scholarly journals Biomechanical and morphological changes of subchondral bone in anterior cruciate ligament transection – Induced rat model of knee osteoarthritis

2015 ◽  
Vol 23 ◽  
pp. A124
Author(s):  
Q. Xu ◽  
J. Pang ◽  
Y. Zheng ◽  
H. Zhan ◽  
Y. Cao ◽  
...  
2020 ◽  
Author(s):  
Che Ji ◽  
Jia Peiyu ◽  
Ma Yantao ◽  
Han Qi ◽  
Wang Xiaolei ◽  
...  

Abstract Background Knee osteoarthritis (KOA) is a progressively degenerative form of arthritis characterized by chondrocyte apoptosis and cartilage degeneration. KOA also involves limb muscle atrophy, especially in the quadriceps muscles. However, there are limited options for the treatment of KOA. miR-29b stimulates apoptosis in the chondrocytes from patients with KOA and muscle atrophy in other models. Therefore, we investigated the therapeutic effect of miR-29b in cartilage autophagy and muscle atrophy. Methods Ten rats comprised the control cohort without anterior cruciate ligament transection. The treatment group (KOA induced in the right knee via anterior cruciate ligament transection) was divided into a model untreated group and a miR-29b-antagomir group (miR-29b antagomir injected 1 wk before surgery). Results Real-time polymerase chain reaction revealed successful downregulation of miR-29b using antagomir in the joints and muscles. A weight-bearing test showed that miR-29b downregulation affected joint function. Enzyme-linked immunosorbent assays demonstrated that downregulating miR-29b reduced pro-inflammatory cytokine expression. Immunohistochemistry revealed that miR-29b depletion enhanced autophagy by activating LC3 and beclin-1 in the cartilage. Autophagy was stimulated by the activation of MAPK and mTOR signaling. Depletion of miR-29b ameliorated the decrease in the weight of the quadriceps and the quadriceps weight/body weight ratio of the rats. Hematoxylin–eosin and periodic acid–Schiff staining showed that miR-29b downregulation inhibited muscular atrophy. Immunofluorescence showed that miR-29b downregulation affected IGF/PI3K/AKT signaling. Conclusions This study demonstrated the therapeutic effect of miR-29b on autophagy in the cartilage and on muscle atrophy in a rat model for KOA, highlighting the potential of miR-29b as a therapeutic target for KOA.


Cartilage ◽  
2019 ◽  
pp. 194760351987847 ◽  
Author(s):  
Nik Aizah ◽  
Pan Pan Chong ◽  
Tunku Kamarul

Objective Advances in research have shown that the subchondral bone plays an important role in the propagation of cartilage loss and progression of osteoarthritis (OA), but whether the subchondral bone changes precede or lead to articular cartilage loss remains debatable. In order to elucidate the subchondral bone and cartilage changes that occur in early OA, an experiment using anterior cruciate ligament transection (ACLT) induced posttraumatic OA model of the rat knee was conducted. Design Forty-two Sprague Dawley rats were divided into 2 groups: the ACLT group and the nonoperated control group. Surgery was conducted on the ACLT group, and subsequently rats from both groups were sacrificed at 1, 2, and 3 weeks postsurgery. Subchondral bone was evaluated using a high-resolution peripheral quantitative computed tomography scanner, while cartilage was histologically evaluated and scored. Results A significant reduction in the subchondral trabecular bone thickness and spacing was found as early as 1 week postsurgery in ACLT rats compared with the nonoperated control. This was subsequently followed by a reduction in bone mineral density and bone fractional volume at week 2, and finally a decrease in the trabecular number at week 3. These changes occurred together with cartilage degeneration as reflected by an increasing Mankin score over all 3 weeks. Conclusions Significant changes in subchondral bone occur very early in OA concurrent with surface articular cartilage degenerative change suggest that factors affecting bone remodeling and resorption together with cartilage matrix degradation occur very early in the disease.


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