Articular cartilage degeneration after acute subchondral bone damage An experimental study in dogs with histopathological grading

2004 ◽  
Vol 75 (6) ◽  
pp. 762-767 ◽  
Author(s):  
Andreas Lahm ◽  
Markus Uhl ◽  
Christoph Erggelet ◽  
Jörg Haberstroh ◽  
Eike Mrosek
2004 ◽  
Vol 75 (6) ◽  
pp. 1-1 ◽  
Author(s):  
Andreas Lahm ◽  
Markus Uhl ◽  
Christoph Erggelet ◽  
Jörg Haberstroh ◽  
Eike Mrosek

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wei Lin ◽  
Huijun Kang ◽  
Yike Dai ◽  
Yingzhen Niu ◽  
Guangmin Yang ◽  
...  

Abstract Background 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. Methods 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. Results 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. Conclusions 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.


2019 ◽  
Vol 234 (10) ◽  
pp. 17946-17958 ◽  
Author(s):  
Zilong Yao ◽  
Peisheng Chen ◽  
Shengnan Wang ◽  
Ganming Deng ◽  
Yanjun Hu ◽  
...  

2016 ◽  
Vol 20 (10) ◽  
pp. 1393-1402 ◽  
Author(s):  
Do Young Park ◽  
Long Hao Jin ◽  
Byoung-Hyun Min ◽  
Kyu-Sung Kwack ◽  
Young-Sil An ◽  
...  

2021 ◽  
Author(s):  
Kohei Arakawa ◽  
Kei Takahata ◽  
Yuichiro Oka ◽  
Kaichi Ozone ◽  
Sumika Nakagaki ◽  
...  

Objective: The effect of the type of mechanical stress on OA onset has not been clarified. The aim of this study was to establish a new model that reproduces the type and increase and decrease of mechanical stress in vivo and to clarify the differences in the mechanism of knee OA onset and progression among the models. Design: To reproduce the difference in mechanical stress, we used the anterior cruciate ligament transection (ACL-T) model and the destabilization of the medial meniscus (DMM) model. In addition, we created a controlled abnormal tibial translation (CATT) model and a controlled abnormal tibial rotation (CATR) model that suppressed the joint instability of the ACL-T and DMM model, respectively. These four models reproduced the increase and decrease in shear force due to joint instability and compressive stress due to meniscal dysfunction. We performed joint instability analysis with soft X-ray, micro computed tomography analysis, histological analysis, and immunohistological analysis in 4 and 6 weeks. Results: Joint instability decreased in the CATT and CATR groups. The meniscus deviated in the DMM and CATR groups. Chondrocyte hypertrophy increased in the ACL-T and DMM groups with joint instability. In the subchondral bone, bone resorption was promoted in the ACL-T and CATT groups, and bone formation was promoted in the DMM and CATR groups. Conclusions: Increased shear force causes articular cartilage degeneration and osteoclast activation in the subchondral bone. In contrast, increased compressive stress promotes bone formation in the subchondral bone earlier than articular cartilage degeneration occurs.


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