Abstract：
Periodontitis, an infectious inflammatory disease influenced by various factors, disrupts the delicate balance between the host microbiota and immunity. The resulting excessive immune response exacerbates the progressive destruction of the supporting periodontal tissue. Macrophages are essential elements of the host innate immune system. They are pivotal components in the periodontal immune microenvironment and actively participate in both physiological and pathological processes of periodontal tissue. When confronted with periodontitis-related irritant factors, macrophages may differentiate to pro- or anti-inflammatory subtypes that affect tissue homeostasis. Additionally, macrophages may die in response to bacterial infections, potentially affecting the severity of periodontitis. This article reviews the typical mechanisms underlying macrophage death and its effects on periodontitis. We describe five forms of macrophage death in periodontitis: apoptosis, pyroptosis, necroptosis, ferroptosis, and ETosis. Our review of macrophage death in the pathophysiology of periodontitis enhances comprehension of the pathogenesis of periodontitis that will be useful for clinical practice. Although our review elucidates the complex mechanisms by which macrophage death and inflammatory pathways perpetuate periodontitis, unresolved issues remain, necessitating further research.
摘要：
牙周炎,受各种因素影响的感染性炎症性疾病，破坏宿主微生物群和免疫力之间的微妙平衡。所产生的过度免疫反应加剧了支持牙周组织的进行性破坏。巨噬细胞是宿主先天免疫系统的基本要素。它们是牙周免疫微环境的重要组成部分，积极参与牙周组织的生理和病理过程。当遇到牙周炎相关的刺激因素时，巨噬细胞可以分化为影响组织稳态的促炎或抗炎亚型。此外,巨噬细胞可能因细菌感染而死亡，可能影响牙周炎的严重程度。本文综述了巨噬细胞死亡的典型机制及其对牙周炎的影响。我们描述了牙周炎中巨噬细胞死亡的五种形式：凋亡，焦亡,坏死,铁性凋亡,和ETosis。我们对牙周炎病理生理学中巨噬细胞死亡的回顾增强了对牙周炎发病机理的理解，这将对临床实践有用。尽管我们的综述阐明了巨噬细胞死亡和炎症途径导致牙周炎持续的复杂机制，悬而未决的问题依然存在，需要进一步研究。
