Electroacupuncture alleviates cartilage degradation: Improvement in cartilage biomechanics via pain relief and potentiation of muscle function in a rabbit model of knee osteoarthritis

•Knee osteoarthritis is the most common joint disease, leading to pain and functional limitation.•Muscle-induced abnormal joint loading to the articular cartilage is a primary pathogenic cause of KOA.•Electroacupuncture relieves pain and potentiates muscle function in KOA rabbit, thus reducing the degradation of cartilage. Knee osteoarthritis (KOA) is a chronic degenerative joint disorder characterized by loss of articular cartilage and progressive deterioration, leading to pain and functional limitation. Abnormal biomechanics play a core role in the onset and development of KOA. The aim of this study was to explore whether electroacupuncture (EA) may relieve pain and adjust the biomechanical properties of the extensor–flexor muscles to improve abnormal joint loading, thus alleviating the degradation of cartilage in a rabbit model of KOA. Firstly, a KOA model was induced by immobilization for 6 weeks. Then, different interventions (EA and celecoxib) were applied for 4 weeks. The levels of pain and disability were assessed using the Lequesne MG index. Muscle function, including function of the rectus femoris and biceps femoris, was tested through hematoxylin-eosin staining (HE staining) and use of a microforce tension-torsion instrument. The cartilage was tested using nanoindentation, Safranin O-Fast Green staining, confocal laser scanning microscopy (immunofluorescence), immunohistochemistry and the enzyme-linked immunosorbent assay (ELISA). Finally, we found that EA and celecoxib resulted in lower behavioral and pain scores than the model group. In addition, it improved the function of muscles. Furthermore, those treatments alleviated the rate of cartilage degradation, manifested as increased loss factor without statistical difference and a significant reduction in the Mankin score. This promoted the metabolism of type II collagen in the cartilage layer and drastically reduced the expression of CTX-II in the synovial fluid and peripheral serum. Concisely, EA promotes pain limitation and ameliorates muscular atrophy-induced inappropriate biomechanical loading on the articular cartilage through pain relief and potentiation of muscle function, thus improving cartilage viscoelasticity, as demonstrated by the retarded degradation of type II collagen in our KOA model.