Aim: This study tested quantitatively whether calculated loading asymmetry of a spine with scoliosis, together with measured bone growth sensitivity to altered compression could explain the observed rate of scoliosis progression during adolescent growth. Scoliosis is thought to progress during growth because angular deformity produces asymmetrical spinal loading, generating asymmetrical growth, etc. in a ‘vicious cycle’.
Materials and Methods: The magnitude of asymmetrical spinal loading was estimated for a spine with scoliosis, assuming physiologically plausible muscle activation strategies. In animal studies of vertebral and tibial growth plates of three different species, the growth plate response to sustained compression was measured and correlated with histological measures of chondrocytic proliferation and hypertrophic enlargement. These data were expressed in a linear formulation of growth G as a function of compressive stress, thus:
G = Gm(1-β(_-_m)); where β=1.68 MPa-1 was the empirically determined constant. (The subscript m signifies the ‘baseline’ growth and physiological stress).
The vertebral and discal contributions to human adolescent spinal growth velocity were measured from stereo-radiographs of 208 patients of with scoliosis. The estimates of level-specific spinal loading asymmetry, together with the relationship expressing growth sensitivity to load were included in an analysis that was used to estimate the resulting asymmetrical vertebral growth, and its contribution to the progression of a scoliosis curvature. The initial geometry represented a lumbar scoliosis of 26° Cobb, averaged and scaled from measurements of fifteen patients’ radiographs. Spinal growth during each of the adolescent years was estimated from growth curves obtained from cross-sectional logistic-correlation of the radiographically determined spinal and vertebral heights versus age.
Results: The analyses of mechanically modulated growth of the spine with an initial 26° Cobb scoliosis predicted curve progression for the majority of eleven loading conditions (effort magnitude and direction) that were analysed. The averaged final lumbar spinal curve magnitude was 34° Cobb at age 16 years when the efforts producing the spinal loading were at 50% of maximum effort, and it was 42° Cobb when the efforts were at 75% of maximum.
Conclusions: An analysis that included analytically determined spinal load asymmetry and empirically determined growth sensitivity to load predicted that a substantial component of scoliosis progression during growth is biomechanically mediated.
Clinical Relevance: The rationale for conservative management of scoliosis during skeletal growth assumes a biomechanical mode of deformity progression (Hueter-Volkmann principle). The present study provides a quantitative basis for this previously qualitative hypothesis. The findings suggest that an important difference between progressive and non-progressive scoliosis might lie in the differing muscle activation strategies adopted by individuals, leading to the possibility of improved prognosis and conservative interventions, as well as treatments employing early minimally invasive localised growth modulation or arrest.
