国际口腔医学杂志

国际口腔医学杂志 ›› 2026, Vol. 53 ›› Issue (3): 370-380.doi: 10.7518/gjkq.2026018

• 综述 • 上一篇    下一篇

细胞焦亡参与牙龈卟啉单胞菌促进动脉粥样硬化发生发展的研究进展

吴子湘(),谭碧云,湛晶蕾,李霞,葛颂()   

  1. 遵义医科大学口腔医学院·附属口腔医院牙周科 遵义 563000
  • 收稿日期:2025-03-26 修回日期:2025-06-23 出版日期:2026-05-01 发布日期:2026-04-24
  • 通讯作者: 葛颂
  • 作者简介:吴子湘，硕士，Email：411004549@qq.com
  • 基金资助:
    国家自然科学基金(82560193);遵义市工业和科学技术局科技计划项目(遵市科合HZ字（2024）342号)

Advances in pyroptosis involved inthepathogenesis and progression of Porphyromonas gingivalis-accelerated atherosclerosis

Zixiang Wu(),Biyun Tan,Jinglei Zhan,Xia Li,Song Ge()   

  1. Dept. of Periodontology, Hospital of Stomatology, School of Stomatology, Zunyi Medical University, Zunyi 563000, China
  • Received:2025-03-26 Revised:2025-06-23 Online:2026-05-01 Published:2026-04-24
  • Contact: Song Ge
  • Supported by:
    National Natural Science Foundation of China(82560193);Science and Technology Plan Projects of Zunyi Municipal Bureau of Industry and Science and Technology [No. (2024) 342]

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摘要：

牙龈卟啉单胞菌（P. gingivalis）作为牙周关键致病菌，不仅引起局部炎症，还可经血液循环或通过炎症介质影响血管系统，与动脉粥样硬化等心血管疾病密切相关。本文围绕P. gingivalis通过细胞焦亡途径促进动脉粥样硬化发生发展的机制展开系统综述，重点阐述P. gingivalis及其毒力因子激活内皮细胞、平滑肌细胞等血管相关细胞的焦亡信号通路，从而导致白细胞介素（IL）-1β、IL-18等促炎细胞因子大量释放，进而驱动血管炎症反应、斑块形成与不稳定化。本文聚焦细胞焦亡这一连接感染、炎症与程序性细胞死亡的关键机制，系统梳理P. gingivalis调控焦亡通路促进动脉粥样硬化的证据，并从分子与细胞层面揭示牙周致病菌影响全身性疾病的新途径。文中还探讨了针对焦亡关键环节的干预策略在治疗牙周炎相关动脉粥样硬化中的潜在价值。通过整合近年来微生物—宿主相互作用与细胞死亡交叉领域的研究进展，本文为理解牙周炎与心血管疾病共病机制提供了新视角，也为开发针对细胞焦亡的靶向防治策略提供了理论依据。

关键词: 牙龈卟啉单胞菌, 细胞焦亡, 牙周炎, 动脉粥样硬化, 心血管疾病

Abstract:

Porphyromonas gingivalis (P. gingivalis), a key periodontal pathogen, induces local inflammation and has been recently confirmed to affect the vascular system via bloodstream dissemination or inflammatory mediators, closely associating it with cardiovascular diseases such as atherosclerosis. This article provides a systematic review of the mechanisms by which P. gingivalis promotes the initiation and progression of atherosclerosis through the pyroptosis pathway. It elucidates how P. gingivalis and its virulence factors activate pyroptosis signaling in vascular-related cells such as endothelial cells and smooth muscle cells, leading to the substantial production of pro-inflammatory cytokines including interleukin (IL)-1β and IL-18. This cascade exacerbates vascular inflammatory responses, promotes plaque formation, and induces instability. Innovatively centered on pyroptosis, which is a critical mechanism linking infection, inflammation, and programmed cell death, this review systematically consolidates evidence on how P. gingivalis regulates pyroptosis pathways to aggravate atherosclerosis. It also reveals novel pathways through which periodontal pathogens influence systemic diseases at the molecular and cellular levels. Furthermore, the article discusses the potential value of intervention strategies targeting key steps of pyroptosis in the treatment of atherosclerosis associated with periodontitis. This review integrates recent advances in microbe-host interactions and cell death to elucidate the comorbi-dity mechanism linking periodontitis and cardiovascular disease, while providing a theoretical basis for the development of targeted therapeutic strategies against pyroptosis.

Key words: Porphyromonas gingivalis, pyroptosis, periodontitis, atherosclerosis, cardiovascular disease

中图分类号: 

  • R780.2

图 1

P. gingivalis及其毒力因子在牙周炎中的致病机制示意图"

图 2

细胞焦亡激活示意图"

图 3

细胞焦亡在P. gingivalis促进As中的作用示意图"

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