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中华口腔医学研究杂志(电子版) ›› 2024, Vol. 18 ›› Issue (03) : 150 -155. doi: 10.3877/cma.j.issn.1674-1366.2024.03.002

青年编委专栏

根尖周病中程序性细胞死亡的研究进展
廖泽楷1, 梁爱琳1, 龚启梅1,()   
  1. 1. 中山大学附属口腔医院,光华口腔医学院,广东省口腔医学重点实验室,广东省口腔疾病临床医学研究中心,广州 510055
  • 收稿日期:2024-01-29 出版日期:2024-06-01
  • 通信作者: 龚启梅

Research progress on programmed cell death in periapical periodontitis

Zekai Liao1, Ailin Liang1, Qimei Gong1,()   

  1. 1. Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Stomatology, Guangdong Provincial Clinical Research Center of Oral Diseases, Guangzhou 510055, China
  • Received:2024-01-29 Published:2024-06-01
  • Corresponding author: Qimei Gong
  • Supported by:
    National Natural Science Foundation of China(81870750); Basic and Applied Basic Research Foundation of Guangdong Province(2023A1515010722)
引用本文:

廖泽楷, 梁爱琳, 龚启梅. 根尖周病中程序性细胞死亡的研究进展[J]. 中华口腔医学研究杂志(电子版), 2024, 18(03): 150-155.

Zekai Liao, Ailin Liang, Qimei Gong. Research progress on programmed cell death in periapical periodontitis[J]. Chinese Journal of Stomatological Research(Electronic Edition), 2024, 18(03): 150-155.

程序性细胞死亡(PCD)是由基因决定的细胞主动、有序的死亡方式,其与根尖周病的进展密切相关。目前在根尖周病灶中发现的PCD途径有细胞凋亡、自噬、坏死性凋亡、细胞焦亡和铁死亡等。这些途径能被内源性和外源性刺激激活,在维持机体稳态和炎症调节中发挥重要作用。本文针对各种PCD途径在根尖周病中的作用进行综述,以期探究根尖周病的发病机制和靶向调控分子,从而为防治根尖周病提供新思路。

Programmed cell death (PCD) is a genetically determined, active, and orderly way of cell death, closely associated with the progression of periapical diseases. Various PCD pathways have been identified in periapical lesions, including apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis. These pathways can be activated by both endogenous and exogenous stimuli, playing crucial roles in maintaining homeostasis and regulating inflammation. This article provided a comprehensive review of the roles of different PCD pathways in periapical diseases, aiming to explore the pathogenesis and target regulatory molecules of periapical diseases, thereby offering new insights into their prevention and treatment.

