| Articular cartilage repair remains a great challenge. The injured articular cartilage has a very limited capacity for repair. Damage to the articular cartilage may therefore progress to osteoarthritis by enzymatic degradation and mechanic wear and result in a painful and disfunction joint. Currently, prosthetic joint replacement is the most common approach for treating severe and extended degeneration of the cartilage, but it has some complications including infection and long-term loosening of the components. Biological resurfacing is an alternative technology, which has potential to re-establish a structurally and functionally competent repair tissue of an enduring nature to prevent the degradation. Some of the strategies currently being investigated include chondrogenic cell transplantation, periosteal and perichondrial tissue grafting, subchondral drilling, osteochondral auto/allografting, and cell recruitment using various growth factors. The best method is unclear, and there is a need to develop new technologies for the repair of articular cartilage lesions.When a fracture occurs, a rapid, intense inflammatory response brings a spectrum of cells and molecules to the fracture site. The site becomes segregated from the surrounding tissue and the accumulated inflammatory cells and molecules provide an environment for mesenchymal progenitor cells to proliferate rapidly and form a repair blastema that spans the break.Post-fracture repair blastema may be another source for autologous graft in reconstruction of articular cartilage. In the current study, the idea of using a post-fracture repair blastema to restore an articular cartilage defect was tested firstly.MATERIALS AND METHODS10 New Zealand White female rabbits (6 months of age) were randomly divided into two groups.First Surgery: In vivo preparation of post-fracture repair blastema implant. New Zealand White rabbits were anesthetized by Sumianxin (0.2mL ?kg -1 im). The skin in the region of the surgery was shaved. All surgical procedures were done according to the same protocol. Bone defect with wide of 0.5 cm was made in random side of radius of rabbits at sterile condition.Second Surgery: Grafting the post-fracture repair blastema into a defect. After 1 week, the post-fracture repair blastema was taken out and both knee joints of the 10 New Zealand white rabbits were approached through a medial parapatellar incision, and each patella was dislocated laterally. A 3-mm diameter full-thickness articular cartilage defects were created in the patellofemoral joint of the femur. The fullthickness defects of random side were filled with the implant. The knee joint at other side was left untreated as a nontreated control. All rabbits were allowed free cage activity after surgery. At 4 and 24 weeks post-operation, rabbit distal femur articular cartilage samples were harvested, and were fixed in 10% formalin for 24h. Each specimen was decalcified in a solution of 5% nitric acid for 3-4 days, then embedded in paraffin and sectioned perpendicularly and mounted onto microscopic slides. Each section was stained with haematoxylin-eosin and Mallory' and observed under light microscopy according to O'Driscoll histological grading scale.RESULTSMACROSCOPIC OBSERVATIONS OF CARTILAGE DEFECTSSigns of inflammation in any operated knee were not observed. As early as 4 weeks after implantation, the defects repaired by the implant were noticeably smoother than the untreated defects. The treated defect sites were more yellow and less translucent than the surrounding cartilage. The junction between the normal and the newly formed cartilage was not clearly visible. The generalappearance of the control defect sites showed varying degrees of cartilage resurfacing of the articular defects with repair tissue, which appeared tan colour. At 24 weeks, the colour in the treated defects was similar to that of normal adjacent cartilage. The colour of the untreated defects was tan-purple, and the texture ranged from irregular to smooth.HISTOLOGIC SCORING OF... |
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