Higashino Kosaku, Sairyo Koichi, Sakamaki Tadanori, Komatsubara Shinji, Yukata Kiminori, Hibino Naohito, Kosaka Hirofumi, Sakai Toshinori, Katoh Shinsuke, Sano Toshiaki, Yasui Natsuo
Department of Orthopedics, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, Tokushima 770-8503, Japan.
Spine (Phila Pa 1976). 2007 Dec 1;32(25):2839-45. doi: 10.1097/BRS.0b013e31815b981f.
A study using rat spondylolisthesis models.
To clarify pathomechanism of vertebral rounding deformity in pediatric spondylolisthesis.
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.
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.
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.
Deficient endochondral ossification of the growth plate in the anterior upper corner of the vertebra could be the pathomechanism of the rounding deformity of the sacrum.
一项使用大鼠脊柱滑脱模型的研究。
阐明小儿脊柱滑脱中椎体圆形畸形的发病机制。
对于高度滑脱,据报道与L5脊柱滑脱相关的骶骨表面圆形化是最主要的危险因素。然而,这种圆形畸形的确切发病机制尚待阐明。
使用脊柱滑脱大鼠模型(4周龄)。术后每周拍摄X线片,共5周。采集腰椎进行组织学检查。采用苏木精-伊红染色、阿尔辛蓝染色和抗酒石酸酸性磷酸酶染色。免疫组织化学方法研究生长板软骨中的II型和X型胶原。还进行了改良的骨组织形态计量学分析。
X线片显示术后1周出现滑脱。术后2周圆形畸形明显。圆形畸形随时间进展。术后3周,生长板前角的特定柱体不清晰,这与X线片上观察到的圆形表面相对应。相反,在该部位观察到大量软骨。除前角外,在生长板附近观察到抗酒石酸酸性磷酸酶阳性细胞。前角的生长板和软骨块II型胶原染色阳性。肥大层的软骨细胞X型胶原染色阳性;然而,前角染色较淡。结果表明,前部的软骨细胞在形态和功能上未形成正常的生长板。从组织形态计量学分析来看,正常的后部生长板每周通过软骨内成骨生长510±20微米,而前角为200±15微米。
椎体前上角生长板软骨内成骨不足可能是骶骨圆形畸形的发病机制。