State Key Laboratory of Oral Diseases and National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
The First Affiliated Hospital of Chengdu Medical College, Chengdu, China.
Oral Dis. 2024 Oct;30(7):4152-4160. doi: 10.1111/odi.15013. Epub 2024 Jun 9.
The gingival mucosal barrier, an important oral cavity barrier, plays a significant role in preventing pathogenic microorganism invasion and maintaining periodontal tissue health. Pathogenic microorganism invasion of the gingival mucosa produces a large number of cytokines. Among them, pyroptosis is an important player in exacerbating immune-inflammatory responses, leading to tissue destruction. However, the mechanism of pyroptosis and the immune response it triggers have not been fully elucidated. We provide an overview of recent advances in understanding gingival physical barrier pyroptosis and inflammation-induced hyperimmunity.
PubMed, Web of Science databases were searched for articles, reviews, and clinical studies published until March 2024.
We summarised the importance of the gingival barrier in terms of the functions of different cells, described the progress in research on gingival epithelial cell and gingival fibroblast pyroptosis and the immune-inflammatory response it induces, and discussed the relationship between pyroptosis and systemic diseases, association of multiple cell death systems. Finally, we propose future directions for pyroptosis research.
Pyroptosis often triggers a range of inflammatory immune responses that lead to associated diseases. Therefore, further study of the molecular mechanisms of pyroptosis and the immune responses is warranted.
牙龈黏膜屏障是口腔重要的屏障，在防止病原微生物入侵和维持牙周组织健康方面发挥着重要作用。病原微生物侵袭牙龈黏膜会产生大量细胞因子，其中，细胞焦亡是加重免疫炎症反应、导致组织破坏的重要参与者。然而，细胞焦亡的机制及其引发的免疫反应尚未完全阐明。我们就理解牙龈物理屏障细胞焦亡和炎症诱导的hyperimmunity 提供了最新进展的综述。
检索了截至 2024 年 3 月在 PubMed、Web of Science 数据库中发表的文章、综述和临床研究。
我们从不同细胞的功能方面总结了牙龈屏障的重要性，描述了牙龈上皮细胞和牙龈成纤维细胞焦亡及其诱导的免疫炎症反应的研究进展，并讨论了细胞焦亡与系统性疾病的关系、多种细胞死亡系统的关联。最后，我们提出了细胞焦亡研究的未来方向。
细胞焦亡常引发一系列炎症免疫反应，进而导致相关疾病。因此，有必要进一步研究细胞焦亡的分子机制及其免疫反应。
