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The study maps fibrocartilage and adjacent connective tissue in human TMJ-OA and finds that perivascular-derived COL5A1+ fibroblasts drive fibrocartilaginous extracellular matrix transformation. Integrin αV/β5 is broadly activated across OA joints, increasing fibrocartilaginous transcription while disrupting coordinated ECM transformation. In OA mouse and TMJ-OA miniature pig models, cilengitide inhibition of αV/β5 promotes transcriptional reprogramming and functional connective tissue remodeling, supporting cilengitide as a clinically relevant route for repair.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/integrin-inhibition-facilitates-fibrocartilaginous-transformation-in-connective-tissue-in-osteoarthritis-ruiye-bi-et-al-article/417101/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/integrin-inhibition-facilitates-fibrocartilaginous-transformation-in-connective-tissue-in-osteoarthritis-ruiye-bi-et-al-article/417101.png","ImageObject",300,407,{"name":92,"@type":93},"WPS_1790064749","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-31","2026-09-28",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",12,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"Why does fibrocartilage injury remain difficult to treat in osteoarthritis?","Question",{"text":113,"@type":114},"Fibrocartilage shows poor self-repair capacity after osteoarthritis, which restricts treatment strategies and results in limited clinical efficacy.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"What role does integrin αV/β5 play in OA-related fibrocartilaginous remodeling?",{"text":118,"@type":114},"Integrin αV/β5 is universally activated in OA joints, leading to increased fibrocartilaginous transcription while also causing disarranged extracellular matrix transformation in connective tissues.",{"name":120,"@type":111,"acceptedAnswer":121},"How does cilengitide affect fibrocartilaginous transformation in OA models?",{"text":122,"@type":114},"In osteoarthritis mouse models and a TMJ-OA miniature pig model, inhibiting integrin αV/β5 activity with cilengitide facilitates transcriptional reprogramming of Col5a1+ fibroblasts and supports functional remodeling of connective tissues.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},417101,1790717432,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146,"preview_page_count":4},3985747859154,"https://ap-avatar.wpscdn.com/davatar_276721f389ce27ea32af1340a28f341c","DISEASES AND DISORDERS  \nIntegrin inhibition facilitates fibrocartilaginous transformation in connective tissue in osteoarthritis  \nRuiye Bi1†, Xianni Yang1†, Haohan Li1†, Yanjing Zhan1†, Qing Yin1,2, Han Fang1, Ziqian Wang1, Binbin Ying3*, HaopengYu4,5*, Songsong Zhu1*  \nOsteoarthritis (OA) is a disabling condition with pathological remodeling of different joints, resulting in impaired function of the whole musculoskeletal system in vertebrates. Fibrocartilage has poor self-repair capacity after OA, leading to restricted treatment strategies and unsatisfying clinical efficacy. Recently, we constructed the spatiotemporal multiomic landscape offibrocartilage and connective tissue in human temporomandibular joint (TMJ)– OA, observing that adjacent connective tissue could transform to fibrocartilage in TMJ-OA. We found that the COL5A1+ fibroblast population, derived from perivascular niche, contributes to fibrocartilaginous extracellular matrix (ECM) transformation. Multijoint analysis showed that integrin αV/β5 was universally activated in OA joints, which led to increased fibrocartilaginous transcription but disarranged ECM transformation in connective tissues. In OA mouse models and a TMJ-OA miniature pig model, inhibition of integrin αV/β5 activity using cilengitide facilitated the transcriptional reprogramming of Col5a1+ fibroblast and functional remodeling of the connective tissues. Our findings verified the effectiveness of cilengitide and provided a clinical route for fibrocartilage injury repair in OA.  \ncopyright © 2026 the Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. no claim to original U.S.  \nGovernment Works. distributed under a creative commons Attribution noncommercial license 4.0 (cc BY-nc) .  \nINTRODUCTION  \nOsteoarthritis (OA) is a widespread and disabling condition with profound impacts on individuals and society (1) . Globally, 595 million people had OA, equal to 7.6% of the total population and an increase of 132.2% in total cases since 1990 (2) . Cellular and molecular changes in OA lead to pathological remodeling of different joints and ultimately resulted in impaired function of the whole musculoskeletal system (3, 4) .  \nFibrocartilage is predominantly located on the surface of different joints and has a broad spectrum of locomotor functions, including tension, compression, and shear (5). OA leads to impairment offibrocartilaginous tissues, such as the knee meniscus, the intervertebral disk (IVD) annulus fibrosus (AF), and the temporomandibular joint (TMJ) disk, which has notable consequences in terms of socioeconomic cost and quality of life (6–8). Despite the importance of these tissues in activities of daily living, the discovery and development of clinical strategies for fibrocartilage repair and regeneration in OA have been hindered by the poor self-repair capacity of these tissues (5, 9).  \nRecent evidence shows that adjacent connective tissues share similarities in terms of cell composition and transcriptional features with fibrocartilage, suggesting that these tissues have fibrocartilaginous transformation potential in OA and cartilage degenerative diseases (10–13). A classic example of fibrocartilaginous transformation under OA condition is TMJ anterior disk displacement (ADD). Patients with ADD may suffer from OA symptoms including myofascial pain, synovitis, and limited motion (14, 15), while there is a subgroup of  \n1State Key laboratory of Oral diseases, national center for Stomatology, national clinical Research center for Oral diseases, department of Orthognathic and tMJ Surgery, West china hospital of Stomatology, Sichuan University, chengdu, china. 2Max-Planck institute for heart and lung Research, W. G. Kerckhoff institute, Badnauheim, Germany. 3department of Stomatology, the First Affiliated hospital of ningbo University, ningbo, china. 4West china Biomedical Big data center, West china hospital, Sichuan University, chengdu, chi","cbCaidQTlhXNVQE4","https://ap.wps.com/l/cbCaidQTlhXNVQE4","pdf",7354232,22,"English","# INTRODUCTION\n## Osteoarthritis burden and cellular remodeling\n## Fibrocartilage function and limited self-repair in OA\n## Fibrocartilaginous transformation potential in adjacent connective tissue\n## TMJ anterior disk displacement and knowledge gaps\n## Study approach and aims","[{\"question\":\"Why does fibrocartilage injury remain difficult to treat in osteoarthritis?\",\"answer\":\"Fibrocartilage shows poor self-repair capacity after osteoarthritis, which restricts treatment strategies and results in limited clinical efficacy.\"},{\"question\":\"What role does integrin αV/β5 play in OA-related fibrocartilaginous remodeling?\",\"answer\":\"Integrin αV/β5 is universally activated in OA joints, leading to increased fibrocartilaginous transcription while also causing disarranged extracellular matrix transformation in connective tissues.\"},{\"question\":\"How does cilengitide affect fibrocartilaginous transformation in OA models?\",\"answer\":\"In osteoarthritis mouse models and a TMJ-OA miniature pig model, inhibiting integrin αV/β5 activity with cilengitide facilitates transcriptional reprogramming of Col5a1+ fibroblasts and supports functional remodeling of connective tissues.\"}]","Integrin inhibition facilitates fibrocartilaginous transformation in connective tissue in osteoarthritis - Ruiye Bi et al. article | PDF",1790608000,55]