The role of remodeling and asymmetric growth in vertebral wedging

Scoliosis with vertebral wedging is thought to be caused by asymmetric growth (Hueter-Volkmann law), but vertebral diaphyseal remodeling (Wolff's law) may also contribute to the deformity. We investigated whether vertebral wedging in scoliosis might involve both mechanisms.

An external fixator was used to impose a 30 degrees scoliosis and compression of 0.1 or 0.2 MPa to the tails of 10 5-week-old and 20 14-week-old Sprague-Dawley rats for 6 weeks. The rats were divided into three groups of 10 animals each: Group 1: 5-week-old animals with 0.1 MPa compression; Group 2: 14-week-old animals with 0.1 MPa compression; Group 3: 14-week-old animals with 0.2 MPa compression. Vertebral wedging and diaphyseal curvature were measured from micro CT scans performed at weeks 1, 3, and 6. Wedging due to asymmetrical growth and remodeling was calculated from a Calcein label administered at week 3 and a Xylenol label at week 6.

The growth rate of the loaded vertebrae as a per cent of control vertebrae was 60% in Group 1, 40% in Group 2, and 30% in Group 3. The growth rate of control vertebrae in 14-week-old animals was 16% that of 5-week-old animals. The animals in all 3 groups developed a scoliosis with vertebral wedging that averaged 18.7 degrees in Group 1, 8.2 degrees in Group 2, and 10.1 degrees in Group 3. Asymmetric growth was much greater in Group 1 (5-week-old) animals. The ossified epiphyses became wedged and diaphyseal remodeling occurred in all groups.

The major contribution to the vertebral wedging was asymmetric growth in the 5-week-old animals and diaphyseal remodeling in the 14-week-old animals. The results support the concept that if appropriate loads can be applied to human vertebrae through minimally invasive techniques, scoliosis and vertebral wedging can be corrected without a spinal fusion in both adolescents and adults.