[1]
|
Zhao Y,An Y,Zhou L,et al. Animal models of temporomandibular joint osteoarthritis: Classification and selection[J]. Front Physiol,2022,13:859517. doi: 10.3389/fphys.2022.859517
|
[2]
|
Hunter D J,Bierma-Zeinstra S. Osteoarthritis[J]. Lancet,2019,393(10182):1745-1759. doi: 10.1016/S0140-6736(19)30417-9
|
[3]
|
Allen K D,Thoma L M,Golightly Y M. Epidemiology of osteoarthritis[J]. Osteoarthritis Cartilage,2022,30(2):184-195. doi: 10.1016/j.joca.2021.04.020
|
[4]
|
Ernberg M. The role of molecular pain biomarkers in temporomandibular joint internal derangement[J]. J Oral Rehabil,2017,44(6):481-491. doi: 10.1111/joor.12480
|
[5]
|
Sanchez-Lopez E,Coras R,Torres A,et al. Synovial inflammation in osteoarthritis progression[J]. Nat Rev Rheumatol,2022,18(5):258-275. doi: 10.1038/s41584-022-00749-9
|
[6]
|
Wu C L,Harasymowicz N S,Klimak M A,et al. The role of macrophages in osteoarthritis and cartilage repair[J]. Osteoarthritis Cartilage,2020,28(5):544-554. doi: 10.1016/j.joca.2019.12.007
|
[7]
|
Resiere D,Mehdaoui H,Neviere R. Inflammation and oxidative stress in snakebite envenomation: A brief descriptive review and clinical implications[J]. Toxins (Basel),2022,14(11):802-815. doi: 10.3390/toxins14110802
|
[8]
|
Ibi M,Horie S,Kyakumoto S,et al. Cell-cell interactions between monocytes/macrophages and synoviocyte-like cells promote inflammatory cell infiltration mediated by augmentation of MCP-1 production in temporomandibular joint[J]. Biosci Rep,2018,38(2):BSR20171217. doi: 10.1042/BSR20171217
|
[9]
|
Wehmeyer C,Pap T,Buckley C D,et al. The role of stromal cells in inflammatory bone loss[J]. Clin Exp Immunol,2017,189(1):1-11. doi: 10.1111/cei.12979
|
[10]
|
Scanzello C R. Chemokines and inflammation in osteoarthritis: Insights from patients and animal models[J]. J Orthop Res,2017,35(4):735-739. doi: 10.1002/jor.23471
|
[11]
|
Pan X,Zhao Z,Huang X,et al. Circ-slain2 alleviates cartilage degradation and inflammation of TMJOA[J]. J Dent Res,2023,102(13):1498-1506. doi: 10.1177/00220345231198448
|
[12]
|
Liu X,Li H,Feng Y,et al. Resatorvid alleviates experimental inflammatory TMJOA by restraining chondrocyte pyroptosis and synovial inflammation[J]. Arthritis Res Ther,2023,25(1):230-244. doi: 10.1186/s13075-023-03214-4
|
[13]
|
Guo H,Callaway J B,Ting J P. Inflammasomes: Mechanism of action,role in disease,and therapeutics[J]. Nat Med,2015,21(7):677-687. doi: 10.1038/nm.3893
|
[14]
|
Zhang S,Teo K Y W,Chuah S J,et al. MSC exosomes alleviate temporomandibular joint osteoarthritis by attenuating inflammation and restoring matrix homeostasis[J]. Biomaterials,2019,200: 35-47.
|
[15]
|
Li B,Guan G,Mei L,et al. Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint[J]. J Cell Mol Med,2021,25(11):4902-4911. doi: 10.1111/jcmm.16514
|
[16]
|
Hu H, Liu W, Sun C, et al. Endogenous repair and regeneration of injured articular cartilage: A challenging but promising therapeutic strategy[J]. Aging Dis,2021,12(3):886-901.
|
[17]
|
Derwich M,Mitus-Kenig M,Pawlowska E. Interdisciplinary approach to the temporomandibular joint osteoarthritis-review of the literature[J]. Medicina (Kaunas),2020,56(5):225-247. doi: 10.3390/medicina56050225
|
[18]
|
Yang H,Wen Y,Zhang M,et al. MTORC1 coordinates the autophagy and apoptosis signaling in articular chondrocytes in osteoarthritic temporomandibular joint[J]. Autophagy,2020,16(2):271-288. doi: 10.1080/15548627.2019.1606647
|
[19]
|
Lian C,Wang X,Qiu X,et al. Collagen type II suppresses articular chondrocyte hypertrophy and osteoarthritis progression by promoting integrin β1-SMAD1 interaction[J]. Bone Res,2019,7:8-23. doi: 10.1038/s41413-019-0046-y
|
[20]
|
Shi Y,Hu X,Cheng J,et al. A small molecule promotes cartilage extracellular matrix generation and inhibits osteoarthritis development[J]. Nat Commun,2019,10(1):1914-1928. doi: 10.1038/s41467-019-09839-x
|
[21]
|
Yan J F,Qin W P,Xiao B C,et al. Pathological calcification in osteoarthritis: an outcome or a disease initiator?[J]. Biol Rev Camb Philos Soc,2020,95(4):960-985. doi: 10.1111/brv.12595
|
[22]
|
Huang Z,Zhou M,Wang Q,et al. Mechanical and hypoxia stress can cause chondrocytes apoptosis through over-activation of endoplasmic reticulum stress[J]. Arch Oral Biol,2017,84: 125-132
|
[23]
|
Ren H,Yang H,Xie M,et al. Chondrocyte apoptosis in rat mandibular condyles induced by dental occlusion due to mitochondrial damage caused by nitric oxide[J]. Arch Oral Biol,2019,101: 108-121
|
[24]
|
Zhang C,Lin S,Li T,et al. Mechanical force-mediated pathological cartilage thinning is regulated by necroptosis and apoptosis[J]. Osteoarthritis Cartilage,2017,25(8):1324-1334. doi: 10.1016/j.joca.2017.03.018
|
[25]
|
Poli G,Fabi C,Sugoni C,et al. The role of NLRP3 inflammasome activation and oxidative stress in varicocele-mediated male hypofertility[J]. Int J Mol Sci,2022,23(9):5233-5248. doi: 10.3390/ijms23095233
|
[26]
|
Nunes P R,Mattioli S V,Sandrim V C. NLRP3 activation and its relationship to endothelial dysfunction and oxidative stress: Implications for preeclampsia and pharmacological interventions[J]. Cells,2021,10(11):2828-2842. doi: 10.3390/cells10112828
|
[27]
|
Liu X, Zhao J, Jiang H, et al. ALPK1 aggravates TMJOA cartilage degradation via NF-κB and ERK1/2 signaling[J]. J Dent Res,2022,101(12):1499-1509.
