{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T10:08:13Z","timestamp":1789034893098,"version":"build-2803163510"},"reference-count":50,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T00:00:00Z","timestamp":1788739200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T00:00:00Z","timestamp":1788739200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/501100012166","name":"National Key Research and Development Program of China","doi-asserted-by":"publisher","award":["2023YFC2413600"],"award-info":[{"award-number":["2023YFC2413600"]}],"id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82130027"],"award-info":[{"award-number":["82130027"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82522020"],"award-info":[{"award-number":["82522020"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Dent Res"],"abstract":"<jats:p>\n                    Excessive osteoclast activation drives rapid subchondral bone destruction, serving as a critical early-stage event precipitating temporomandibular joint osteoarthritis (TMJ-OA). Although epigenetic remodeling is widely recognized as an important interface between pathological environmental signals and genomic response, the specific epigenetic mechanisms translating TMJ-OA\u2013associated stimulation into pathological osteoclast activation remain to be elucidated. Here, using a mechanically induced TMJ-OA mouse model, we identify aberrant reactive oxygen species (ROS) accumulation as a critical upstream driver initiating excessive osteoclast activation and subsequent joint deterioration. By integrating transcriptomic and epigenomic analyses, we delineate the chromatin remodeler AT-rich interaction domain 1A (ARID1A) as an essential oxidative stress sensor within the osteoclast lineage. Mechanistically, ROS accumulation induces ARID1A upregulation and recruitment to the\n                    <jats:italic toggle=\"yes\">Src<\/jats:italic>\n                    enhancer, transcriptionally activating\n                    <jats:italic toggle=\"yes\">Src<\/jats:italic>\n                    and amplifying PI3K-AKT signaling to drive pathological osteoclastogenesis. Conditional knockout of\n                    <jats:italic toggle=\"yes\">Arid1a<\/jats:italic>\n                    in myeloid cells effectively abrogates subchondral bone loss and cartilage destruction in TMJ-OA. Translating these mechanistic insights, we engineered an ROS-responsive, osteoclast-targeting hydrogel for the on-demand delivery of an ARID1A-dependent canonical BRG1\/BRM-associated factor complex inhibitor, which successfully alleviates TMJ-OA progression. Our findings establish the epigenetic response to ROS accumulation as a key pathogenic mechanism in TMJ-OA and highlight ARID1A as a promising therapeutic target for early disease intervention.\n                  <\/jats:p>","DOI":"10.1177\/00220345261471409","type":"journal-article","created":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T07:42:17Z","timestamp":1788766937000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["ARID1A Mediates ROS-Induced Osteoclast Activation in TMJ Osteoarthritis"],"prefix":"10.1177","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-6009-6691","authenticated-orcid":false,"given":"Y.L.","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Prosthodontics, Shanghai Stomatological Hospital &amp; School of Stomatology, Fudan University, Shanghai, China"},{"name":"Department of Prosthodontics, Shanghai Ninth People\u2019s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China"},{"name":"College of Stomatology, Shanghai Jiao Tong University, Shanghai, China"},{"name":"National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-4710-0163","authenticated-orcid":false,"given":"J.Y.","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics, Shanghai