Residual kyphotic deformity is considered the main factor for the increased risk of new fractures after an osteoporotic vertebral fracture. We hypothesized that even in the absence of kyphotic deformity, the altered pressure profile of the disc after a fracture will increase the risk for subsequent fractures.

Materials and Methods: Six fresh-frozen, human thoracolumbar specimens, consisting of 5 adjacent vertebrae, were used. A void was randomly created under the upper (n=3) or the lower (n=3) endplate of the middle vertebra. The specimen was then compressed in flexion until a selective fracture of the weakened endplate was observed. Vertebral kyphosis was reduced with extension. After cementation of the fracture, the rest of the trabecular content was evacuated and was filled with cement. Specimens were tested in flexion-extension (±6Nm) under 400N preload before and after the index fracture. Pressure was recorded at the discs above and below the fractured VB and strain at the anterior wall of the adjacent VBs. Finally, the specimen was loaded in flexion until a subsequent fracture was observed on fluoroscopy.

Results: In the intact specimens, nucleus pressure increased by 26.4±13.9% in full flexion compared to neutral posture. After the index fracture, the pressure in full flexion increased by 15.2±11 % in the discs with unfractured endplates, but decreased by 19±26.7% in the discs with the fractured endplate (p< 0.05). Anterior wall strain at the VB adjacent to the fractured endplate increased by 94.2%±22.8% (p=0.02), compared to an 18.2%±7.1% (p=0.98) increase at the VB adjacent to the unfractured endplate. Subsequent loading of the specimens after cementation of the index fracture resulted in a fracture of the adjacent VB close to the fractured endplate of the middle vertebra in 4 specimens and at the upper potted VB in one specimen. Maximum load applied with the actuators failed to create a fracture in one specimen.

Discussion: The effects of the fractured endplate were isolated by eliminating other known parameters. Vertebral kyphosis was reduced and cement was similarly distributed under both endplates.

In the intact specimens, nucleus pressure gradually increased during flexion. This can more evenly distribute the load during flexion to the entire surface of the endplate and avoid excessive load concentration to the anterior portion. After an endplate fracture, the nucleus pressure gradually decreased during flexion, meaning that the anterior annulus was forced to bear more load. This uneven load transfer to the anterior part of the VB resulted in doubling the strain at the VB adjacent to the fractured end plate. All adjacent factures were observed at the vertebra next to the damaged endplate. The altered mechanical behavior of the nucleus can be ascribed to the increased available space after the endplate depression.

Purpose: The purpose of this biomechanical study was to assess: (1) the effect of thoracic vertebral compression fracture (VCF) on kyphosis and physiologic compressive load path, and (2) the effect of balloon kyphoplasty and spinal extension on restoration of normal geometric and loading alignment.

Methods: Six fresh human thoracic specimens, each consisting of three adjacent vertebrae were used. In order to create a VCF, IBTs were placed transpedicularly into the middle VB and cancellous bone was disrupted by inflation of IBTs. After cancellous bone disruption the specimens were compressed using bilateral loading cables until a fracture was observed. Fracture reduction by spinal extension, and then by balloon kyphoplasty was performed under a physiologic compressive preload of 250 N. The vertebral body heights, kyphotic deformity, and location of compressive load path were measured on video-fluoroscopy images.

Results: The VCF caused anterior VB height loss of 3715%, middle-height loss of 3416%, segmental kyphosis increase of 147.0 degrees, and vertebral kyphosis increase of 135.5 degrees (p< 0.05). The compressive load path shifted anteriorly by 20% of A-P endplate width in the fractured and adjacent VBs (p=0.01). IBT inflation alone restored anterior VB height to 918.9%, middle-height to 9114%, and segmental kyphosis to within 5.65.9 degrees of pre-fracture values. The compressive load path returned posteriorly in all three VBs (p=0.00): the load path remained anterior to the pre-fracture location by 9–11% of the A-P endplate width. The extension moment fully restored the compressive load path to its pre-fracture location. Under this moment, the anterior and middle VB heights were restored to 858.6% and 749.4% of pre-fracture values, respectively. The segmental kyphosis was fully restored to its pre-fracture value; however, the middle height and kyphotic deformity of the fractured VB remained smaller than the pre-fracture values (p< 0.05).

Conclusions: An anterior shift of the compressive load path in VBs adjacent to VCF can induce additional flexion moments. The eccentric loading may contribute to the increased risk of new VB fractures adjacent to an uncorrected VCF deformity. Extension moment could fully correct the segmental kyphosis but could not restore the middle height of the fractured vertebral body. Balloon kyphoplasty reduced the VCF deformity and partially restored the compressive load path to normal alignment.