Mente P L, Stokes I A, Spence H, Aronsson D D
University of Vermont, Department of Orthopaedics and Rehabilitation, McClure Musculoskeletal Research Center, Burlington, USA.
Spine (Phila Pa 1976). 1997 Jun 15;22(12):1292-6. doi: 10.1097/00007632-199706150-00003.
A rat tail model was used to test the hypothesis that angulation and asymmetric axial compressive loading would lead to vertebral wedging because of asymmetric longitudinal growth in the physes.
To study the effect of angulation and asymmetric loading on the progression of spinal curvature in a rat tail model.
Large idiopathic scoliotic curves in children with significant growth remaining are the curves most likely to progress. The mechanism of progression of skeletal deformities is thought to be controlled by the Hueter-Volkmann law, whereby additional axial compression decelerates growth, and reduced axial compression accelerates growth. It has been hypothesized that spinal curvature leads to asymmetric loading transversely along the vertebral growth plate, causing progressive vertebral wedging by means of a vicious cycle.
Two 32-mm diameter external ring fixators were glued to 0.7-mm pins that had been inserted percutaneously through the eighth and 10th caudal vertebra of 10 6-week-old Sprague-Dawley rats. Calibrated springs and 15 degrees wedges, mounted on stainless steel threaded rods passing through holes distributed around the rings, imposed a 30 degrees Cobb angle and axially compressed the instrumented vertebrae. Fluorochrome labels and radiographs were used to document the progression of vertebral wedging.
The wedging initially was entirely in the intervertebral discs, but by 6 weeks the wedging of the discs and vertebrae were approximately equal. Fluorochrome labeling confirmed that the vertebral wedging resulted from asymmetric growth in the physes.
This study shows that vertebrae, when asymmetrically loaded, become wedged. This is consistent with the concept of mechanically provoked progression of scoliotic deformities according to the Hueter-Volkmann law.
采用大鼠尾部模型来检验以下假设,即成角和不对称轴向压缩负荷会由于生长板纵向生长不对称而导致椎体楔形变。
在大鼠尾部模型中研究成角和不对称负荷对脊柱侧凸进展的影响。
在仍有显著生长的儿童中,大型特发性脊柱侧凸曲线是最有可能进展的曲线。骨骼畸形进展的机制被认为受休特尔-福尔克曼定律控制,即额外的轴向压缩会减缓生长,而轴向压缩减少则会加速生长。据推测,脊柱侧凸会导致沿椎体生长板横向的不对称负荷,通过恶性循环导致椎体逐渐楔形变。
将两个直径32毫米的外环固定器粘贴到10只6周龄的斯普拉格-道利大鼠的第8和第10尾椎经皮插入的0.7毫米销钉上。校准过的弹簧和15度楔形物安装在穿过环绕固定器环分布的孔的不锈钢螺纹杆上,施加30度的科布角并轴向压缩受试椎体。使用荧光染料标记和X线片记录椎体楔形变的进展情况。
最初楔形变完全发生在椎间盘,但到6周时,椎间盘和椎体的楔形变大致相等。荧光染料标记证实椎体楔形变是由生长板不对称生长引起的。
本研究表明,椎体在不对称负荷时会发生楔形变。这与根据休特尔-福尔克曼定律机械性诱发脊柱侧凸畸形进展的概念一致。