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CREEP DEFORMITY OF HUMAN VERTEBRAE



Abstract

Introduction: Anterior vertebral body deformities lead to senile kyphosis in many elderly people. Metabolic weakening of bone plays a major role in such osteoporotic “fractures”, but there is evidence also that altered load-sharing in the elderly spine pre-disposes the anterior vertebral body to damage. The insidious onset of many vertebral deformities suggests that gradual time-dependent “creep” processes may contribute, as well as sudden injury. Bone is known to have viscoelastic properties, but creep deformity of whole vertebrae has not previously been investigated.

Methods: 17 cadaveric thoraco-lumbar “motion segments”, consisting of two vertebrae and the intervening disc and ligaments, were obtained from 11 human cadavers aged 42–89 yrs (mean 66 yrs). Each was subjected to a constant compressive load of 1.0 kN for 30 minutes. Vertebral deformations in the sagittal plane were monitored at 50 Hz using an optical MacReflex system, which located pins in the lateral cortex of each vertebral body to an accuracy of < 10 μm. Two pins each defined the anterior, middle and posterior vertebral body height, and deformations were expressed as a % of original (unloaded) height. Elastic deformations included those recorded in the first 10 sec after load application; creep deformation was the continuing deformation (under constant load) during the following 30 min. After 30 min. recovery, 10 of the motion segments were positioned in flexion and damaged by compressive overload. The creep test was then repeated. Additional experiments investigated longer-term creep and recovery.

Results: Creep deformations were similar to the elastic (recoverable) deformations (Table 1). They were greatest anteriorly, giving rise to a typical permanent wedging of the vertebral body of 0.1–1.0o. Creep increased markedly after fracture. Creep continued beyond 2 hrs, but showed little recovery during 2 hrs of unloading.

Discussion: Even at laboratory temperature, creep mechanisms can cause measurable deformity in old vertebrae, and the processes increase greatly after macroscopic fracture. In old spines with degenerated discs, compressive load is concentrated on to the vertebral body margins, and bone loss is greatest anteriorly. This explains why creep was greatest anteriorly. Future work will characterize creep (and recovery) at body temperatures, and determine how it depends on bone density.

Correspondence should be addressed to Sue Woordward, Britspine Secretariat, 9 Linsdale Gardens, Gedling, Nottingham NG4 4GY, England. Email: sue.britspine@hotmail.com