Stomatological Hospital &amp; School of Stomatology, Fudan University, Shanghai, China"},{"name":"Department of Prosthodontics, Shanghai Ninth People\u2019s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China"},{"name":"College of Stomatology, Shanghai Jiao Tong University, Shanghai, China"},{"name":"National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.Q.","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics, Shanghai Stomatological Hospital &amp; School of Stomatology, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.L.","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics, Shanghai Stomatological Hospital &amp; School of Stomatology, Fudan University, Shanghai, China"},{"name":"Department of Prosthodontics, Shanghai Ninth People\u2019s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China"},{"name":"College of Stomatology, Shanghai Jiao Tong University, Shanghai, China"},{"name":"National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-2673-2535","authenticated-orcid":false,"given":"E.H.","family":"Yao","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics, Shanghai Stomatological Hospital &amp; School of Stomatology, Fudan University, Shanghai, China"},{"name":"Department of Prosthodontics, Shanghai Ninth People\u2019s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China"},{"name":"College of Stomatology, Shanghai Jiao Tong University, Shanghai, China"},{"name":"National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.L.","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics, Shanghai Stomatological Hospital &amp; School of Stomatology, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7856-8091","authenticated-orcid":false,"given":"M.L.","family":"Mei","sequence":"additional","affiliation":[{"name":"Sir John Walsh Research Institute, Faculty of Dentistry, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1305-7287","authenticated-orcid":false,"given":"P. R.","family":"Cooper","sequence":"additional","affiliation":[{"name":"Sir John Walsh Research Institute, Faculty of Dentistry, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3238-0469","authenticated-orcid":false,"given":"J.H.","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics, Shanghai Stomatological Hospital &amp; School of Stomatology, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1490-281X","authenticated-orcid":false,"given":"X.Q.","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics, Shanghai Stomatological Hospital &amp; School of Stomatology, Fudan University, Shanghai, China"},{"name":"Department of Prosthodontics, Shanghai Ninth People\u2019s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China"},{"name":"College of Stomatology, Shanghai Jiao Tong University, Shanghai, China"},{"name":"National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, Shanghai Engineering Research Center of Advanced Dental Technology and Materials, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,9,7]]},"reference":[{"key":"e_1_3_2_2_1","doi-asserted-by":"crossref","unstructured":"Abraham A et al. 2024. Arid1a-dependent canonical BAF complex suppresses inflammatory programs to drive efficient germinal center B cell responses. Nat Immunol. 25(9):1704\u20131717. https:\/\/doi.org\/10.1038\/s41590-024-01920-y","DOI":"10.1038\/s41590-024-01920-y"},{"key":"e_1_3_2_3_1","doi-asserted-by":"crossref","unstructured":"Bli\u017aniak F et al. 2024. Non-steroidal anti-inflammatory drugs administered intra-articularly in temporomandibular joint disorders: a systematic review and meta-analysis. J Clin Med. 13(14):4056. https:\/\/doi.org\/10.3390\/jcm13144056","DOI":"10.3390\/jcm13144056"},{"key":"e_1_3_2_4_1","doi-asserted-by":"crossref","unstructured":"Brown TJ Laurent UB Fraser JR. 1991. Turnover of hyaluronan in synovial joints: elimination of labelled hyaluronan from the knee joint of the rabbit. Exp Physiol. 