[1]
Chang MCWang TMChien HH,et al. Effect of butyrate,a bacterial by-product,on the viability and ICAM-1 expression/production of human vascular endothelial cells:Role in infectious pulpal/periapical diseases[J]. Int Endod J202255(1):38-53. DOI:10.1111/iej.13614.
[2]
Pei FLin HLiu H,et al. Dual role of autophagy in lipopolysaccharide-induced preodontoblastic cells[J]. J Dent Res201594(1):175-182. DOI:10.1177/0022034514553815.
[3]
Wu ZLi MRen X,et al. Double-edged sword effect of pyroptosis:The role of Caspase-1/-4/-5/-11 in different levels of apical periodontitis[J]. Biomolecules202212(11):1660. DOI:10.3390/biom12111660.
[4]
Liu HFan WFan B. Necroptosis in apical periodontitis:A programmed cell death with multiple roles[J]. J Cell Physiol2023238(9):1964-1981. DOI:10.1002/jcp.31073.
[5]
Yang MShen ZZhang X,et al. Ferroptosis of macrophages facilitates bone loss in apical periodontitis via NRF2/FSP1/ROS pathway[J]. Free Radic Biol Med2023208:334-347. DOI:10.1016/j.freeradbiomed.2023.08.020.
[6]
Moujalled DStrasser ALiddell JR. Molecular mechanisms of cell death in neurological diseases[J]. Cell Death Differ202128(7):2029-2044. DOI:10.1038/s41418-021-00814-y.
[7]
Ribeiro-Sobrinho APRabelo FFigueiredo CB,et al. Bacteria recovered from dental pulp induce apoptosis of lymph node cells[J]. J Med Microbiol200554(Pt 4):413-416. DOI:10.1099/jmm.0.45728-0.
[8]
Yang CNLin SKKok SH,et al. The possible role of sirtuin 5 in the pathogenesis of apical periodontitis[J]. Oral Dis202127(7):1766-1774. DOI:10.1111/odi.13723.
[9]
Lin XLv XLi B,et al. Heterogeneity of T cells in periapical lesions and in vitro validation of the proangiogenic effect of GZMA on HUVECs[J]. Int Endod J202356(10):1254-1269. DOI:10.1111/iej.13951.
[10]
Jia TYuan FTao J,et al. CRISPR/Cas13d targeting GZMA in PARs pathway regulates the function of osteoclasts in chronic apical periodontitis[J]. Cell Mol Biol Lett202328(1):70. DOI:10.1186/s11658-023-00477-2.
[11]
Lin LMHuang GTRosenberg PA. Proliferation of epithelial cell rests,formation of apical cysts,and regression of apical cysts after periapical wound healing[J]. J Endod200733(8):908-916. DOI:10.1016/j.joen.2007.02.006.
[12]
Martins CARivero ERDufloth RM,et al. Immunohistochemical detection of factors related to cellular proliferation and apoptosis in radicular and dentigerous cysts[J]. J Endod201137(1):36-39. DOI:10.1016/j.joen.2010.09.010.
[13]
Xie YLei XZhao G,et al. mTOR in programmed cell death and its therapeutic implications[J]. Cytokine Growth Factor Rev202371-72:66-81. DOI:10.1016/j.cytogfr.2023.06.002.
[14]
Liu SYao SYang H,et al. Autophagy:Regulator of cell death[J]. Cell Death Dis202314(10):648. DOI:10.1038/s41419-023-06154-8.
[15]
Parzych KRKlionsky DJ. An overview of autophagy:Morphology,mechanism,and regulation[J]. Antioxid Redox Signal201420(3):460-473. DOI:10.1089/ars.2013.5371.
[16]
Li JYue YChan W,et al. RGS10 negatively regulates apical periodontitis via TFEB-mediated autophagy in BABL/c mice model and in vitro[J]. Int Endod J202356(7):854-868. DOI:10.1111/iej.13924.
[17]
Zhu ZYang JZhang J,et al. The presence of autophagy in human periapical lesions[J]. J Endod201339(11):1379-1384. DOI:10.1016/j.joen.2013.07.013.
[18]
Lai EHHong CYKok SH,et al. Simvastatin alleviates the progression of periapical lesions by modulating autophagy and apoptosis in osteoblasts[J]. J Endod201238(6):757-763. DOI:10.1016/j.joen.2012.02.023.
[19]
Deng ZLin BLiu F,et al. Role of Enterococcus faecalis in refractory apical periodontitis:From pathogenicity to host cell response[J]. J Oral Microbiol202315(1):2184924. DOI:10.1080/20002297.2023.2184924.
[20]
Huang HYWang WCLin PY,et al. The roles of autophagy and hypoxia in human inflammatory periapical lesions[J]. Int Endod J201851(Suppl 2):e125-e145. DOI:10.1111/iej.12782.
[21]
Yang CNKok SHWang HW,et al. Simvastatin alleviates bone resorption in apical periodontitis possibly by inhibition of mitophagy-related osteoblast apoptosis[J]. Int Endod J201952(5):676-688. DOI:10.1111/iej.13055.
[22]
Ye KChen ZXu Y. The double-edged functions of necroptosis[J]. Cell Death Dis202314(2):163. DOI:10.1038/s41419-023-05691-6.
[23]
Dai XMa RJiang W,et al. Enterococcus faecalis-induced macrophage necroptosis promotes refractory apical periodontitis[J]. Microbiol Spectr202210(4):e104522. DOI:10.1128/spectrum.01045-22.
[24]
