Zhan Yanjing, Shi Ziwen, Yang Xianni, Cao Pinyin, Yu Haopeng, Wang Peng, Zhu Songsong, Bi Ruiye
State Key Laboratory of Oral Diseases, Sichuan University, Chengdu, China.
Department of Orthognathic and TMJ Surgery, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Oral Dis. 2025 Apr 28. doi: 10.1111/odi.15355.
Condylar fibrocartilage regeneration after injury has been hindered by its poor self-repair capacity. Injection of parathyroid hormone (PTH) has been proven to effectively delay cartilage damage in osteoarthritis. In this study, we investigated the regulatory effect of PTH on the homeostasis of condylar fibrocartilage.
FCSCs were extracted and exposed to a high PTH environment from rats to analyze the transcriptional changes. The condyles of mice were cultured ex vivo and exposed to high PTH to observe changes in cartilage. Parathyroidectomy induced PTH-deficient rats were locally injected with PTH to observe its effects on cartilage homeostasis.
High PTH environment could promote chondrogenic differentiation of FCSCs early, while weakening at late phase. The ex vivo culture of mouse condyle under PTH stimulation enhanced the proliferation of chondrocytes early, which were replaced by hypertrophic chondrocytes. The degradation of cartilage matrix also grew distinct under high PTH. PTH deficiency induced osteoarthritis-like changes in rats, characterized by cartilage layers disorder, chondrocyte reduction, and matrix degradation. Exogenous PTH could reverse fibrocartilage degeneration.
The maintenance of PTH homeostasis is crucial for maintaining the function of temporomandibular condylar FCSCs. Exogenous PTH can ameliorate the characteristics associated with rat temporomandibular joint osteoarthritis.
髁突纤维软骨损伤后自我修复能力较差，阻碍了其再生。甲状旁腺激素（PTH）注射已被证明可有效延缓骨关节炎中的软骨损伤。在本研究中，我们研究了PTH对髁突纤维软骨稳态的调节作用。
从大鼠中提取髁突纤维软骨干细胞（FCSCs）并将其置于高PTH环境中，以分析转录变化。将小鼠髁突进行体外培养并暴露于高PTH环境中，以观察软骨的变化。对甲状旁腺切除诱导的PTH缺乏大鼠进行局部注射PTH，以观察其对软骨稳态的影响。
高PTH环境早期可促进FCSCs的软骨形成分化，而后期则减弱。PTH刺激下小鼠髁突的体外培养早期增强了软骨细胞的增殖，随后被肥大软骨细胞取代。在高PTH作用下，软骨基质的降解也变得明显。PTH缺乏诱导大鼠出现骨关节炎样改变，其特征为软骨层紊乱、软骨细胞减少和基质降解。外源性PTH可逆转纤维软骨退变。
PTH稳态的维持对于维持颞下颌关节髁突FCSCs的功能至关重要。外源性PTH可改善大鼠颞下颌关节骨关节炎相关特征。
