Departments of Orthopaedic Surgery (K. Kubota, K. Kobayakawa, Y.M., K.H., Y.I.) and Advanced Medical Initiatives (M.M., M.H., S.O.), Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582. E-mail address fro K. Kubota:
J Bone Joint Surg Am. 2013 Sep 18;95(18):e130. doi: 10.2106/JBJS.L.01381.
The pathomechanism underlying idiopathic scoliosis remains unclear, and, to our knowledge, a consistent and relevant animal model has not been established previously. The goal of this study was to examine whether a disturbance of rib cage development is a causative factor for scoliosis and to establish a nonsurgical mouse model of progressive scoliosis.
To examine the relationship between rib cage development and the pathogenesis of progressive scoliosis, a plastic restraint limiting anteroposterior rib cage development was placed on the chest of four-week-old mice. All mice were evaluated with whole-spine radiographs, and the severity of scoliosis was consecutively measured. The rib cage rotation angle and the anteroposterior chest dimension were measured with use of micro-computed tomography scanning. To examine whether the imbalanced load transmission through the ribs to the vertebral body was involved in our model, we performed a rib-neck osteotomy in a subgroup of the mice.
The thoracic restraint did not provoke spinal curvature immediately after it was applied, but nine of ten mice that wore the restraint but did not have rib osteotomy gradually developed progressive scoliosis. Radiographs and computed tomography images showed a right thoracic curvature, vertebral rotation, and narrow chest in the mice that had worn the restraint for eleven weeks but did not have rib osteotomy even after the restraint was removed. The anteroposterior chest dimension was significantly correlated with both the curve magnitude and the rib cage rotation angle. The progression of spinal deformity was observed only during the adolescent growth spurt, and it plateaued thereafter. The left-side rib osteotomy led to the development of progressive left-thoracic curvature, whereas the bilateral rib osteotomy did not cause scoliosis, even with restraint wear.
We established a nonsurgical experimental model of progressive scoliosis and also demonstrated that a rib cage deformity with an imbalanced load to the vertebral body resulted in progressive structural scoliosis.
特发性脊柱侧凸的发病机制仍不清楚，据我们所知，之前尚未建立一致且相关的动物模型。本研究旨在探讨胸廓发育障碍是否是脊柱侧凸的一个致病因素，并建立进展性脊柱侧凸的非手术小鼠模型。
为了研究胸廓发育与进行性脊柱侧凸发病机制的关系，在 4 周龄小鼠的胸部放置一个限制胸廓前后径发育的塑料限制器。所有小鼠均接受全脊柱 X 线片评估，并连续测量脊柱侧凸的严重程度。使用 micro-CT 扫描测量胸廓旋转角度和胸廓前后径。为了研究肋骨向椎体不平衡传递负荷是否参与了我们的模型，我们在部分小鼠中进行了肋骨颈截骨术。
胸廓限制器在应用后并不会立即引起脊柱弯曲，但在未进行肋骨截骨的 10 只佩戴限制器的小鼠中，有 9 只逐渐出现进行性脊柱侧凸。在去除限制器后，佩戴限制器 11 周但未进行肋骨截骨的小鼠的 X 线片和 CT 图像显示出右胸侧凸、椎体旋转和胸廓变窄。胸廓前后径与曲线幅度和胸廓旋转角度均有显著相关性。脊柱畸形的进展仅发生在青少年生长突增期，此后趋于稳定。左侧肋骨截骨导致进行性左侧胸侧凸，而双侧肋骨截骨即使佩戴限制器也不会导致脊柱侧凸。
我们建立了一种进展性脊柱侧凸的非手术实验模型，并证实了胸廓畸形和向椎体不平衡传递负荷导致进行性结构性脊柱侧凸。
