Ma Lingzhi, Zhang Hongrong, Liu Yali, Liu Yan, Zhou Jing, Yang Hefeng, Xu Biao
Affiliated Stomatology Hospital of Kunming Medical University, Kunming, China; Yunnan Key Laboratory of Stomatology, Kunming, China.
Affiliated Stomatology Hospital of Kunming Medical University, Kunming, China; Yunnan Key Laboratory of Stomatology, Kunming, China.
Int Dent J. 2025 Jun;75(3):2204-2221. doi: 10.1016/j.identj.2024.12.012. Epub 2025 Jan 3.
Periodontitis (PD) is a common chronic inflammatory oral disease that severely affects patients' quality of life. Fisetin has been shown to possess antioxidant and anti-inflammatory properties in various biological systems.
This study first identified the molecular targets of fisetin for PD through network pharmacology analysis. The therapeutic effects of fisetin were then evaluated in an animal model of PD and validated through in vitro experiments. Additionally, we utilised single-cell and spatial transcriptomics technologies to identify key cell populations in PD and their spatial distribution.
The study demonstrated that fisetin significantly reduced alveolar bone destruction in the rat model of PD. Single-cell transcriptomics revealed that fisetin primarily affects fibroblast populations. In vitro experiments showed that fisetin alleviated the cytotoxicity caused by high oxidative stress levels in human periodontal ligament fibroblasts (PDLFs) .
Fisetin inhibits the progression of periodontitis by reducing oxidative stress levels in fibroblast populations. These findings support the potential of fisetin as a therapeutic agent for periodontitis and provide a scientific basis for future clinical trials and treatment strategies.
By significantly reducing alveolar bone destruction and modulating fibroblast function, fisetin presents a novel therapeutic strategy for managing periodontitis. These results provide a scientific foundation for the design of clinical trials aimed at evaluating the efficacy of fisetin in PD patients. If validated in clinical settings, fisetin could be incorporated into treatment regimens, offering a pharmacological option that complements conventional periodontal therapies, thereby improving patient outcomes and quality of life.
牙周炎（PD）是一种常见的慢性炎症性口腔疾病，严重影响患者的生活质量。已证明非瑟酮在各种生物系统中具有抗氧化和抗炎特性。
本研究首先通过网络药理学分析确定非瑟酮对牙周炎的分子靶点。然后在牙周炎动物模型中评估非瑟酮的治疗效果，并通过体外实验进行验证。此外，我们利用单细胞和空间转录组学技术来识别牙周炎中的关键细胞群及其空间分布。
研究表明，非瑟酮可显著减少牙周炎大鼠模型中的牙槽骨破坏。单细胞转录组学显示，非瑟酮主要影响成纤维细胞群。体外实验表明，非瑟酮可减轻人牙周膜成纤维细胞（PDLFs）中高氧化应激水平引起的细胞毒性。
非瑟酮通过降低成纤维细胞群中的氧化应激水平来抑制牙周炎的进展。这些发现支持非瑟酮作为牙周炎治疗药物的潜力，并为未来的临床试验和治疗策略提供了科学依据。
通过显著减少牙槽骨破坏和调节成纤维细胞功能，非瑟酮为牙周炎的治疗提供了一种新的治疗策略。这些结果为设计旨在评估非瑟酮对牙周炎患者疗效的临床试验提供了科学基础。如果在临床环境中得到验证，非瑟酮可纳入治疗方案，提供一种补充传统牙周治疗的药理学选择，从而改善患者的治疗效果和生活质量。
