Early Patellofemoral Articular Cartilage Degeneration In a Rat Model of Patellar Instability associated with activation of NF-κB Signal Pathway
Abstract Background Patellar instability (PI) often increases the possibility of lateral patellar dislocation and early osteoarthritis. The early articular cartilage degeneration of patellofemoral osteoarthritis (PFOA) in molecular mechanism still needs further investigation. It is commonly known that NF-κB signal pathway plays an important part in articular cartilage degeneration. The aim of this study was to investigate the relationship between NF-κB signaling pathway and degeneration of patellofemoral joint cartilage. Methods We established a model of PFOA caused by patellar instability in SD rats. 120 female Sprague-Dawley rats aged 4 weeks were randomly divided into two groups: patellar instability(PI, n=60) group and control group (n=60). The cartilage of the PI model group and the control group were separated at the stages of 4, 8, 12 weeks for comparison. The morphological structure of the trochlear cartilage and subchondral bone were evaluated by micro-computed tomographic (Micro-CT) and histological staining. The expression of NF-κB, Matrix metalloproteinase (MMP)-13, Collagen X and TNF-a were evaluated by immunohistochemistry and real-time polymerase chain reaction (RT-PCR). Results Micro-CT and histological staining showed that subchondral bone loss was found from 8 weeks after surgery in PI model group. Compared with the control group, the protein and mRNA expression of NF-κB, TNF-a were remarkably increased in PI model group at 4, 8 and 12 weeks after surgery. In addition, the markers of cartilage degeneration MMP-13 and Collagen X were found higher in PI model group at different stages after surgery. Conclusion This study proved that early patellofemoral joint cartilage degeneration can be caused by PI in growing rats, accompanied by significant subchondral bone loss. In addition, the degeneration of articular cartilage might associated with the activation of NF-κB signal pathway and become aggravated with time in PI model group.