{"title":"Single-Cell RNA Sequencing Study on Two Synovial Derived Tumors in the Temporomandibular Joint.","authors":"Weihua Han, Tiansong Xu, Zonghan He, Haiyan Luo, Chuanbin Guo, Juanhong Meng","doi":"10.1111/odi.70003","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the cellular composition and differentiation trajectory of synovial chondromatosis (SC) and diffuse tenosynovial giant cell tumor (D-TSGCT) in the temporomandibular joint (TMJ).</p><p><strong>Materials and methods: </strong>Single-cell RNA sequencing was applied to analyze the cellular composition, differentiation trajectory, and intercellular communication of SC and D-TSGCT. Cell culture and morphological experiments were applied to validate the chondrogenic differentiation potential of fibroblast-like synoviocytes (FLS) in the initial stage of SC and to explore the expression and regulation of differential genes during chondrogenic differentiation.</p><p><strong>Results: </strong>SC was mainly composed of FLS and chondrocytes, while D-TSGCT had a relatively complex cellular composition. Genetically, chondrogenesis-related genes such as COMP and SMAD2 were upregulated in the early stage of SC. TGFβ pathway and collagen catabolic process were subsequently activated, ultimately leading to cartilage formation. CSF1 and CD68 were overexpressed at the forming stage of D-TSGCT, and the macrophage pathway was enriched in the later phase. Based on experimental verification, COMP could induce chondrogenic differentiation of FLS by activating TGFβ/SMAD signal pathways in vitro.</p><p><strong>Conclusions: </strong>FLS are the common starting point of synovial-derived tumors, but differentiate toward different endpoints in the SC and D-TSGCT. COMP/TGFβ/SMAD signaling pathways can promote chondrogenic differentiation of synovium in SC.</p>","PeriodicalId":19615,"journal":{"name":"Oral diseases","volume":" ","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oral diseases","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/odi.70003","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: To investigate the cellular composition and differentiation trajectory of synovial chondromatosis (SC) and diffuse tenosynovial giant cell tumor (D-TSGCT) in the temporomandibular joint (TMJ).
Materials and methods: Single-cell RNA sequencing was applied to analyze the cellular composition, differentiation trajectory, and intercellular communication of SC and D-TSGCT. Cell culture and morphological experiments were applied to validate the chondrogenic differentiation potential of fibroblast-like synoviocytes (FLS) in the initial stage of SC and to explore the expression and regulation of differential genes during chondrogenic differentiation.
Results: SC was mainly composed of FLS and chondrocytes, while D-TSGCT had a relatively complex cellular composition. Genetically, chondrogenesis-related genes such as COMP and SMAD2 were upregulated in the early stage of SC. TGFβ pathway and collagen catabolic process were subsequently activated, ultimately leading to cartilage formation. CSF1 and CD68 were overexpressed at the forming stage of D-TSGCT, and the macrophage pathway was enriched in the later phase. Based on experimental verification, COMP could induce chondrogenic differentiation of FLS by activating TGFβ/SMAD signal pathways in vitro.
Conclusions: FLS are the common starting point of synovial-derived tumors, but differentiate toward different endpoints in the SC and D-TSGCT. COMP/TGFβ/SMAD signaling pathways can promote chondrogenic differentiation of synovium in SC.
期刊介绍:
Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.