76(1):125\u2013134. https:\/\/doi.org\/10.1113\/expphysiol.1991.sp003474","DOI":"10.1113\/expphysiol.1991.sp003474"},{"key":"e_1_3_2_5_1","doi-asserted-by":"crossref","unstructured":"Chang L et al. 2018. The SWI\/SNF complex is a mechanoregulated inhibitor of YAP and TAZ. Nature. 563(7730):265\u2013269. https:\/\/doi.org\/10.1038\/s41586-018-0658-1","DOI":"10.1038\/s41586-018-0658-1"},{"key":"e_1_3_2_6_1","doi-asserted-by":"crossref","unstructured":"Embree M et al. 2011. Role of subchondral bone during early-stage experimental TMJ osteoarthritis. J Dent Res. 90(11):1331\u20131338. https:\/\/doi.org\/10.1177\/0022034511421930","DOI":"10.1177\/0022034511421930"},{"key":"e_1_3_2_7_1","doi-asserted-by":"crossref","unstructured":"Eustermann S Patel AB Hopfner KP He Y Korber P. 2024. Energy-driven genome regulation by ATP-dependent chromatin remodellers. Nat Rev Mol Cell Biol. 25(4):309\u2013332. https:\/\/doi.org\/10.1038\/s41580-023-00683-y","DOI":"10.1038\/s41580-023-00683-y"},{"key":"e_1_3_2_8_1","doi-asserted-by":"crossref","unstructured":"Fang B et al. 2022. Mechanical strain regulates osteoclastogenesis via modulating the PTEN\/PI3K\/Akt signal pathway through miR-21. Cytotechnology. 74(1):65\u201375. https:\/\/doi.org\/10.1007\/s10616-021-00507-x","DOI":"10.1007\/s10616-021-00507-x"},{"key":"e_1_3_2_9_1","doi-asserted-by":"crossref","unstructured":"Feng SY et al. 2022. Increased joint loading induces subchondral bone loss of the temporomandibular joint via the RANTES-CCRs-Akt2 axis. JCI Insight. 7(21):e158874. https:\/\/doi.org\/10.1172\/jci.insight.158874","DOI":"10.1172\/jci.insight.158874"},{"key":"e_1_3_2_10_1","doi-asserted-by":"crossref","unstructured":"Gantner BN et al. 2024. Histone oxidation as a new mechanism of metabolic control over gene expression. Trends Genet. 40(9):739\u2013746. https:\/\/doi.org\/10.1016\/j.tig.2024.05.012","DOI":"10.1016\/j.tig.2024.05.012"},{"key":"e_1_3_2_11_1","doi-asserted-by":"crossref","unstructured":"Ge Q et al. 2025. Slit2 inhibits SRC-PI3K signaling pathway regulates osteoclast differentiation of macrophages and reduces bone resorption. Front Cell Dev Biol. 13:1632882. https:\/\/doi.org\/10.3389\/fcell.2025.1632882","DOI":"10.3389\/fcell.2025.1632882"},{"key":"e_1_3_2_12_1","doi-asserted-by":"crossref","unstructured":"Goettsch C et al. 2013. NADPH oxidase 4 limits bone mass by promoting osteoclastogenesis. J Clin Invest. 123(11):4731\u20134738. https:\/\/doi.org\/10.1172\/jci67603","DOI":"10.1172\/JCI67603"},{"key":"e_1_3_2_13_1","doi-asserted-by":"crossref","unstructured":"Guo Q et al. 2021. Inhibition of ACLY leads to suppression of osteoclast differentiation and function via regulation of histone acetylation. J Bone Miner Res. 36(10):2065\u20132080. https:\/\/doi.org\/10.1002\/jbmr.4399","DOI":"10.1002\/jbmr.4399"},{"key":"e_1_3_2_14_1","doi-asserted-by":"crossref","unstructured":"Guo YN et al. 2022. Chondrocyte apoptosis in temporomandibular joint osteoarthritis promotes bone resorption by enhancing chemotaxis of osteoclast precursors. Osteoarthritis Cartilage. 30(8):1140\u20131153. https:\/\/doi.org\/10.1016\/j.joca.2022.04.002","DOI":"10.1016\/j.joca.2022.04.002"},{"key":"e_1_3_2_15_1","doi-asserted-by":"crossref","unstructured":"Han L et al. 2019. Chromatin remodeling mediated by ARID1A is indispensable for normal hematopoiesis in mice. Leukemia. 33(9):2291\u20132305. https:\/\/doi.org\/10.1038\/s41375-019-0438-4","DOI":"10.1038\/s41375-019-0438-4"},{"key":"e_1_3_2_16_1","doi-asserted-by":"crossref","unstructured":"Hota SK Bruneau BG. 2016. Atp-dependent chromatin remodeling during mammalian development. Development. 