首页> 外文期刊>Spine >Vertebral rounding deformity in pediatric spondylolisthesis occurs due to deficient of endochondral ossification of the growth plate: radiological, histological and immunohistochemical analysis of a rat spondylolisthesis model.
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Vertebral rounding deformity in pediatric spondylolisthesis occurs due to deficient of endochondral ossification of the growth plate: radiological, histological and immunohistochemical analysis of a rat spondylolisthesis model.

机译:小儿腰椎滑脱症的椎体四舍五入畸形是由于生长板的软骨内骨化不足所致:大鼠腰椎滑脱症模型的放射学,组织学和免疫组化分析。

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STUDY DESIGN: A study using rat spondylolisthesis models. OBJECTIVE: To clarify pathomechanism of vertebral rounding deformity in pediatric spondylolisthesis. SUMMARY OF BACKGROUND DATA: For high-grade slippage, rounding of sacrum surface associated with L5 spondylolisthesis is reported to be the most responsible risk factor. However, the exact pathomechanism of the rounding deformity is yet to be clarified. METHODS: Spondylolisthesis rat model (4-week-old) was used. Radiographs were taken weekly for 5 weeks after the surgery. The lumbar spines were harvested for histology. Hematoxylin and eosin, alcian blue staining, and tartrate-resistant acid phosphatase staining were used. Immunohistochemically, the growth plate cartilage was studied for type II and X collagen. A modified bone histomorphometric analysis was also performed. RESULTS: Radiographs showed slippage 1 week after surgery. Rounding deformity was obvious 2 weeks after surgery. The rounding deformity progressed with time. Three weeks after surgery, the specific columns of growth plate were unclear at the anterior corner, which corresponded to the rounding surface observed on radiographs. Instead, a huge mass of cartilage was observed at that site. Tartrate-resistant acid phosphatase-positive cells were observed in the vicinity of the growth plate except in relation with the anterior corner. The growth plate and cartilage mass at the anterior corner stained positive for type II collagen. Chondrocytes in the hypertrophied layer stained positively for type X collagen; however, staining was faint at the anterior corner. The results suggested that the chondrocytes at the anterior did not form, morphologically and functionally, the normal growth plate. From histomorphometrical analysis, the normal posterior growth plate made endochondral bone growth in 510 +/- 20 microm for a week, whereas the anterior corner in 200 +/- 15 microm. CONCLUSION: Deficient endochondral ossification of the growth plate in the anterior upper corner of the vertebra could bethe pathomechanism of the rounding deformity of the sacrum.
机译:研究设计:使用大鼠腰椎滑脱模型的研究。目的:明确小儿脊柱滑脱椎椎体变圆的发病机理。背景数据摘要:对于高度打滑,与L5腰椎滑脱相关的骨表面变圆据报道是最负责任的危险因素。但是,圆形畸形的确切发病机理尚待阐明。方法:采用腰椎滑脱大鼠模型(4周龄)。手术后每周进行X射线照相,持续5周。收获腰椎用于组织学。使用苏木精和曙红,阿尔辛蓝染色和抗酒石酸盐的酸性磷酸酶染色。免疫组织化学研究了生长板软骨中的II型和X型胶原蛋白。还进行了改良的骨组织形态分析。结果:X线片显示术后1周出现滑脱。术后2周明显变圆。圆角变形随时间而发展。手术后三周,在前角不清楚生长板的特定柱,这对应于射线照片上观察到的圆形表面。相反,在该部位观察到大量软骨。除了前角以外,在生长板附近观察到抗酒石酸的酸性磷酸酶阳性细胞。前角的生长板和软骨块对II型胶原染色为阳性。肥大层中的软骨细胞对X型胶原染色呈阳性。然而,在前角染色较弱。结果表明,在形态和功能上,前软骨细胞没有形成正常的生长板。从组织形态学分析,正常的后生长板使软骨内骨生长在510 +/- 20微米范围内一周,而前角在200 +/- 15微米。结论:椎骨前上角生长板软骨内骨化不足可能是ac骨变圆的致病机制。

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