title: Contributions of Remodeling and Asymmetrical Growth to Vertebral Wedging in a Scoliosis Model.
abstract: METHODS
  We performed a laboratory study of rats of 3 different ages with imposed angulation and compressive loading to caudal vertebrae to determine causes of vertebral wedging.
  
  
  OBJECTIVE
  The purpose was to determine the percentage of total vertebral wedging that was caused by asymmetric growth, vertebral body, and epiphyseal wedging. Approval from the Institutional Animal Care and Use Committee, the University of Vermont, was obtained for the live animal procedures used in this study.
  Vertebral wedging from asymmetrical growth (Hueter-Volkmann law) is reported to cause vertebral wedging in scoliosis with little attention to the possible contribution of bony remodeling (Wolff's law).
  
  
  METHODS
  In our study, an external fixator imposed a 30° lateral curvature and compression of 0.1 megapascal (MPa) in 5- and 14-week-old animals (Groups 1 and 2) and 0.2 MPa in 14- and 32-week-old animals (groups 3 and 4). Total vertebral wedging was measured from micro CT scans. Wedging due to asymmetrical growth and epiphyseal remodeling was calculated from fluorescent labels and the difference was attributed to vertebral body wedging.
  
  
  RESULTS
  Total vertebral wedging averaged 18°, 6°, 10° and 5° in Groups 1, 2, 3, and 4, respectively. Metaphyseal asymmetrical growth averaged 8°, 1°, 4°, 0° (44%, 17%, 40% and 0% of total). Epiphyseal wedging averaged 9°, 0°, 3°, and -1°. The difference (vertebral body) averaged 1°, 5°, 3°, and 7° (6%, 83%, 30% and 140% of total). The growth of the loaded vertebrae as a percentage of control vertebrae was 56%, 39% and 25% in Groups 1, 2 and 3; negligible in Group 4. Vertebral body cortical remodeling, with increased thickness and increased curvature on the concave side was evident in young animals and 0.2 MPa loaded older animals.
  
  
  CONCLUSIONS
  We conclude that asymmetrical growth was the largest contributor to vertebral wedging in young animals; vertebral body remodeling was the largest contributor in older animals. If, conversely, vertebral wedging can be corrected by appropriate loading in young and old animals, it has important implications for the nonfusion treatment of scoliosis.
authors.affiliation: Department of Orthopaedics and Rehabilitation, University of Vermont, Robert T. Stafford Hall, 95 Carrigan Drive Burlington, VT, 05405, USA. Electronic address: david.aronsson@uvm.edu.
authors.forename: David D
authors.initials: DD
authors.lastname: Aronsson
authors.affiliation: Department of Orthopaedics and Rehabilitation, University of Vermont, Robert T. Stafford Hall, 95 Carrigan Drive Burlington, VT, 05405, USA.
authors.forename: Ian A F
authors.initials: IA
authors.lastname: Stokes
authors.affiliation: Department of Orthopaedics and Rehabilitation, University of Vermont, Robert T. Stafford Hall, 95 Carrigan Drive Burlington, VT, 05405, USA.
authors.forename: Carole A
authors.initials: CA
authors.lastname: McBride
keywords: Asymmetric growth (Heuter-Volkmann law); Mechanical modulation; Scoliosis; Vertebral remodeling (Wolff’s law); Vertebral wedging