Abstract
Introduction: Cement augmentation of osteoporotic vertebral fractures by vertebroplasty can alleviate pain, possibly by restoring normal load-sharing to the affected motion segment. Fracture is known to decrease vertebral compressive stiffness (1), and also affects the compressive stress distribution acting on the vertebral body, causing stress concentrations to appear in the adjoining intervertebral discs (2). We hypothesise that vertebro-plasty can reverse these fracture-induced changes.
Methods: Nineteen cadaver thoraco-lumbar motion segments (64–90 yrs) were used. Each was mounted on a hydraulic materials testing machine and induced to fracture by compressive overload in moderate flexion. Vertebroplasty was performed by injecting 7 cc of poly-methylmethacrylate cement (Simplex P, Stryker Howmedica, NJ) into the fractured vertebral body. Specimens were then creep loaded at 1.5 kN for 1 hour to allow consolidation. Before and after each procedure, profiles of the compressive stress distribution were obtained by pulling a miniature pressure transducer along the mid-sagittal diameter of the intervertebral disc whilst it was compressed at 1.5kN. Using these profiles, stress peaks in the anterior and posterior annulus were measured by subtracting the nucleus pressure from the peak stress in each region (2). Compressive stiffness of the motion segment was also measured before and after vertebroplasty from the tangent of the load-displacement curve at 1 kN. Changes were compared using ANOVA.
Results: Following fracture, motion segment compressive stiffness was reduced by 37% from 2478 N/mm, STD 966N/mm, to 1583 N/mm, STD 585 N/mm (p = 0.0001), stress peaks in the posterior annulus were increased by 139% from 0.24 MPa, STD 0.24 MPa, to 0.57 MPa, STD 0.47 MPa (p = 0.016), and stress peaks in the anterior annulus showed no significant change. The decrease in compressive stiffness was significantly correlated with the increase in the size of the posterior stress peak (Rsq = 0.65, p< 0.001). Following vertebroplasty and subsequent creep loading, compressive stiffness was increased to 2156 N/mm, STD 718 N/mm, and stress peaks in the posterior annulus were reduced to 0.31 MPa, STD 0.43 MPa. These changes were again highly correlated with each other (Rsq = 0.68, p< 0.001). Both compressive stiffness and the size of posterior stress peaks after vertebroplasty showed no significant difference when compared to pre-fracture values.
Discussion: Fracture reduces the ability of vertebrae to resist deformation, thereby decreasing compressive stiffness. These changes impair the disc’s ability to press evenly on the vertebral body, giving rise to increased stress peaks in the posterior annulus. Vertebroplasty can reverse these fracture induced changes by increasing vertebral compressive stiffness which acts to restore pressure in the nucleus. This enables the disc to press more evenly on the vertebral body and thereby reduces the size of stress peaks in the posterior annulus. This restoration of normal load-sharing may possibly contribute to pain relief in patients undergoing this procedure.
Correspondence should be addressed to Dr Carlos Wigderowitz, Honorary Secretary of BORS, Division of Surgery & Oncology, Section of Orthopaedic & Trauma Surgery, Ninewells Hospital & Medical School Tort Centre, Dundee, DD1 9SY.
References:
(1) Kopperdahl et al, J Orthop Res18: 685–690, 2000. Google Scholar
(2) Adams MA et al, Spine25: 1625–1635, 2000. Google Scholar
