[1] Zhao YP, Zhang ZY, Wu YT, et al. Investigation of the clinical and radiographic features of osteoarthrosis of the temporomandibular joints in adolescents and young adults [J]. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2011, 111(2):e27-e34. [2] Liu Y, Wu JS, Tang YL, et al. Multiple treatment meta-analysis of intra-articular injection for temporomandibular osteoarthritis [J] J Oral Maxillofac Surg, 2020, 78: 373.e1-373.e18. [3] Charlier E, Relic B, Deroyer C, et al. Insights on molecular mechanisms of chondrocytes death in osteoarthritis [J]. Int J Mol Sci, 2016, 17(12):2146. [4] Schweichel JU, Merker HJ. The morphology of various types of cell death in prenatal tissues [J]. Teratology, 1973, 7(3):253-266. [5] Vanden BT, Kaiser WJ, Bertrand MJ, et al. Molecular crosstalk between apoptosis, necroptosis, and survival signaling [J]. Mol Cell Oncol, 2015, 2(4):e975093. [6] 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(6):489-95. [7] 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(2):112-119. [8] Pasparakis M, Vandenabeele P. Necroptosis and its role in inflammation [J]. Nature, 2015, 517(7534):311-320. [9] Siegmund D, Lang I, Wajant H. Cell death-independent activities of the death receptors CD95, TRAILR1, and TRAILR2 [J]. FEBS J, 2017, 284(8):1131-1159. [10] Yang H, Zhang M, Wang X, et al. TNF accelerates death of mandibular condyle chondrocytes in rats with biomechanical stimulation-induced temporomandibular joint disease [J]. PLoS One, 2015,10(11):e0141774. [11] Hsu H, Huang J, Shu HB, et al. TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex [J]. Immunity, 1996,4(4):387-396. [12] Weinlich R, Oberst A, Beere HM, et al. Necroptosis in development, inflammation and disease [J]. Nat Rev Mol Cell Biol, 2017, 18(2):127-136. [13] Yuan J, Amin P, Ofengeim D. Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases [J]. Nat Rev Mol Cell Biol, 2019, 20(1):19-33. [14] Dasgupta A, Nomura M, Shuck R, et al. Cancer's Achilles' Heel: apoptosis and necroptosis to the rescue [J]. Int J Mol Sci, 2016,18(1):23. [15] 孙玉环,赵茜,何冬梅,等.高浓度肿瘤坏死因子-α环境下髁突软骨细胞死亡情况研究[J].中国实用口腔科杂志,2015,8(9):527-531. [16] Lee SW, Rho JH, Lee SY, et al. Leptin protects rat articular chondrocytes from cytotoxicity induced by TNF-α in the presence of cyclohexamide [J]. Osteoarthritis Cartilage, 2015, 23(12):2269-2278. [17] Riegger J, Brenner RE. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis [J]. Cell Death Dis, 2019,10(10):683. [18] 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. [19] Liang S, Lv Z, Zhang J, et al. Necrostatin-1 attenuates trauma-induced mouse osteoarthritis and IL-1β induced apoptosis via HMGB1/TLR4/SDF-1 in primary mouse chondrocytes [J]. Front Pharmacol, 2018, 9:1378. [20] Amin AR, Islam AB. Genomic analysis and differential expression of HMG and S100A family in human arthritis: upregulated expression of chemokines, IL-8 and nitric oxide by HMGB1 [J]. DNA Cell Biol, 2014, 33(8):550-565. [21] Rosenberg JH, Rai V, Dilisio MF, et al. Increased expression of damage-associated molecular patterns (DAMPs) in osteoarthritis of human knee joint compared to hip joint [J]. Mol Cell Biochem, 2017,436(1-2):59-69. [22] Feng Y, Fang W, Li C, et al. The expression of high-mobility group box protein-1 in temporomandibular joint osteoarthritis with disc perforation [J]. J Oral Pathol Med, 2016, 45(2):148-152. [23] Hamada T, Torikai M, Kuwazuru A, et al. Extracellular high mobility group box chromosomal protein 1 is a coupling factor for hypoxia and inflammation in arthritis [J]. Arthritis Rheum, 2008, 58(9):2675-2685. [24] Ye T, He F, Lu L, et al. The effect of oestrogen on mandibular condylar cartilage via hypoxia-inducible factor-2α during osteoarthritis development [J]. Bone, 2020, 130: 115123. [25] Wang XY, Chen Y, Tang XJ, et al. AMD3100 attenuates matrix metalloprotease-3 and -9 expressions and prevents cartilage degradation in a monosodium iodo-acetate-induced rat model of temporomandibular osteoarthritis [J]. J Oral Maxillofac Surg, 2016, 74(5): 927.e1-927.e13. [26] Cremers N, van den Bosch M, van Dalen S, et al. S100A8/A9 increases the mobilization of pro-inflammatory Ly6C monocytes to the synovium during experimental osteoarthritis [J]. Arthritis Res Ther, 2017,19(1):217. [27] Wang L, Zhang H, Shao L, et al. S100A12 levels in synovial fluid may reflect clinical severity in patients with primary knee osteoarthritis [J]. Biomarkers, 2013,18(3):216-220. [28] Nakashima M, Sakai T, Hiraiwa H, et al. Role of S100A12 in the pathogenesis of osteoarthritis [J]. Biochem Biophys Res Commun, 2012, 422(3):508-514. [29] Ding L, Buckwalter JA, Martin JA. DAMPs synergize with cytokines or fibronectin fragment on inducing chondrolysis but lose effect when acting alone [J]. Mediators Inflamm, 2017, 2017:2642549. [30] Yun J, Jiang G, Wang Y, et al. The HMGB1-CXCL12 Complex Promotes Inflammatory Cell Infiltration in Uveitogenic T Cell-Induced Chronic Experimental Autoimmune Uveitis [J]. Front Immunol, 2017,8:142. [31] Liu-Bryan R, Terkeltaub R. Chondrocyte innate immune myeloid differentiation factor 88-dependent signaling drives procatabolic effects of the endogenous Toll-like receptor 2/Toll-like receptor 4 ligands low molecular weight hyaluronan and high mobility group box chromosomal protein 1 in mice [J]. Arthritis Rheum, 2010, 62(7):2004-2012. [32] Sokolove J, Lepus CM. Role of inflammation in the pathogenesis of osteoarthritis: latest findings and interpretations [J]. Ther Adv Musculoskelet Dis, 2013, 5(2):77-94. |