The anterior disc displacement (ADD) leads to temporomandibular joint osteoarthritis (TMJOA) and mandibular growth retardation in adolescents. To investigate the potential functional role of fibrocartilage stem cells (FCSCs) during the process, a surgical ADD-TMJOA mouse model was established. From 1 week after model generation, ADD mice exhibited aggravated mandibular growth retardation with osteoarthritis (OA)-like joint cartilage degeneration, manifesting with impaired chondrogenic differentiation and loss of subchondral bone homeostasis. Lineage tracing using Gli1-CreER⁺; Tm^fl/-mice and Sox9-CreER⁺;Tm^fl/-mice showed that ADD interfered with the chondrogenic capacity of Gli1⁺ FCSCs as well as osteogenic differentiation of Sox9⁺ lineage, mainly in the middle zone of TMJ cartilage. Then, a surgically induced disc reposition (DR) mouse model was generated. The inhibited FCSCs capacity was significantly alleviated by DR treatment in ADD mice. And both the ADD mice and adolescent ADD patients had significantly relieved OA phenotype and improved condylar growth after DR treatment. In conclusion, ADD-TMJOA leads to impaired chondrogenic progenitor capacity and osteogenesis differentiation of FCSCs lineage, resulting in cartilage degeneration and loss of subchondral bone homeostasis, finally causing TMJ growth retardation. DR at an early stage could significantly alleviate cartilage degeneration and restore TMJ cartilage growth potential.

椎间盘前移（ADD）会导致青少年颞下颌关节骨关节炎（TMJOA）和下颌生长迟缓。为了研究纤维软骨干细胞（FCSC）在此过程中的潜在功能作用，建立了手术ADD-TMJOA小鼠模型。从模型生成后1周开始，ADD小鼠表现出下颌生长迟缓加剧，并伴有骨关节炎（OA）样关节软骨变性，表现为软骨分化受损和软骨下骨稳态丧失。使用Gli1-CreER ⁺进行谱系追踪； Tm ^fl/-小鼠和Sox9-CreER ⁺ ;Tm ^fl/-小鼠表明，ADD 干扰Gli1 ⁺ FCSC 的软骨形成能力以及Sox9 ⁺谱系的成骨分化，主要是在 TMJ 软骨的中部区域。然后，生成手术诱导椎间盘复位（DR）小鼠模型。ADD小鼠中的DR治疗显着减轻了受抑制的FCSCs能力。DR治疗后，ADD小鼠和青少年ADD患者的OA表型均得到显着缓解，髁突生长得到改善。总之，ADD-TMJOA导致FCSC谱系的软骨祖细胞能力和成骨分化受损，导致软骨退化和软骨下骨稳态丧失，最终导致TMJ生长迟缓。早期的DR可以显着减轻软骨退化并恢复颞下颌关节软骨的生长潜力。