Stature and growth compensation for spinal curvature.

UNLABELLED: Spinal curvatures alter measured stature and may influence the evaluation of skeletal maturity and growth based on stature measurements. METHODS: A dataset of calibrated measurements of vertebral positions of 407 radiographs in the frontal plane, together with clinically measured Cobb angles was used to determine the difference between spinal length and spinal height ('height loss') as a function of Cobb angles for radiographs indicating both single (N=182) and double (N=225) curves. RESULTS: An apparently quadratic relationship: Height loss (mm)=1.0+0.066*Cobb+0.0084*Cobb*Cobb was found between height loss and each patient's mean Cobb angle for double curves. There was close agreement of the regression coefficients for single and double curves, and the present findings were very similar to the relationship reported by Ylikoski (Eur Spine J, 2003, 12:288-291). The relationships differed substantially from those proposed by Bjure (Clin Orthop, 1973 93:44-52) and by Brookenthal (SRS Exhibit 15, 2002). DISCUSSION AND CONCLUSIONS: The findings of the present study indicate that height loss (in mm) occurring with a 10 degrees increase in mean Cobb angle (for two curves) would be 1.1+0.16 times the mean Cobb angle (in degrees). For example, for a Cobb angle change from 30 to 40 degrees, the expected height loss would be 1.1+35*0.16 mm=6.7 mm. This assumes that height loss occurs only as a result of altered curvature, without alteration in disc height associated with an increase in scoliosis.

Intervertebral disc changes in an animal model representing altered mechanics in scoliosis.

The intervertebral discs become wedged and narrowed in a scoliosis curve, and this may be due in part to altered biomechanical environment. To study this, external rings were attached by percutaneous pins transfixing adjacent vertebrae in 5-week-old Sprague-Dawley rats and four permutations of mechanical conditions (4 groups of animals) were compared: (A) 15 degrees Angulation, (B) Angulation with 0.1 MPa Compression, (C) 0.1 MPa Compression, and (D) Reduced mobility. These altered mechanical conditions were applied for 5 weeks. After 5 weeks, disc narrowing at the intervention levels was evident in micro-CT images. Average disc space loss as a percent of the initial values over the 5 weeks was 19%, 28%, 22% and 20% four groups listed above. Increased lateral bending stiffness relative to within-animal controls was also observed at all groups. The minimum stiffness was recorded at an angle close to the in vivo value, indicating that angulated discs had adapted to the imposed deformity. In the angulated and compressed discs there was a small difference in the amount of collagen crimping in the disc annuli between concave and convex sides. All experimental interventions produced substantial changes in the intervertebral discs of these growing animals. 'Reduced mobility' was present in all interventions, and the changes in the discs with reduced mobility alone were comparable with those in loaded and angulated discs. This suggests that imposed reduced mobility is the major source of disc changes, and may be a factor in disc degeneration in scoliosis. Further studies are in progress to characterize gene expression, matrix protein synthesis and composition in these discs.

Biomechanical modeling of posterior instrumentation of the scoliotic spine.

Scoliosis is a three-dimensional deformation of the spine that can be treated by vertebral fusion using surgical instrumentation. However, the optimal configuration of instrumentation remains controversial. Simulating the surgical maneuvers with personalized biomechanical models may provide an analytical tool to determine instrumentation configuration during the pre-operative planning. Finite element models used in surgical simulations display convergence difficulties as a result of discontinuities and stiffness differences between elements. A kinetic model using flexible mechanisms has been developed to address this problem, and this study presents its use in the simulation of Cotrel-Dubousset Horizon surgical maneuvers. The model of the spine is composed of rigid bodies corresponding to the thoracic and lumbar vertebrae, and flexible elements representing the intervertebral structures. The model was personalized to the geometry of three scoliotic patients (with a thoracic Cobb angle of 45 degrees, 49 degrees and 39 degrees ). Binary joints and kinematic constraints were used to represent the rod-implant-vertebra joints. The correction procedure was simulated using three steps: (1) Translation of hooks and screws on the first rod; (2) 90 degrees rod rotation; (3) Hooks and screws look-up on the rod. After the simulation, slight differences of 0-6 degrees were found for the thoracic spine scoliosis and the kyphosis, and of 1-8 degrees for the axial rotation of the apical vertebra and for the orientation of the plane of maximum deformity, compared to the real post-operative shape of the patient. Reaction loads at the vertebra-implant link were mostly below 1000 N, while reaction loads at the boundary conditions (representing the overall action of the surgeon) were in the range 7-470 N and maximum torque applied to the rod was 1.8 Nm. This kinetic modeling approach using flexible mechanisms provided a realistic representation of the surgical maneuvers. It may offer a tool to predict spinal geometry correction and assist in the pre-operative planning of surgical instrumentation of the scoliotic spine.

Mechanical effects on skeletal growth.

The growth (i.e. increase of external dimensions) of long bones and vertebrae occurs longitudinally by endochondral ossification at the growth plates, and radially by apposition of bone at the periosteum. It is thought that mechanical loading influences the rate of longitudinal growth. The 'Hueter-Volkmann Law' proposes that growth is retarded by increased mechanical compression, and accelerated by reduced loading in comparison with normal values. The present understanding of this mechanism of bone growth modulation comes from a combination of clinical observation (where altered loading and growth is implicated in some skeletal deformities) and animal experiments in which growth plates of growing animals have been loaded. The gross effect of growth modulation has been demonstrated qualitatively and semi-quantitatively. Sustained compression of physiological magnitude inhibits growth by 40% or more. Distraction increases growth rate by a much smaller amount. Experimental studies are underway to determine how data from animal studies can be scaled to other growth plates. Variables include: differing sizes of growth plate, different anatomical locations, different species and variable growth rate at different stages of skeletal maturity. The two major determinants of longitudinal growth are the rate of chondrocytic proliferation and the amount of chondrocytic enlargement (hypertrophy) in the growth direction. It is largely unknown what are the relative changes in these key variables in mechanically modulated growth, and what are the signaling pathways that produce these changes.