STUDY DESIGN

Vertebral defects were created in a validated 3D finite element model (FEM) to simulate destructive tubercular lesions of increasing severity. Forces in various parts of the spine were then calculated and correlated to deformity progression and growth modulation (GM) changes.

OBJECTIVE

To understand the biomechanical basis of GM, which governs spinal growth and the progression of kyphosis in posttubercular kyphotic (PTK) deformities.

SUMMARY OF BACKGROUND DATA

Hueter-Volkmann Law (HVL), chondral growth force response curve (CGFRC), and regional growth acceleratory phenomenon have all been proposed to explain the modulation of growth in limbs but have not been tested in vertebral end plates (VEP). We have previously documented various GM changes in posttubercular kyphotic. By simulating the kyphotic collapse in a validated FEM, the mechanical basis of GM can be established.

METHODS

Sixty-three children with tuberculosis treated conservatively formed the clinical material. The progress of deformity and GM changes in the fusion mass and the kyphotic curve was documented. Defects simulating lesions of four levels of severity (types A, B, C, and D) were created in a validated 3D FEM and subjected to load till restabilization occurred. The stresses at the end plates, discs, facet joints, and the points of contact were calculated.

RESULTS

Regional growth acceleratory phenomenon and favorable growth changes were found in type A collapse where the facets were intact. With increasing destruction, the forces in the facet capsules increased beyond 30 MPa predicting facet dislocations in types B, C, and D collapse. As the contact stress on the VEP increased to 16.6 MPa (type B) and 40 MPa (type C), this was associated with growth suppression. Type D collapse involved facet dislocation at multiple levels leading to "buckling collapse". Acceleratory growth was found both in tension and compression phases proving that VEP growth followed principles of CGFRC rather than HVL.

CONCLUSION

This is the first study in the current literature to demonstrate that spinal growth follows CGFRC rather than HVL. This observation opens a potential window of opportunity to treat spinal deformities by mechanical GM.