Gulotta Lawrence V, Rudzki Jonas R, Kovacevic David, Chen Christopher C T, Milentijevic Dejan, Williams Riley J
Laboratory for Soft Tissue Research, Hospital for Special Surgery, New York, New York 10021, USA.
Am J Sports Med. 2009 Jul;37(7):1324-33. doi: 10.1177/0363546509333476. Epub 2009 May 15.
Autologous osteochondral transplantation surgery requires an impact force on the graft that may cause chondrocyte death and matrix degradation. This study attempted to determine the degree to which this occurs in a rabbit model shortly after the procedure.
Impaction of a press-fit autologous osteochondral graft in vivo results in chondrocyte necrosis, apoptosis, and matrix degradation at early time points.
Controlled laboratory study.
Twenty New Zealand White rabbits underwent unilateral osteochondral transplantation (OT) surgeries, and 10, bilateral sham surgeries. Fifteen animals were sacrificed at time zero (10 sham-0 limbs, 10 OT-0 limbs), and 15, 4 days after surgery (10 sham-4 limbs, 10 OT-4 limbs). Chondrocyte viability/necrosis was determined with cell vital staining. Chondrocyte apoptosis was determined by TUNEL, Bcl-2, and M30 assays. Cartilage matrix degradation was determined by routine light and polarized light microscopy and COL2-3/4C(short) immunohistochemistry. Statistical analysis was performed with a 2-way analysis of variance (P < .05).
There were significantly fewer viable cells in OT-4 than in sham-4. A similar difference in cell viability was found in OT-0 versus sham-0. There were more TUNEL-positive cells in OT-4 as compared with OT-0, sham-0, and sham-4; however, there was little or no staining of Bcl-2 and M30. Mankin scores were higher in both OT groups versus both sham groups at time zero and day 4. The OT-4 group had positive staining for COL2-3/4C(short) that corresponded with a loss of collagen birefringence at the superficial zone.
Osteochondral transplantation procedures performed by tamping a press-fit graft induce chondrocyte necrosis and matrix metalloproteinase-mediated cartilage matrix degradation. However, apoptosis was not found to a major contributor to cell death in this model.
Results of osteochondral transplantation procedures may be improved by atraumatic insertion and fixation techniques or by pharmacologic agents that can block these degradative processes.
自体骨软骨移植手术需要对移植物施加冲击力，这可能导致软骨细胞死亡和基质降解。本研究试图确定该情况在兔模型中术后不久的发生程度。
体内压配式自体骨软骨移植物的冲击在早期时间点会导致软骨细胞坏死、凋亡和基质降解。
对照实验室研究。
20只新西兰白兔接受单侧骨软骨移植（OT）手术，10只接受双侧假手术。15只动物在零时（10只假手术-0肢体，10只OT-0肢体）处死，15只在术后4天（10只假手术-4肢体，10只OT-4肢体）处死。通过细胞活性染色确定软骨细胞活力/坏死情况。通过TUNEL、Bcl-2和M30检测确定软骨细胞凋亡情况。通过常规光镜和偏振光显微镜以及COL2-3/4C（短）免疫组织化学确定软骨基质降解情况。采用双向方差分析进行统计分析（P <.05）。
OT-4组的活细胞明显少于假手术-4组。OT-0组与假手术-0组在细胞活力方面也存在类似差异。与OT-0、假手术-0和假手术-4组相比，OT-4组的TUNEL阳性细胞更多；然而，Bcl-2和M30几乎没有或没有染色。在零时和第4天，两个OT组的Mankin评分均高于两个假手术组。OT-4组COL2-3/4C（短）染色呈阳性，这与表层胶原双折射丧失相对应。
通过夯实压配式移植物进行的骨软骨移植手术会诱导软骨细胞坏死和基质金属蛋白酶介导的软骨基质降解。然而，在该模型中未发现凋亡是细胞死亡的主要原因。
通过无创插入和固定技术或通过能够阻断这些降解过程的药物制剂，可能会改善骨软骨移植手术的结果。