|
[28]
|
Lu K,Ma F,Yi D,et al. Molecular signaling in temporomandibular joint osteoarthritis[J]. J Orthop Translat,2021,32: 21-27
|
[29]
|
Zhou Y,Wang T,Hamilton J L,et al. Wnt/β-catenin signaling in osteoarthritis and in other forms of arthritis[J]. Curr Rheumatol Rep,2017,19(9):53-65. doi: 10.1007/s11926-017-0679-z
|
[30]
|
Zhou Y,Shu B,Xie R,et al. Deletion of Axin1 in condylar chondrocytes leads to osteoarthritis-like phenotype in temporomandibular joint via activation of β-catenin and FGF signaling[J]. J Cell Physiol,2019,234(2):1720-1729. doi: 10.1002/jcp.27043
|
[31]
|
Li W,Zhao S,Yang H,et al. Potential novel prediction of TMJ-OA: MiR-140-5p regulates inflammation through Smad/TGF-β signaling[J]. Front Pharmacol,2019,10:15-24. doi: 10.3389/fphar.2019.00015
|
[32]
|
Ghassemi Nejad S, Kobezda T, Tar I, et al. Development of temporomandibular joint arthritis: The use of animal models[J]. Joint Bone Spine,2017,84(2):145-151.
|
[33]
|
Wang Z,Huang J,Zhou S,et al. Loss of Fgfr1 in chondrocytes inhibits osteoarthritis by promoting autophagic activity in temporomandibular joint[J]. J Biol Chem,2018,293(23):8761-8774. doi: 10.1074/jbc.RA118.002293
|
[34]
|
Saito T,Tanaka S. Molecular mechanisms underlying osteoarthritis development: Notch and NF-κB[J]. Arthritis Res Ther,2017,19(1):94-101. doi: 10.1186/s13075-017-1296-y
|
[35]
|
Luo X,Jiang Y,Bi R,et al. Inhibition of notch signaling pathway temporally postpones the cartilage degradation progress of temporomandibular joint arthritis in mice[J]. J Craniomaxillofac Surg,2018,46(7):1132-1138. doi: 10.1016/j.jcms.2018.04.026
|
[36]
|
Ruscitto A,Scarpa V,Morel M,et al. Notch regulates fibrocartilage stem cell fate and is upregulated in inflammatory TMJ arthritis[J]. J Dent Res,2020,99(10):1174-1181. doi: 10.1177/0022034520924656
|
[37]
|
Chen Y,Zhao B,Zhu Y,et al. HIF-1-VEGF-Notch mediates angiogenesis in temporomandibular joint osteoarthritis[J]. Am J Transl Res,2019,11(5):2969-2982.
|
[38]
|
Yang H,Zhang M,Liu Q,et al. Inhibition of Ihh reverses temporomandibular joint osteoarthritis via a PTH1R signaling dependent mechanism[J]. Int J Mol Sci,2019,20(15):3797-3815. doi: 10.3390/ijms20153797
|
[39]
|
Nachury M V,Mick D U. Establishing and regulating the composition of cilia for signal transduction[J]. Nat Rev Mol Cell Biol,2019,20(7):389-405. doi: 10.1038/s41580-019-0116-4
|
[40]
|
Zhang Q,Lenardo M J,Baltimore D. 30 Years of NF-κB: A blossoming of relevance to human pathobiology[J]. Cell,2017,168(1-2):37-57. doi: 10.1016/j.cell.2016.12.012
|
[41]
|
Yuan J,Ding W,Wu N,et al. Protective effect of genistein on condylar cartilage through downregulating NF-κB expression in experimentally created osteoarthritis rats[J]. Biomed Res Int,2019,2019:2629791.
|
[42]
|
Taleuan A, Kamal D, Aouinti L, et al. Arthrotic ankylosis of the temporomandibular joint[J]. Pan Afr Med J,2019,32:151-160.
|