Department of Orthopedic Surgery, Third Hospital of Hebei Medical University, No. 139 Ziqiang Road, 050051, Shijiazhuang, Hebei, China.
BMC Musculoskelet Disord. 2021 Jan 18;22(1):90. doi: 10.1186/s12891-021-03965-8.
Patellar instability (PI) often increases the possibility of lateral patellar dislocation and early osteoarthritis. The molecular mechanism of early articular cartilage degeneration during patellofemoral osteoarthritis (PFOA) still requires further investigation. However, it is known that the NF-κB signaling pathway plays an important role in articular cartilage degeneration. The aim of this study was to investigate the relationship between the NF-κB signaling pathway and patellofemoral joint cartilage degeneration.
We established a rat model of PI-induced PFOA. Female 4-week-old Sprague-Dawley rats (n = 120) were randomly divided into two groups: the PI (n = 60) and control group (n = 60). The distal femurs of the PI and control group were isolated and compared 4, 8, and 12 weeks after surgery. The morphological structure of the trochlear cartilage and subchondral bone were evaluated by micro-computed tomography and histology. The expression of NF-κB, matrix metalloproteinase (MMP)-13, collagen X, and TNF-ɑ were evaluated by immunohistochemistry and quantitative polymerase chain reaction.
In the PI group, subchondral bone loss and cartilage degeneration were found 4 weeks after surgery. Compared with the control group, the protein and mRNA expression of NF-κB and TNF-ɑ were significantly increased 4, 8, and 12 weeks after surgery in the PI group. In addition, the markers of cartilage degeneration MMP-13 and collagen X were more highly expressed in the PI group compared with the control group at different time points after surgery.
This study has demonstrated that early patellofemoral joint cartilage degeneration can be caused by PI in growing rats, accompanied by significant subchondral bone loss and cartilage degeneration. In addition, the degeneration of articular cartilage may be associated with the activation of the NF-κB signaling pathway and can deteriorate with time as a result of PI.
髌骨不稳定(PI)常增加外侧髌骨脱位和早期骨关节炎的可能性。髌股骨关节炎(PFOA)早期关节软骨退变的分子机制仍需进一步研究。然而,已知 NF-κB 信号通路在关节软骨退变中起重要作用。本研究旨在探讨 NF-κB 信号通路与髌股关节软骨退变的关系。
我们建立了 PI 诱导的 PFOA 大鼠模型。4 周龄雌性 Sprague-Dawley 大鼠(n=120)随机分为两组:PI 组(n=60)和对照组(n=60)。PI 组和对照组的远端股骨在手术后 4、8 和 12 周进行分离和比较。通过微计算机断层扫描和组织学评估滑车软骨和软骨下骨的形态结构。通过免疫组织化学和定量聚合酶链反应评估 NF-κB、基质金属蛋白酶(MMP)-13、胶原 X 和 TNF-ɑ 的表达。
在 PI 组中,手术后 4 周发现软骨下骨丢失和软骨退变。与对照组相比,PI 组 NF-κB 和 TNF-ɑ 的蛋白和 mRNA 表达在手术后 4、8 和 12 周时均显著增加。此外,与对照组相比,PI 组在手术后不同时间点的软骨退变标志物 MMP-13 和胶原 X 的表达更高。
本研究表明,生长大鼠的 PI 可导致早期髌股关节软骨退变,伴有明显的软骨下骨丢失和软骨退变。此外,关节软骨的退变可能与 NF-κB 信号通路的激活有关,并且由于 PI 会随着时间的推移而恶化。