Objective: The interplay between periodontitis (PD) and rheumatoid arthritis (RA) is well recognized, with aging being a central risk factor for both. However, the shared aging-related molecular mechanisms remain unclear. We aimed to identify common aging-related hub genes linking PD and RA and elucidate their underlying functional mechanisms.

Material and methods: PD and RA gene expression profiles were obtained from Gene Expression Omnibus database. Crosstalk genes were identified via differential expression analysis and intersected with aging-related genes from GeneCards. Functional enrichment (GO/KEGG) was performed. Hub genes were screened using protein-protein interaction network analysis and two machine learning algorithms and validated with external datasets. Diagnostic performance was evaluated by nomogram and receiver operating characteristic analysis. Immune cell infiltration was analyzed using CIBERSORT.

Results: We identified 191 aging-related crosstalk genes, enriched in immune-inflammatory pathways. Five hub genes (RAC2, CSF2RB, IL2RG, ENTPD1, and IL10RA) were confirmed, showing significant overexpression in PD and RA tissues with excellent diagnostic value. Immune infiltration revealed coordinated dysregulation of plasma cells and γδ T cells in both diseases.

Conclusions: This study reveals shared aging-related genes, pathways, and immune cell dysregulation between PD and RA, elucidating how aging exacerbates both diseases through immune-inflammatory mechanisms. These findings provide a theoretical basis for novel biomarkers and therapies.

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生物信息学分析揭示了牙周炎和类风湿关节炎在衰老背景下的共同基因特征和分子机制。

目的：牙周炎（PD）和类风湿关节炎（RA）之间的相互作用是公认的，而衰老是两者的主要危险因素。然而，衰老相关的分子机制尚不清楚。我们的目的是确定连接PD和RA的常见衰老相关中心基因，并阐明其潜在的功能机制。材料和方法：PD和RA基因表达谱来源于gene expression Omnibus数据库。通过差异表达分析鉴定了相声基因，并与GeneCards中的衰老相关基因交叉。进行功能富集（GO/KEGG）。使用蛋白-蛋白相互作用网络分析和两种机器学习算法筛选枢纽基因，并使用外部数据集进行验证。通过nomogram和receiver operating characteristic分析来评价诊断效果。采用CIBERSORT分析免疫细胞浸润情况。结果：我们鉴定了191个与衰老相关的串扰基因，这些基因在免疫炎症途径中富集。5个中心基因（RAC2、CSF2RB、IL2RG、ENTPD1、IL10RA）在PD和RA组织中均有过表达，具有很好的诊断价值。免疫浸润显示两种疾病中浆细胞和γδ T细胞的协同失调。结论：本研究揭示了PD和RA之间共同的衰老相关基因、途径和免疫细胞失调，阐明了衰老如何通过免疫炎症机制加剧这两种疾病。这些发现为新的生物标志物和治疗提供了理论基础。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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