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BACKGROUND: Ischemia/reperfusion can induce degenerative alterations in articular cartilage. However, the precise mechanism remains poorly understood. OBJECTIVE: To observe the morphological changes and the apoptosis of articular cartilage of femoral head epiphyses with ischemia/reperfusion. METHODS: A total of 80 Sprague-Dawley rats were randomly assigned to two groups: ischemia/reperfusion (model of ischemia/reperfusion in hip joint) and sham-surgery (exposure of abdominal aorta for 5 minutes) groups, with 40 animals in each group. Articular cartilages of femoral head epiphysis were col ected in 6, 12, 24, and 48 hours, 5 days, and 2 and 4 weeks after operation. Morphology of articular cartilage of femoral head epiphyses was examined by light microscope, and cel apoptosis was detected by TUNEL method. RESULTS AND CONCLUSION: Light microscopy showed chondrocytes degeneration and reduction, as wel as fibrosis in matrix of cartilage in the ischemia/reperfusion group. Chondrocyte apoptosis was observed in both groups by TUNEL. Several apoptotic cells, less than five, were observed in the sham-surgery, while 10-30 apoptotic cells were found in ischemia/reperfusion group at 48 hours. Results indicated that ischemia/reperfusion can induce degenerative changes in articular cartilage of femoral head epiphyses, and cel apoptosis in developing hip joint may participate in damage of articular cartilage. Inhibition of chondrocyte apoptosis in articular cartilage may be useful for the prevention and cure of early osteoarthritis.
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Objective To study the biomechanical mechanism of Essex-Lopresti injury, and provide biomechanical basis for diagnosis and treatment of Essex-Lopresti injury. Methods Twelve fresh frozen adult upper limbs were addressed. Firstly, 12 samples ("complete state group") were loaded 100 N of a compressive force lasting 30 seconds in pronation, supination and neutral position on the mechanical testing machine. Secondly, 12 specimens were randomly divided into 2 groups. In the group named resection of radial head, the radial head was removed and interosseous membrane (IOM)was intact. In the group named the section of interosseous membrane, IOM was cut off. Finally, the radial head were removed and IOM was cut off in all specimens. The group was named as resection of radial head and IOM. Each sample was tested according to the method as described. Results The forearm rotation or single excision of the IOM had no effect on radial longitudinal displacement. Simple radial head excision or resection of the IOM and the radial head increased the vertical displacement of the radius. The radial stiffness had a gradual decline in forearm supination, neutral position and pronation. Simple excision IOM has no effect on the radial stiffness. The radial stiffness had decreased under the condition of excision of radial head or resection of the IOM and the radial head. Conclusion These in vitro measurements validate that the radial head fracture with IOM injury may be important reason for complications of the Essex-Lopresti injury. Radial head fracture play a key role for Essex-Lopresti injury and the injury of IOM is secondary cause. IOM is responsible for maintaining the vertical stability of the forearm after radial head resection.
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AIM: To investigate the effects of dehydroepiandrosterone (DHEA) on experimental osteoarthritis in rats. METHODS: Forty rats were randomly divided into four groups. Group A is normal control group. Osteoarthritic models of rats were established by intraarticular injections of papain into the right knee joints of groups B, C and D. Then the right knee joints of rats in groups C and D, respectively, received 150 ?l intraarticular injections of DHEA at a concentration of 50 ?mol?L~(-1) and 100 ?mol?L~(-1), and the right knee joints of rats in groups A and B both received 150 ?l physiological saline, twice weekly for five weeks. Six weeks later, all rats were sacrificed, and the articular cartilage was assessed by gross morphologic, histologic, biochemical and immunohistochemical methods. RESULTS: The cartilage damage in groups C and D was much less than that in group B through observation under a surgical microscope. The Mankin's score, nitric oxide (NO) in the douche of articular cavity, malondialdehyde (MDA) in synovium, the expression of matrix metalloproteinase-1 and 9 in articular cartilage in groups C and D decreased in comparison with group B, and the foregoing indexes in group D decreased significantly compared with group C. However, the activities of superoxide dismutase (SOD) in the douche of articular cavity and blood serum in groups C and D increased in comparison with group B, and the foregoing indexes in group D increased significantly compared with group C. CONCLUSIONS:DHEA shows a cartilage-protecting effect which is in a dosage-dependent manner. The mechanism probably is to inhibit the expression of matrix metalloproteinases and to decrease the release of (NO and enhance the antioxidation.