143(16):2882\u20132897. https:\/\/doi.org\/10.1242\/dev.128892","DOI":"10.1242\/dev.128892"},{"key":"e_1_3_2_17_1","doi-asserted-by":"crossref","unstructured":"Hu Y Chen X Wang S Jing Y Su J. 2021. Subchondral bone microenvironment in osteoarthritis and pain. Bone Res. 9(1):20. https:\/\/doi.org\/10.1038\/s41413-021-00147-z","DOI":"10.1038\/s41413-021-00147-z"},{"key":"e_1_3_2_18_1","doi-asserted-by":"crossref","unstructured":"Hu Y et al. 2021. Chromatin remodeler ARID1A binds IRF3 to selectively induce antiviral interferon production in macrophages. Cell Death Dis. 12(8):743. https:\/\/doi.org\/10.1038\/s41419-021-04032-9","DOI":"10.1038\/s41419-021-04032-9"},{"key":"e_1_3_2_19_1","doi-asserted-by":"crossref","unstructured":"Huang Z et al. 2021. BRD4 inhibition alleviates mechanical stress-induced TMJ OA-like pathological changes and attenuates TREM1-mediated inflammatory response. Clin Epigenetics. 13(1):10. https:\/\/doi.org\/10.1186\/s13148-021-01008-6","DOI":"10.1186\/s13148-021-01008-6"},{"key":"e_1_3_2_20_1","doi-asserted-by":"crossref","unstructured":"Jiao K et al. 2015. \u03b22-adrenergic signal transduction plays a detrimental role in subchondral bone loss of temporomandibular joint in osteoarthritis. Sci Rep. 5:12593. https:\/\/doi.org\/10.1038\/srep12593","DOI":"10.1038\/srep12593"},{"key":"e_1_3_2_21_1","doi-asserted-by":"crossref","unstructured":"Lee NK et al. 2005. A crucial role for reactive oxygen species in RANKL-induced osteoclast differentiation. Blood. 106(3):852\u2013859. https:\/\/doi.org\/10.1182\/blood-2004-09-3662","DOI":"10.1182\/blood-2004-09-3662"},{"key":"e_1_3_2_22_1","doi-asserted-by":"crossref","unstructured":"Lennicke C Cochem\u00e9 HM. 2021. Redox metabolism: ROS as specific molecular regulators of cell signaling and function. Mol Cell. 81(18):3691\u20133707. https:\/\/doi.org\/10.1016\/j.molcel.2021.08.018","DOI":"10.1016\/j.molcel.2021.08.018"},{"key":"e_1_3_2_23_1","doi-asserted-by":"crossref","unstructured":"Liu J et al. 2021. Exosomal transfer of osteoclast-derived miRNAs to chondrocytes contributes to osteoarthritis progression. Nat Aging. 1(4):368\u2013384. https:\/\/doi.org\/10.1038\/s43587-021-00050-6","DOI":"10.1038\/s43587-021-00050-6"},{"key":"e_1_3_2_24_1","doi-asserted-by":"crossref","unstructured":"Liu Q et al. 2021. Initiation and progression of dental-stimulated temporomandibular joints osteoarthritis. Osteoarthritis Cartilage. 29(5):633\u2013642. https:\/\/doi.org\/10.1016\/j.joca.2020.12.016","DOI":"10.1016\/j.joca.2020.12.016"},{"key":"e_1_3_2_25_1","doi-asserted-by":"crossref","unstructured":"Marian CA et al. 2018. Small molecule targeting of specific BAF (mSWI\/SNF) complexes for HIV latency reversal. Cell Chem Biol. 25(12):1443\u20131455.e14. https:\/\/doi.org\/10.1016\/j.chembiol.2018.08.004","DOI":"10.1016\/j.chembiol.2018.08.004"},{"key":"e_1_3_2_26_1","doi-asserted-by":"crossref","unstructured":"Mathur R. 2018. ARID1A loss in cancer: towards a mechanistic understanding. Pharmacol Ther. 190:15\u201323. https:\/\/doi.org\/10.1016\/j.pharmthera.2018.05.001","DOI":"10.1016\/j.pharmthera.2018.05.001"},{"key":"e_1_3_2_27_1","doi-asserted-by":"crossref","unstructured":"Matsubara T Yasuda K Mizuta K Kawaue H Kokabu S. 2022. Tyrosine kinase Src is a regulatory factor of bone homeostasis. Int J Mol Sci. 23(10):5508. https:\/\/doi.org\/10.3390\/ijms23105508","DOI":"10.3390\/ijms23105508"},{"key":"e_1_3_2_28_1","doi-asserted-by":"crossref","unstructured":"Miao MZ et al. 2023. Redox-active endosomes mediate \u03b15\u03b21 integrin signaling and promote chondrocyte matrix metalloproteinase production in osteoarthritis. Sci Signal. 16(809):eadf8299. https:\/\/doi.org\/10.1126\/scisignal.adf8299","DOI":"10.1126\/scisignal.adf8299"},{"key":"e_1_3_2_29_1","doi-asserted-by":"crossref","unstructured":"Monasterio G et al. 2018. Th1\/th17\/th22 immune response and their association with joint pain imagenological bone loss RANKL expression and osteoclast activity in temporomandibular joint osteoarthritis: a preliminary report. J Oral Rehabil. 