Department of Biosciences, Vascular & Exercise Biology Unit, University of Salzburg, 5020 Salzburg, Austria.
Clinic of Operative Dentistry, Periodontology and Preventive Dentistry, Saarland University, 66424 Homburg, Germany.
Cells. 2020 Dec 5;9(12):2614. doi: 10.3390/cells9122614.
Periodontitis is a general term for diseases characterised by inflammatory destruction of tooth-supporting tissues, gradual destruction of the marginal periodontal ligament and resorption of alveolar bone. Early-onset periodontitis is due to disturbed neutrophil extracellular trap (NET) formation and clearance. Indeed, mutations that inactivate the cysteine proteases cathepsin C result in the massive periodontal damage seen in patients with deficient NET formation. In contrast, exaggerated NET formation due to polymorphonuclear neutrophil (PMN) hyper-responsiveness drives the pathology of late-onset periodontitis by damaging and ulcerating the gingival epithelium and retarding epithelial healing. Despite the gingival regeneration, periodontitis progression ends with almost complete loss of the periodontal ligament and subsequent tooth loss. Thus, NETs help to maintain periodontal health, and their dysregulation, either insufficiency or surplus, causes heavy periodontal pathology and edentulism.
牙周炎是一种以支持牙齿的组织炎症性破坏为特征的疾病，表现为边缘牙周韧带的逐渐破坏和牙槽骨的吸收。早发性牙周炎是由于中性粒细胞胞外陷阱（NET）形成和清除障碍所致。事实上，失活半胱氨酸蛋白酶组织蛋白酶 C 的突变导致形成 NET 的能力缺陷的患者出现大量牙周破坏。相反，由于多形核中性粒细胞（PMN）过度反应导致 NET 过度形成，通过破坏和溃疡牙龈上皮并延缓上皮愈合，导致迟发性牙周炎的病理学变化。尽管有牙龈再生，牙周炎的进展仍以牙周韧带几乎完全丧失和随后的牙齿脱落而告终。因此，NET 有助于维持牙周健康，其失调（不足或过剩）会导致严重的牙周病和无牙症。
