Jia Shuyuan, Liang Qin, Zhang Yanling, Diao Jing, Liu Yizhou, Ye Yulin, Xu Shaojia, Yang Wenying, Zhao Ya, Ma Bowen, Li Xiaodong, Zheng Shuguo, Yuan Chao
Department of Preventive Dentistry, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices& Beijing Key Laboratory of Digital Stomatology & NHC Key Laboratory of Digital Stomatology & NMPA Key Laboratory for Dental Materials, Beijing 100081, P. R. China.
Department of Stomatology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 100730, P. R. China.
J Proteome Res. 2025 Mar 7;24(3):1161-1179. doi: 10.1021/acs.jproteome.4c00701. Epub 2025 Feb 26.
Diabetes and periodontitis, as widespread chronic diseases, often exacerbate each other's conditions. Nonsurgical periodontal treatments can improve the oral and systemic health in these patients, with salivary proteins offering potential insights into disease mechanisms and treatment effectiveness. However, there is a lack of comprehensive data on salivary proteomics in this context. By assigning patients with diabetes-associated periodontitis to a test group (supragingival scaling, subgingival scraping and root planing) or a control group (supragingival scaling only), analyzing nonstimulated whole saliva samples using liquid chromatography-tandem mass spectrometry, and establishing the in vivo and in vitro models, we found significant differential expression of salivary proteins related to Apelin signaling pathway, hematopoietic cell profiling, stress response and immune regulation, identifying four candidate proteins: superoxide dismutase 1 (SOD1), profilin 1 (PFN1), S100 calcium-binding protein A11 (S100A11) and kallikrein-related peptidase 6 (KLK6). All four proteins were significantly elevated, with a combined area under the curve of 0.933, while SOD1 alone reached 0.915. Additionally, we observed high glucose and inflammatory conditions reduced SOD1 expression. In conclusion, SOD1 emerges as a promising regulatory target for managing diabetes and periodontitis by modulating the oral oxidative stress microenvironment.
糖尿病和牙周炎作为广泛存在的慢性疾病,常常相互加剧病情。非手术牙周治疗可以改善这些患者的口腔和全身健康,唾液蛋白为疾病机制和治疗效果提供了潜在的见解。然而,在这种情况下,缺乏关于唾液蛋白质组学的全面数据。通过将糖尿病相关性牙周炎患者分为试验组(龈上洁治、龈下刮治和根面平整)或对照组(仅龈上洁治),使用液相色谱 - 串联质谱法分析非刺激性全唾液样本,并建立体内和体外模型,我们发现与阿片肽信号通路、造血细胞谱、应激反应和免疫调节相关的唾液蛋白存在显著差异表达,鉴定出四种候选蛋白:超氧化物歧化酶1(SOD1)、肌动蛋白结合蛋白1(PFN1)、S100钙结合蛋白A11(S100A11)和激肽释放酶相关肽酶6(KLK6)。这四种蛋白均显著升高,曲线下面积总和为0.933,而仅SOD1就达到0.915。此外,我们观察到高糖和炎症条件会降低SOD1的表达。总之,通过调节口腔氧化应激微环境,SOD1有望成为管理糖尿病和牙周炎的调控靶点。