45(8):589\u2013597. https:\/\/doi.org\/10.1111\/joor.12649","DOI":"10.1111\/joor.12649"},{"key":"e_1_3_2_30_1","doi-asserted-by":"crossref","unstructured":"Neves LBM Lima BC Coutinho de Mello R Baldessarini BL Peres RV. 2025. Intra-articular therapies for synovial joint dysfunction: a comprehensive integrative review. Oral Surg Oral Med Oral Pathol Oral Radiol. 141(5):598\u2013609. https:\/\/doi.org\/10.1016\/j.oooo.2025.10.026","DOI":"10.1016\/j.oooo.2025.10.026"},{"key":"e_1_3_2_31_1","doi-asserted-by":"crossref","unstructured":"Ning W Schmalz G Li P Huang S. 2022. Oral health-related quality of life in patients with osteoarthritis of the temporomandibular joint\u2014results of a systematic review. J Oral Rehabil. 49(11):1106\u20131114. https:\/\/doi.org\/10.1111\/joor.13363","DOI":"10.1111\/joor.13363"},{"key":"e_1_3_2_32_1","doi-asserted-by":"crossref","unstructured":"Nishikawa K et al. 2021. Osteoclasts adapt to physioxia perturbation through DNA demethylation. EMBO Rep. 22(12):e53035. https:\/\/doi.org\/10.15252\/embr.202153035","DOI":"10.15252\/embr.202153035"},{"key":"e_1_3_2_33_1","doi-asserted-by":"crossref","unstructured":"Qi H et al. 2022. Loss of RAP2A aggravates cartilage degradation in TMJOA via YAP signaling. J Dent Res. 102(3):302\u2013312. https:\/\/doi.org\/10.1177\/00220345221132213","DOI":"10.1177\/00220345221132213"},{"key":"e_1_3_2_34_1","doi-asserted-by":"crossref","unstructured":"Qu YL et al. 2019. Arid1a regulates insulin sensitivity and lipid metabolism. EBioMedicine. 42:481\u2013493. https:\/\/doi.org\/10.1016\/j.ebiom.2019.03.021","DOI":"10.1016\/j.ebiom.2019.03.021"},{"key":"e_1_3_2_35_1","doi-asserted-by":"crossref","unstructured":"Rong K et al. 2025. Inflammatory macrophage-derived itaconate inhibits DNA demethylase TET2 to prevent excessive osteoclast activation in rheumatoid arthritis. Bone Res. 13(1):60. https:\/\/doi.org\/10.1038\/s41413-025-00437-w","DOI":"10.1038\/s41413-025-00437-w"},{"key":"e_1_3_2_36_1","doi-asserted-by":"crossref","unstructured":"Spadon-Brito LG et al. 2025. Effectiveness of treatments for temporomandibular joint osteoarthritis: a systematic review and meta-analysis. Clin Oral Investig. 29(11):513. https:\/\/doi.org\/10.1007\/s00784-025-06581-1","DOI":"10.1007\/s00784-025-06581-1"},{"key":"e_1_3_2_37_1","doi-asserted-by":"crossref","unstructured":"Su W et al. 2020. Angiogenesis stimulated by elevated PDGF-BB in subchondral bone contributes to osteoarthritis development. JCI Insight. 5(8):e135446. https:\/\/doi.org\/10.1172\/jci.insight.135446","DOI":"10.1172\/jci.insight.135446"},{"key":"e_1_3_2_38_1","doi-asserted-by":"crossref","unstructured":"Tao H et al. 2024. Redox signaling and antioxidant defense in osteoclasts. Free Radic Biol Med. 212:403\u2013414. https:\/\/doi.org\/10.1016\/j.freeradbiomed.2023.12.043","DOI":"10.1016\/j.freeradbiomed.2023.12.043"},{"key":"e_1_3_2_39_1","doi-asserted-by":"crossref","unstructured":"Tian K et al. 2026. METTL3-mediated fibroblast-like synoviocytes senescence promotes temporomandibular joint osteoarthritis progression. Commun Biol. 9(1):510. https:\/\/doi.org\/10.1038\/s42003-026-09773-x","DOI":"10.1038\/s42003-026-09773-x"},{"key":"e_1_3_2_40_1","doi-asserted-by":"crossref","unstructured":"Tomida M et al. 2004. Intra-articular oxidative state correlated with the pathogenesis of disorders of the temporomandibular joint. Br J Oral Maxillofac Surg. 42(5):405\u2013409. https:\/\/doi.org\/10.1016\/j.bjoms.2004.06.003","DOI":"10.1016\/j.bjoms.2004.06.003"},{"key":"e_1_3_2_41_1","doi-asserted-by":"crossref","unstructured":"Tu Y et al. 2025. Anti-resorptive dihydrophenanthrene coelonin alleviates arthritic bone destruction by inhibiting osteoclast formation and synovial inflammation through Src regulation. Phytomedicine. 