Zhu Xuanzhi, Huang Hanyao, Zhao Lei
State Key Laboratory of Oral Diseases, Department of Periodontics, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
State Key Laboratory of Oral Diseases, Department of Oral and Maxillofacial Surgery, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Front Cell Dev Biol. 2022 Feb 25;10:856118. doi: 10.3389/fcell.2022.856118. eCollection 2022.
Atherosclerosis is a chronic artery disease characterized by plaque formation and vascular inflammation, eventually leading to myocardial infarction and stroke. Innate immunity plays an irreplaceable role in the vascular inflammatory response triggered by chronic infection. Periodontitis is a common chronic disorder that involves oral microbe-related inflammatory bone loss and local destruction of the periodontal ligament and is a risk factor for atherosclerosis. Periodontal pathogens contain numerous pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide, CpG DNA, and Peptidoglycan, that initiate the inflammatory response of the innate immunity depending on the recognition of pattern-recognition receptors (PRRs) of host cells. The immune-inflammatory response and destruction of the periodontal tissue will produce a large number of damage-associated molecular patterns (DAMPs) such as neutrophil extracellular traps (NETs), high mobility group box 1 (HMGB1), alarmins (S100 protein), and which can further affect the progression of atherosclerosis. Molecular patterns have recently become the therapeutic targets for inflammatory disease, including blocking the interaction between molecular patterns and PRRs and controlling the related signal transduction pathway. This review summarized the research progress of some representative PAMPs and DAMPs as the molecular pathological mechanism bridging periodontitis and atherosclerosis. We also discussed possible ways to prevent serious cardiovascular events in patients with periodontitis and atherosclerosis by targeting molecular patterns.
动脉粥样硬化是一种慢性动脉疾病，其特征在于斑块形成和血管炎症，最终导致心肌梗死和中风。固有免疫在慢性感染引发的血管炎症反应中发挥着不可替代的作用。牙周炎是一种常见的慢性疾病，涉及与口腔微生物相关的炎症性骨质流失以及牙周韧带的局部破坏，是动脉粥样硬化的一个危险因素。牙周病原体包含众多病原体相关分子模式（PAMP），如脂多糖、CpG DNA和肽聚糖，这些分子模式依赖于宿主细胞模式识别受体（PRR）的识别来启动固有免疫的炎症反应。牙周组织的免疫炎症反应和破坏会产生大量损伤相关分子模式（DAMP），如中性粒细胞胞外陷阱（NET）、高迁移率族蛋白B1（HMGB1）、警报素（S100蛋白）等，这些分子模式会进一步影响动脉粥样硬化的进展。分子模式最近已成为炎症性疾病的治疗靶点，包括阻断分子模式与PRR之间的相互作用以及控制相关信号转导通路。本综述总结了一些具有代表性的PAMP和DAMP作为连接牙周炎和动脉粥样硬化的分子病理机制的研究进展。我们还讨论了通过靶向分子模式来预防牙周炎和动脉粥样硬化患者发生严重心血管事件的可能方法。
