EXPLORING CHONDROCYTE DEATH IN TEMPOROMANDIBULAR JOINT OSTEOARTHRITIS: A PROGRAMMED CELL DEATH PERSPECTIVE
Abstract
Temporomandibular joint osteoarthritis (TMJ OA) is a condition characterized by severe pain and joint dysfunction in the temporomandibular joint. The main pathological change in TMJ OA is cartilage degeneration, and chondrocytes are the primary cell type within cartilage tissue. This paper explores the hypothesis that chondrocyte death plays a central role in the process of cartilage degeneration in TMJ OA. Specifically, it focuses on programmed cell death (PCD) as a regulated mechanism involved in the development of OA. The research progress on PCD in OA cartilage degeneration is discussed, offering new insights and ideas for future basic research on cartilage degeneration in TMJ OA.
Keywords:
Temporomandibular Joint Osteoarthritis, Chondrocyte Death, Programmed Cell Death, Cartilage Degeneration, Joint DysfunctionDownloads
Published
Issue
Section
How to Cite
License
Copyright (c) 2023 Wei Zhang
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
References
Wang X D, Zhang J N, Gan Y H, et al. Current understanding of pathogenesis and treatment of TMJ osteoarthritis [J]. J Dent Res, 2015, 94:666-673.
Scrivani S J, Keith D A, Kaban L B. Temporomandibular disorders [J]. N Engl J Med, 2008, 359:2693-2705.
Yang J, Hu S, Bian Y, et al. Targeting Cell Death: Pyroptosis, Ferroptosis, Apoptosis and Necroptosis in Osteoarthritis [J]. Front Cell Dev Biol, 2021, 9:789948.
Kerr J F, Wyllie A H, Currie A R. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics [J]. Br J Cancer, 1972, 26:239-257.
Zhang Y, Chen X, Gueydan C, et al. Plasma membrane changes during programmed cell deaths [J]. Cell Res, 2018, 28:9-21.doi: 10.1038/cr.2017.133
Kesavardhana S, Malireddi R K S, Kanneganti T D. Caspases in Cell Death, Inflammation, and Pyroptosis [J]. Annu Rev Immunol, 2020, 38:567-595.
Yuan X, Gajan A, Chu Q, et al. Developing TRAIL/TRAIL death receptor-based cancer therapies [J]. Cancer Metastasis Rev, 2018, 37:733-748.
Cheng C, Tian J, Zhang F, et al. WISP1 Protects Against Chondrocyte Senescence and Apoptosis by Regulating αvβ3 and PI3K/Akt Pathway in Osteoarthritis [J]. DNA Cell Biol, 2021, 40:629-637.
Wang X D, Kou X X, He D Q, et al. Progression of cartilage degradation, bone resorption and pain in rat temporomandibular joint osteoarthritis induced by injection of iodoacetate [J]. PLoS One, 2012, 7:e45036.
Hwang H S, Kim H A. Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis [J]. Int J Mol Sci, 2015, 16:26035-26054.
Mino-Oka A, Izawa T, Shinohara T, et al. Roles of hypoxia inducible factor-1α in the temporomandibular joint [J]. Arch Oral Biol, 2017, 73:274-281.
Wang B W, Jiang Y, Yao Z L, et al. Aucubin Protects Chondrocytes Against IL-1β-Induced Apoptosis In Vitro And Inhibits Osteoarthritis In Mice Model [J]. Drug Des Devel Ther, 2019, 13:3529-3538.
Ding Y, Wang L, Zhao Q, et al. MicroRNA‑93 inhibits chondrocyte apoptosis and inflammation in osteoarthritis by targeting the TLR4/NF‑κB signaling pathway [J]. Int J Mol Med, 2019, 43:779-790.
Duve C D. Structure and Functions of Lysosomes [M]. Funktionelle und Morphologische Organisation der Zelle, 1963.
Liu X, Tang Y, Cui Y, et al. Autophagy is associated with cell fate in the process of macrophagederived foam cells formation and progress [J]. J Biomed Sci, 2016, 23:57.
Kanayama M, Shinohara M L. Roles of Autophagy and Autophagy-Related Proteins in Antifungal Immunity [J]. Front Immunol, 2016, 7:47.
Kovács A L, Pálfia Z, Réz G, et al. Sequestration revisited: integrating traditional electron microscopy, de novo assembly and new results [J]. Autophagy, 2007, 3:655-662.
Caramés B, Taniguchi N, Otsuki S, et al. Autophagy is a protective mechanism in normal cartilage, and its aging-related loss is linked with cell death and osteoarthritis [J]. Arthritis Rheum, 2010, 62:791801.
Xue J F, Shi Z M, Zou J, et al. Inhibition of PI3K/AKT/mTOR signaling pathway promotes autophagy of articular chondrocytes and attenuates inflammatory response in rats with osteoarthritis [J]. Biomed Pharmacother, 2017, 89:1252-1261.
Bao J, Chen Z, Xu L, et al. Rapamycin protects chondrocytes against IL-18-induced apoptosis and ameliorates rat osteoarthritis [J]. Aging (Albany NY), 2020, 12:5152-5167.
Zhong G, Long H, Ma S, et al. miRNA-335-5p relieves chondrocyte inflammation by activating autophagy in osteoarthritis [J]. Life Sci, 2019, 226:164-172.
Duan R, Xie H, Liu Z Z. The Role of Autophagy in Osteoarthritis [J]. Frontiers in Cell and Developmental Biology, 2020, 8.
Cookson B T, Brennan M A. Pro-inflammatory programmed cell death [J]. Trends Microbiol, 2001, 9:113-114.
Ball D P, Taabazuing C Y, Griswold A R, et al. Caspase-1 interdomain linker cleavage is required for pyroptosis [J]. Life Sci Alliance, 2020, 3.
Xia X, Wang X, Cheng Z, et al. The role of pyroptosis in cancer: pro-cancer or pro-"host"? [J]. Cell Death Dis, 2019, 10:650.
Man S M, Kanneganti T D. Regulation of inflammasome activation [J]. Immunol Rev, 2015, 265:621.
Zu Y, Mu Y, Li Q, et al. Icariin alleviates osteoarthritis by inhibiting NLRP3-mediated pyroptosis [J]. J Orthop Surg Res, 2019, 14:307.
Yan J, Ding D, Feng G, et al. Metformin reduces chondrocyte pyroptosis in an osteoarthritis mouse model by inhibiting NLRP3 inflammasome activation [J]. Exp Ther Med, 2022, 23:222.
Liu Q, Wu Z, Hu D, et al. Low dose of indomethacin and Hedgehog signaling inhibitor administration synergistically attenuates cartilage damage in osteoarthritis by controlling chondrocytes pyroptosis [J]. Gene, 2019, 712:143959.
Holler N, Zaru R, Micheau O, et al. Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule [J]. Nat Immunol, 2000, 1:489-495.
Degterev A, Huang Z, Boyce M, et al. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury [J]. Nat Chem Biol, 2005, 1:112-119.
Pasparakis M, Vandenabeele P. Necroptosis and its role in inflammation [J]. Nature, 2015, 517:311320.