146:157147. https:\/\/doi.org\/10.1016\/j.phymed.2025.157147","DOI":"10.1016\/j.phymed.2025.157147"},{"key":"e_1_3_2_42_1","doi-asserted-by":"crossref","unstructured":"Turosz N et al. 2024. Temporomandibular joint injections and lavage: an overview of reviews. J Clin Med. 13(10):2855. https:\/\/doi.org\/10.3390\/jcm13102855","DOI":"10.3390\/jcm13102855"},{"key":"e_1_3_2_43_1","doi-asserted-by":"crossref","unstructured":"Wang XD Zhang JN Gan YH Zhou YH. 2015. Current understanding of pathogenesis and treatment of TMJ osteoarthritis. J Dent Res. 94(5):666\u2013673. https:\/\/doi.org\/10.1177\/0022034515574770","DOI":"10.1177\/0022034515574770"},{"key":"e_1_3_2_44_1","doi-asserted-by":"crossref","unstructured":"Wu H Eckhardt CM Baccarelli AA. 2023. Molecular mechanisms of environmental exposures and human disease. Nat Rev Genet. 24(5):332\u2013344. https:\/\/doi.org\/10.1038\/s41576-022-00569-3","DOI":"10.1038\/s41576-022-00569-3"},{"key":"e_1_3_2_45_1","doi-asserted-by":"crossref","unstructured":"Xu L et al. 2023. Osteoclast-targeted delivery of anti-miRNA oligonucleotides by red blood cell extracellular vesicles. J Control Release. 358:259\u2013272. https:\/\/doi.org\/10.1016\/j.jconrel.2023.04.043","DOI":"10.1016\/j.jconrel.2023.04.043"},{"key":"e_1_3_2_46_1","doi-asserted-by":"crossref","unstructured":"Yang T et al. 2015. Wnt5a\/Ror2 mediates temporomandibular joint subchondral bone remodeling. J Dent Res. 94(6):803\u2013812. https:\/\/doi.org\/10.1177\/0022034515576051","DOI":"10.1177\/0022034515576051"},{"key":"e_1_3_2_47_1","doi-asserted-by":"crossref","unstructured":"Yuan W et al. 2022. A new frontier in temporomandibular joint osteoarthritis treatment: exosome-based therapeutic strategy. Front Bioeng Biotechnol. 10:1074536. https:\/\/doi.org\/10.3389\/fbioe.2022.1074536","DOI":"10.3389\/fbioe.2022.1074536"},{"key":"e_1_3_2_48_1","doi-asserted-by":"crossref","unstructured":"Zhang Y et al. 2026. Inflammation barrier role of piezo1 in chondrocytes under aberrant loading. J Dent Res. 105(5):637\u2013646. https:\/\/doi.org\/10.1177\/00220345251371674","DOI":"10.1177\/00220345251371674"},{"key":"e_1_3_2_49_1","doi-asserted-by":"crossref","unstructured":"Zhen G et al. 2013. Inhibition of TGF-\u03b2 signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis. Nat Med. 19(6):704\u2013712. https:\/\/doi.org\/10.1038\/nm.3143","DOI":"10.1038\/nm.3143"},{"key":"e_1_3_2_50_1","doi-asserted-by":"crossref","unstructured":"Zheng F et al. 2020. Redox toxicology of environmental chemicals causing oxidative stress. Redox Biol. 34:101475. https:\/\/doi.org\/10.1016\/j.redox.2020.101475","DOI":"10.1016\/j.redox.2020.101475"},{"key":"e_1_3_2_51_1","doi-asserted-by":"crossref","unstructured":"Zhu S et al. 2019. Subchondral bone osteoclasts induce sensory innervation and osteoarthritis pain. J Clin Invest. 129(3):1076\u20131093. https:\/\/doi.org\/10.1172\/jci121561","DOI":"10.1172\/JCI121561"}],"container-title":["Journal of Dental Research"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/00220345261471409","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/full-xml\/10.1177\/00220345261471409","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/00220345261471409","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T09:17:38Z","timestamp":1789031858000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.1177\/00220345261471409"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,9,7]]},"references-count":50,"alternative-id":["10.1177\/00220345261471409"],"URL":"https:\/\/doi.org\/10.1177\/00220345261471409","relation":{},"ISSN":["0022-0345","1544-0591"],"issn-type":[{"value":"0022-0345","type":"print"},{"value":"1544-0591","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,9,7]]},"article-number":"00220345261471409"}}