Abstract
BackgroundPatellar 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.MethodsWe 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.ResultsIn 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.ConclusionsThis 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.
Highlights
Patellar instability (PI) often increases the possibility of lateral patellar dislocation and early osteoarthritis
We investigated the relationship between cartilage degeneration during patellofemoral osteoarthritis (PFOA) and the NF-κB signaling pathway by employing immunohistochemistry to assess the histological characteristics of cartilage and quantitative real-time polymerase chain reaction to assess the different expressions of NF-κB, Matrix metalloproteinase-13 (MMP-13), collagen X, and TNF-ɑ in cartilage at different time points in a growing rat model of PI
Micro-CT measurements of subchondral bone In the PI group, significant bone loss was observed at 4 weeks compared with the time-matched controls; the loss of bone mass gradually increased, and the subchondral bone plate became obviously thinner (Fig. 4)
Summary
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. The aim of this study was to investigate the relationship between the NF-κB signaling pathway and patellofemoral joint cartilage degeneration. OA most strongly affects the knee joint, a threecompartment structure that includes the patellofemoral joint (PFJ) and the medial and lateral tibiofemoral joints. Patellar instability (PI) is frequently caused by pathological changes involving PFJ stabilizers, which increase the likelihood of lateral patellar dislocation and early OA [8]. The incidence of primary PI is 5.8 per 100,000, with a higher incidence in more active and younger individuals [11] Some risk factors, such as lateralization of tibial tuberosity, trochlear dysplasia, and the medial patellofemoral ligament, are believed to promote PI [12].
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