The concept of modulating spinal growth to correct scoliosis is intriguing, and this study proposes a new model. Inhibition of vertebral growth on the convex side of a curve would allow continued normal growth on the concave side to correct the scoliosis. In an earlier study, we induced bony bridges across the physis of the femur producing an epiphysiodesis in rabbits by using a stimulator modified to deliver a current of 50 μA. This study builds on this finding to design a model with an aim of inhibiting growth in a unilateral peripheral portion of the vertebral endplate physis, which induces asymmetric spinal growth.
The study was conducted with 8-week-old rabbits; 6 were treated with electrical current through an implantable 4-lead device; 3 were age-matched normal rabbits. The device was implanted and delivered a constant current of 50 μA from each electrode, continuously for 6 weeks. Weekly radiograph monitoring and endpoint histology were carried out.
Spinal growth was modified by inducing asymmetric growth of the vertebra of young rabbits using electric stimulators delivering 50 μA of direct current through electrodes implanted in a left peripheral portion of the endplate physis.
This concept study, based on our earlier study, involved a method and device for inhibiting growth in one aspect of the vertebral endplate using electrical current at an amplitude that induced a hemiepiphysiodesis. Our results showed that this technique both establishes an in vivo model of scoliosis and suggests that if this technique were applied to an existing curve it could potentially induce asymmetrical growth of the spine, thereby correcting scoliosis by continuing the normal growth on the concavity of the curve.
A potential new method for modulating spinal growth was developed, and, with further research, this method may be useful in treating children with scoliosis by delivering a growth-inhibiting current to the physeal areas of vertebra through electrodes placed percutaneously.
*Bone & Cartilage Research Laboratory, Nemours Biomedical Research
†Department of Orthopaedics, Alfred I. duPont Hospital for Children, Wilmington
‡Department of Biological Sciences, University of Delaware, Newark, DE
Financial support provided by EBI-Biomet and Nemours Foundation and NIH, AR045242.
Reprints: George R. Dodge, PhD, McKay Orthopaedic Research Laboratory, Department of Orthopaedic Surgery University of Pennsylvania, 424 Stemmler Hall, 36th Street and Hamilton Walk, Philadelphia, PA 19104-6081. E-mail: firstname.lastname@example.org