ADSC-enriched adipose extract alleviates cartilage fibrosis in temporomandibular joint osteoarthritis by inhibiting chondrocyte senescence

作者：Zerou Zhang, Dan Jin, Bingshuai Jing, Shanluo Zhou, Yi Sun, Jeroen Van Dessel, Rui Ren, Fuwei Liu, Mian Zhang, Yunpeng Li · 发表于：Journal of Translational Medicine · 年份：2025 · DOI：10.1186/s12967-025-07108-8 · 被引用次数：3 · 研究领域：Osteoarthritis Treatment and Mechanisms、Mesenchymal stem cell research、Temporomandibular Joint Disorders

BACKGROUND: Temporomandibular joint osteoarthritis (TMJOA) is a degenerative joint disease causing chronic pain and restricted mandibular movement. Its complex pathology and lack of effective therapies make it a clinical challenge. Recent studies have demonstrated that cartilage fibrosis correlates closely with TMJOA progression. Inflammatory microenvironments induce chondrocyte senescence, altering secretory phenotypes and driving fibrocartilage formation, characterized by hardened texture and poor mechanical properties, compromising joint biomechanics. Targeting cartilage fibrosis represents a key therapeutic strategy. Stem cell therapies show antifibrotic potential but face clinical limitations due to complex preparation and safety risks. METHODS: Synovial lavage fluid from TMJOA patients was collected and analyzed for fibrosis marker ACTA2 and inflammatory factor IL-1β expression to confirm intra-articular fibrosis and explore contributing factors. Adipose-derived mesenchymal stem cell (ADSC)-enriched adipose extract (ARDE) was prepared using mechanical emulsification with low-speed centrifugation. Its efficacy was assessed in a prospective clinical trial evaluating pain, mouth opening, and radiographic changes. ARDE's modulation of inflammation and repair of fibrocartilage were histologically assessed in a rabbit TMJOA model. In vitro TMJOA chondrocyte models induced by inflammatory factors (IL-1β, TNF-α) were co-cultured with ARDE's core component, ADSCs, to observe the...