P L Mente1, I A Stokes, H Spence, D D Aronsson. 1. University of Vermont, Department of Orthopaedics and Rehabilitation, McClure Musculoskeletal Research Center, Burlington, USA.
Abstract
STUDY DESIGN: 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. OBJECTIVES: To study the effect of angulation and asymmetric loading on the progression of spinal curvature in a rat tail model. SUMMARY OF BACKGROUND DATA: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
STUDY DESIGN: 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. OBJECTIVES: To study the effect of angulation and asymmetric loading on the progression of spinal curvature in a rat tail model. SUMMARY OF BACKGROUND DATA: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: Patricia M Kallemeier; Glenn R Buttermann; Brian P Beaubien; Xinqian Chen; David J Polga; William D Lew; Kirkham B Wood Journal: Eur Spine J Date: 2005-11-04 Impact factor: 3.134