Liu JWang JRen J,et al. Inhibition of receptor-interacting protein kinase-3 in the necroptosis pathway attenuates inflammatory bone loss in experimental apical periodontitis in Balb/c mice[J]. Int Endod J202154(9):1538-1547. DOI:10.1111/iej.13534.
[25]
Dai XDeng ZLiang Y,et al. Enterococcus faecalis induces necroptosis in human osteoblastic MG63 cells through the RIPK3/MLKL signalling pathway[J]. Int Endod J202053(9):1204-1215. DOI:10.1111/iej.13323.
[26]
Chai QLei ZLiu CH. Pyroptosis modulation by bacterial effector proteins[J]. Semin Immunol202369:101804. DOI:10.1016/j.smim.2023.101804.
[27]
Li XJi LMen X,et al. Pyroptosis in bone loss[J]. Apoptosis202328(3-4):293-312. DOI:10.1007/s10495-022-01807-z.
[28]
Cheng RFeng YZhang R,et al. The extent of pyroptosis varies in different stages of apical periodontitis[J]. Biochim Biophys Acta Mol Basis Dis20181864(1):226-237. DOI:10.1016/j.bbadis.2017.10.025.
[29]
Wang KLiu JYue J,et al. Nlrp3 inflammasome drives regulatory T cell depletion to accelerate periapical bone erosion[J]. Int Endod J2024. DOI:10.1111/iej.14062.
[30]
Ran SHuang JLiu B,et al. Enterococcus faecalis activates NLRP3 inflammasomes leading to increased interleukin-1 beta secretion and pyroptosis of THP-1 macrophages[J]. Microb Pathog2021154:104761. DOI:10.1016/j.micpath.2021.104761.
[31]
Ran SChu MGu S,et al. Enterococcus faecalis induces apoptosis and pyroptosis of human osteoblastic MG63 cells via the NLRP3 inflammasome[J]. Int Endod J201952(1):44-53. DOI:10.1111/iej.12965.
[32]
Conti LCSegura-Egea JJCardoso CBM,et al. Relationship between apical periodontitis and atherosclerosis in rats:Lipid profile and histological study[J]. Int Endod J202053(10):1387-1397. DOI:10.1111/iej.13350.
[33]
Azuma MMGomes-Filho JEErvolino E,et al. Omega-3 fatty acids reduce inflammation in rat apical periodontitis[J]. J Endod201844(4):604-608. DOI:10.1016/j.joen.2017.12.008.
[34]
Costa SAMoreira AROCosta CPS,et al. Iron overload and periodontal status in patients with sickle cell anaemia:A case series[J]. J Clin Periodontol202047(6):668-675. DOI:10.1111/jcpe.13284.
[35]
Liu PWang WLi Z,et al. Ferroptosis:A new regulatory mechanism in osteoporosis[J]. Oxid Med Cell Longev20222022:2634431. DOI:10.1155/2022/2634431.
[36]
Lu JYang JZheng Y,et al. Extracellular vesicles from endothelial progenitor cells prevent steroid-induced osteoporosis by suppressing the ferroptotic pathway in mouse osteoblasts based on bioinformatics evidence[J]. Sci Rep20199(1):16130. DOI:10.1038/s41598-019-52513-x.
[37]
Hussein HKishen A. Proteomic profiling reveals engineered chitosan nanoparticles mediated cellular crosstalk and immunomodulation for therapeutic application in apical periodontitis[J]. Bioact Mater202211:77-89. DOI:10.1016/j.bioactmat.2021.09.032.
[38]
Fritsch MGunther SDSchwarzer R,et al. Caspase-8 is the molecular switch for apoptosis,necroptosis and pyroptosis[J]. Nature2019575(7784):683-687. DOI:10.1038/s41586-019-1770-6.
[39]
Moriwaki KChan FK. The inflammatory signal adaptor RIPK3:Functions beyond necroptosis[J]. Int Rev Cell Mol Biol2017328:253-275. DOI:10.1016/bs.ircmb.2016.08.007.
[40]
Jiang WDeng ZDai X,et al. PANoptosis:A new insight into oral infectious diseases[J]. Front Immunol202112:789610. DOI:10.3389/fimmu.2021.789610.
[41]
Geng FLiu JYin C,et al. Porphyromonas gingivalis lipopolysaccharide induced RIPK3/MLKL-mediated necroptosis of oral epithelial cells and the further regulation in macrophage activation[J]. J Oral Microbiol202214(1):2041790. DOI:10.1080/20002297.2022.2041790.
[42]
Song BZhou TYang WL,et al. Programmed cell death in periodontitis:Recent advances and future perspectives[J]. Oral Dis201723(5):609-619. DOI:10.1111/odi.12574.
[43]
Tao HGe GLiang X,et al. ROS signaling cascades:Dual regulations for osteoclast and osteoblast[J]. Acta Biochim Biophys Sin(Shanghai)202052(10):1055-1062. DOI:10.1093/abbs/gmaa098.
[44]
Chi DLin XMeng Q,et al. Real-time induction of macrophage apoptosis,pyroptosis,and necroptosis by Enterococcus faecalis OG1RF and two root canal isolated strains[J]. Front Cell Infect Microbiol202111:720147. DOI:10.3389/fcimb.2021.720147.
[45]
Chi DZhang YLin X,et al. Caspase-1 inhibition reduces occurrence of PANoptosis in macrophages infected by E.faecalis OG1RF[J]. J Clin Med202211(20):6204. DOI:10.3390/jcm11206204.
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