Abstract
Introduction
Senile kyphosis arises from anterior ‘wedge’ deformity of thoracolumbar vertebrae, often in the absence of trauma. It is difficult to reproduce these deformities in cadaveric spines, because a vertebral endplate usually fails first. We hypothesise that endplate fracture concentrates sufficient loading on to the anterior cortex that a wedge deformity develops subsequently under physiological repetitive loading.
Methods
Thirty-four cadaveric thoracolumbar “motion segments,” aged 70–97 yrs, were overloaded in combined bending and compression. Physiologically-reasonable cyclic loading was then applied, at progressively higher loads, for up to 2 hrs. Before and after fracture, and again after cyclic loading the distribution of compressive loading on the vertebral body was assessed from recordings of compressive stress along the sagittal mid-plane of the adjacent intervertebral disc. Vertebral deformity was assessed from radiographs at the beginning and end of testing.
Results
Initial overload usually fractured a vertebral endplate, at 2.31 kN (STD 0.85). There was minimal anterior wedging, but pressure in the nucleus of the adjacent disc was reduced by 65.2% on average, and relatively elevated in the annulus and neural arch. Subsequent cyclic loading then caused anterior wedge deformity of the vertebral body, with the height of the anterior and posterior cortex decreasing by 34.3% (13.2) and 12.7% (7.5) respectively, and wedge angle increasing from 5.0° (3.76) to 11.4° (3.93) (all p<0.001).
Discussion and Conclusion
Our hypothesis is supported: initial minor damage facilitates progressive anterior wedge deformity by transferring compressive loading on to the anterior cortex. Detecting initial endplate damage is important to minimise subsequent vertebral deformity in patients with osteoporosis. 256 words (250 excluding section headings) Acknowledgements Funding was provided by a Royal College of Surgeons of England Research Fellowship and by the Gloucestershire Arthritis Trust.
