Introduction: Painful anterior vertebral wedge “fractures” can occur without any remembered trauma, suggesting that vertebral deformity could accumulate gradually through sustained loading by the process of “creep”. If the adjacent intervertebral discs are degenerated, they press unevenly on the vertebral body in a posture- dependent manner, producing differential creep of the vertebra. We hypothesise that differential creep due to sustained asymmetrical loading of a vertebral body can cause anterior vertebral wedge deformity.

Materials And Methods: Eleven thoracolumbar motion segments aged 64–88 yrs were subjected to a 1.5 kN compressive force for 2 hrs, applied via plaster moulded to its outer surfaces. Specimens were positioned in 2° flexion to simulate a stooped posture. Reflective markers attached to pins inserted into the lateral cortex of each vertebral body enabled anterior, middle and posterior vertebral body heights to be measured at 1Hz using an optical tracking device. Compressive ‘stress’ acting vertically on the vertebral body was quantified by pulling a miniature pressure transducer along the midsagittal diameter of adjacent discs.

Results: Elastic deformation (strain) was higher anteriorly (−2018 ± 2983 μ strain) than posteriorly (−1675 ± 1305 μ strain). Creep strain (−2867 ± 2527 μ strain) was significantly higher anteriorly (p< 0.05) than posteriorly (−1164 ± 1026 μ strain), and was associated with a higher compressive stress in the anterior annulus of the adjacent disc. Non-recoverable creep deformations were significantly higher anteriorly (p< 0.05), and were equivalent to a wedging angle of 0.01–0.3°.

Conclusion: Creep can cause anterior wedge deformity of the vertebral body. In the long term, accumulating creep could cause more severe (and painful?) deformity.

Introduction: Atraumatic vertebral deformity could possibly arise from sustained loading by the adjacent intervertebral discs, especially when discs are degenerated and press unevenly on the vertebra (1). Creep phenomena have been studied in samples of cancellous and cortical bone, but little is known about their potential to deform whole bones. We hypothesise that sustained asymmetrical loading of a vertebral body can cause differential creep, and vertebral deformity.

Materials and methods: Five thoracolumbar ‘motion segments’ (two vertebrae with intervening soft tissues) were dissected from human cadavers aged 64-88 yrs. Each specimen was subjected to a 1.5 kN compressive force for 2 hrs, applied via plaster moulded to its outer surfaces. Specimens were positioned in 2 deg flexion to simulate a stooped posture. Six reflective markers were attached to pins inserted into the lateral cortex of each vertebral body. Anterior, middle and posterior vertebral body heights were measured at 1 Hz to an accuracy of 7 microns, using a MacReflex 2D optical tracking device. This enabled elastic and creep strains in the vertebral cortex to be plotted against time. Compressive ‘stress’ acting vertically on the vertebral body was quantified by pulling a miniature pressure transducer along the mid-sagittal diameter of adjacent discs (1).

Results: Maximum elastic compressive strains in the posterior, middle and anterior cortex were 500-700, 800-2000 and 600-2500 microstrains respectively. Corresponding creep strains were 200-1500, 200-3200 and 500-5500 microstrains. Increased strains in the anterior vertebral body corresponded to increased stresses in the anterior annulus of adjacent discs. Creep was greater in older specimens, and was only partially reversible. ‘Permanent’ anterior wedging of the vertebral body could reach 0.7 deg after 2 hrs.

Discussion: These preliminary results suggest that vertebral deformity in-vivo can arise by creep mechanisms, when total (elastic+creep) strain locally exceeds the yield strain of bone (2). Future experiments will consider the middle vertebra in three-vertebra specimens.