OBJECTIVE: To study the allograft antigenicity of human ear cartilage and the effect of the cell extraction on antigenicity. METHODS: The human ear cartilage was acellular by cell extraction with Triton X-100. Then the cartilage and the acellular cartilage were analyzed by anti-MHC-I immunohistochemical staining, the reaction of the peripheral blood mononuclear(PBM) cells to the cartilage and the acellular cartilage and the migration of the PBM cells toward the cartilage and the acellular cartilage. RESULTS: The result of human ear cartilage was positive for the anti-MHC-I immunohistochemical staining, whereas that of the acellular cartilage was negative for the staining. The reactive proliferation of the PBM cells was more when they were co-cultured with human ear cartilage than that when they were cultured alone in vitro(P lt; 0.05), but the acellular cartilage did not show the same phenomena (P gt; 0.05); when the cartilage and the acellular cartilage were co-cultured with the PBM cells, the PBM cells migrated to the cartilage much more than that to acellular cartilage(P lt; 0.01). CONCLUSION: Human ear cartilage has allograft antigenicity and its antigenicity can be removed by cell extraction with Triton X-100.
To study how to repair the cartilage defect according to the principles of tissue engineering with acellular cartilage matrix as scaffold material. Methods The ear cartilage was obtained from a New Zealand white rabbit(weighing 2.4 kg )and then treated by a modified Courtman’s four-step method to produce the acellular cartilage matrix. Eighteen New Zealand white rabbits (aged 6 months, weighing 2.4-2.6 kg) with no sex l imit were divided into three groups. Forevery rabbit, two pieces of ear cartilage measured 1 cm × 1 cm were excised in each ear. Defects were repaired as follows: group A with the combined graft of acellular cartilage matrix and perichondium, group B with acellular cartilage matrix and group C with perichondium. Three animals in each group were killed 4 and 12 weeks postoperatively, respectively. Tissue samples obtained were analyzed with gross observation, hematoxyl in-eosin stain, Safranine O-alcian blue stain and type II collagen messenger RNA in situ hybridization respectively. Results In gross observation, the repaired sites in groups A and B were not change meaningfully in their shape 4 weeks postoperatively; but they felt a bit of thicker and harder 12 weeks postoperatively. In group C two repaired sites formed scabs at 2 weeks and perforated at 5 weeks. In histological observation, there was a sl ight inflammatory reaction surrounding the acellular cartilage matrix 4 weeks after it was implanted in groups A and B. The inflammatory cells were mainly lymphocytes. The perichondrium graft in group C was collapsed in the defects in HE stain. The defect sites were negative for Safranine O-alcian blue stain and type II collagen mRNA in situ hybridization in all groups. At 12 weeks cells were found in the acellular matrix which arranged in irregular manner in group A in HE stain and was positive for Safranine O-alcian blue stain and type II collagen mRNA in site hybridization. In groups B and C, no new cell was found in HE stain and the repaired sites were negative for Safranine O-alcian blue stain and type II collagen mRNA in situ hybridization. Conclusion Acellular