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Parathyroid Hormone (1–34) Attenuates Cartilage Degradation and Preserves Subchondral Bone Micro-architecture in Rats with Patella Baja-Induced-Patellofemoral Joint Osteoarthritis

骨关节炎 髌骨 软骨 医学 阿格里坎 骨质疏松症 合成代谢 分解代谢 内科学 外科 解剖 病理 关节软骨 新陈代谢 替代医学
作者
Hongfei Zhang,Ming-Jian Bei,Zhiyuan Zheng,Ning Liu,Xuehui Cao,Yaping Xiao,Qiangqiang Lian,Yudan Wang,Xiaoli Hou,Faming Tian
出处
期刊:Calcified Tissue International [Springer Science+Business Media]
卷期号:111 (1): 87-95 被引量:4
标识
DOI:10.1007/s00223-022-00958-0
摘要

Several studies have revealed that PTH1-34 may possess the potential for treating osteoarthritis (OA) and osteoporosis. However, no study has yet determined whether PTH1-34 can be used for the treatment of patella baja-induced patellofemoral joint OA (PFJOA). Thus, this study sought to assess the efficacy of PTH1-34 for the treatment of PFJOA in a rat model. Patella baja was induced in 3-month-old female Sprague–Dawley (SD) rats by patellar ligament shortening (PLS), after which the rats were randomly divided into three groups (n = 12): Sham, PLS, and PTH group (PTH + PLS, PTH1-34, 30 µg/kg/d, 5 days per week for 10 weeks). Thereafter, radiographic imaging, macroscopic and microscopic analyses, immunohistochemistry, and microcomputed tomography (CT) analysis were performed. The appearance of PLS-induced PFJOA promoted obvious changes in the patellar position and structure in the PLS group, which were characterized by cartilage degeneration, subchondral bone microstructure deterioration, patella baja, and increasing patella length. However, these negative characteristics were markedly ameliorated by PTH1-34, which not only inhibited cartilage catabolism by decreasing MMP-13 and ADAMTS-4 but also enhanced anabolism by increasing Col-II and Aggrecan. Furthermore, the micro-CT results showed a marked improvement in subchondral bone microarchitecture. The findings presented herein demonstrated that early treatment with PTH1-34 could improve cartilage metabolism and subchondral bone health in this PFJOA model.
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