NLRP3炎症小体调节正畸牙移动过程中组织改建的研究进展  

Research progress on NLRP3 inflammasome⁃mediated regulation of tissue remodeling during orthodontic tooth movement

作　　者：王佳佳 张疆弢 曾福磊 WANG Jiajia;ZHANG Jiangtao;ZENG Fulei(Affiliated Stomatological Hospital of Zunyi Medical Uni-versity,Zunyi 563000,China)

机构地区：[1]遵义医科大学附属口腔医院,贵州遵义563000

出　　处：《口腔疾病防治》2025年第2期169-176,共8页Journal of Prevention and Treatment for Stomatological Diseases

基　　金：国家自然科学基金项目(82160183);贵州省科技计划项目(黔科合基础-ZK[2021]一般434);贵州省教育厅普通高等学校青年科技人才成长项目(黔教合KY字[2021]232)。

摘　　要：核苷酸结合寡聚化结构域样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)炎症小体通过其下游的半胱氨酸蛋白酶1(Caspase-1)依赖性促炎细胞因子白细胞介素1β(interleukin-1β,IL-1β)和白细胞介素18(interleukin-18,IL-18)的成熟和分泌,介导炎症并诱导细胞焦亡,调节牙周组织改建。正畸力通过介导牙周组织无菌性炎症引发牙周组织适应性改建,进而促进正畸牙移动与稳定。NLRP3炎症小体在正畸牙移动过程中发挥重要作用,但同时也是导致正畸患者牙周组织炎症和正畸炎性牙根吸收的原因之一。文献复习结果表明,NLRP3炎症小体参与正畸牙移动组织改建中牙周膜成纤维细胞、牙周膜干细胞、巨噬细胞、成骨细胞和破骨细胞的活化与分化过程,并且靶向NLRP3炎症小体上游NF-κB信号通路、下游Caspase-1、IL-1β和IL-18等效应分子及NLRP3炎症小体组成蛋白本身在调节牙移动以及治疗和预防正畸伴发牙周组织炎症、正畸炎性牙根吸收等方面具有重要意义。未来研究可重点关注NLRP3炎症小体在正畸牙移动过程中组织改建的具体作用机制。本文就NLRP3炎症小体信号通路在正畸牙移动过程中相应组织改建的影响及其调控机制进行综述。NOD-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome mediates inflam-mation,induces pyroptosis,and regulates periodontal tissue remodeling through the maturation and secretion of its down-stream cysteine protease 1(Caspase-1)-dependent pro-inflammatory cytokines,interleukin(IL)-1βand IL-18.Orthodon-tic force mediates the aseptic inflammation of periodontal tissues and triggers adaptive alteration of periodontal tissues,thereby promoting the movement and stability of orthodontic teeth.NLRP3 inflammasome plays an important role in orth-odontic tooth movement and causes periodontal tissue inflammation and orthodontic inflammatory root resorption in orth-odontic patients.Literature review suggests that NLRP3 inflammasome is involved in the activation and differentiation of periodontal ligament fibroblasts,periodontal ligament stem cells,macrophages,osteoblasts,and osteoclasts in orthodontic tooth mobile tissue remodeling.Additionally,it targets the upstream nuclear factor kappa-B signaling pathway;down-stream effectors,such as Caspase-1,IL-1β,and IL-18;and the NLRP3 inflammasome components for regulating tooth movement as well as treating and preventing orthodontics-associated periodontitis and orthodontic-induced inflammatory root resorption.Future studies can be focused on the specific mechanism of NLRP3 inflammasome tissue modification during orthodontic tooth movement.This article reviews the effects and regulatory mechanisms of the NLRP3 inflamma-some signaling pathway on the corresponding tissue remodeling during orthodontic tooth movement.

关 键 词：NLRP3炎症小体 正畸牙移动 白细胞介素1Β 白细胞介素18 细胞焦亡 牙槽骨 牙周炎 牙根吸收 

分 类 号：R78[医药卫生—口腔医学]