Guo Jing, He Ying
Department of Stomatology, Xi'an No. 3 Hospital, Affiliated Hospital of Northwest University, No. 10, Fengcheng 3rd Road East, Weiyang District, Xi'an City, 710010, Shaanxi Province, China.
Odontology. 2025 Mar 27. doi: 10.1007/s10266-025-01094-5.
Chronic periodontitis (CP) is a prevalent oral condition that can elicit a broad spectrum of inflammatory responses. This study investigates the impact of lncRNA HOTTIP on inflammatory responses of CP via targeting and regulating miR-205-5p. This study involved 117 CP patients and 101 controls. The expression levels of HOTTIP and miR-101-3p in the gingival crevicular fluid (GCF) of CP patients were quantified using qPCR. The levels of inflammatory factors IL-1β, IL-6, IL-10, and TNF-α, were measured through ELISA. ROC analysis was conducted to evaluate the diagnostic efficacy. The LPS-induced hPDLFs injury model was established to investigate the effects of HOTTIP silencing, as well as the concurrent inhibition of HOTTIP and miR-101-3p expression, on cellular functionality and inflammatory responses. HOTTIP was elevated in the GCF of CP patients, whereas miR-101-3p was reduced (P < 0.001). HOTTIP exhibited a positive correlation with inflammatory markers and periodontal indicators (r > 0, P < 0.01). HOTTIP possessed the potential to serve a specific biomarker for the auxiliary diagnosis of CP (AUC = 0.967, P < 0.001), as well as a critical parameter for assessing the periodontal condition of patients. In LPS-induced hPDLFs model, the silencing of HOTTIP was found to enhance cell proliferation (P < 0.01), reduce apoptosis (P < 0.001), and the release of inflammatory factors (P < 0.05). However, the simultaneous inhibition of both HOTTIP and miR-101-3p, this inhibitory effect on inflammatory response was counteracted (P < 0.05). HOTTIP regulated cellular function and the release of inflammatory factors via miR-101-3p, thereby exacerbating the inflammatory response with CP patients. HOTTIP is anticipated to emerge as a promising biomarker for the diagnosis of CP.
慢性牙周炎（CP）是一种常见的口腔疾病，可引发广泛的炎症反应。本研究通过靶向和调控miR-205-5p来探究lncRNA HOTTIP对CP炎症反应的影响。本研究纳入了117例CP患者和101例对照。采用qPCR定量CP患者龈沟液（GCF）中HOTTIP和miR-101-3p的表达水平。通过ELISA检测炎症因子IL-1β、IL-6、IL-10和TNF-α的水平。进行ROC分析以评估诊断效能。建立脂多糖（LPS）诱导的人牙周膜成纤维细胞（hPDLFs）损伤模型，以研究HOTTIP沉默以及同时抑制HOTTIP和miR-101-3p表达对细胞功能和炎症反应的影响。CP患者GCF中HOTTIP升高，而miR-101-3p降低（P < 0.001）。HOTTIP与炎症标志物和牙周指标呈正相关（r > 0，P < 0.01）。HOTTIP有潜力作为CP辅助诊断的特异性生物标志物（AUC = 0.967，P < 0.001），也是评估患者牙周状况的关键参数。在LPS诱导的hPDLFs模型中，发现沉默HOTTIP可增强细胞增殖（P < 0.01），减少细胞凋亡（P < 0.001）以及炎症因子释放（P < 0.05）。然而，同时抑制HOTTIP和miR-101-3p，这种对炎症反应的抑制作用被抵消（P < 0.05）。HOTTIP通过miR-101-3p调节细胞功能和炎症因子释放，从而加剧CP患者的炎症反应。HOTTIP有望成为CP诊断的有前景的生物标志物。
