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.

Introduction

Osteoporotic vertebral fractures can cause severe vertebral wedging and kyphotic deformity. This study tested the hypothesis that kyphoplasty restores vertebral height, shape and mechanical function to a greater extent than vertebroplasty following severe wedge fractures.

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.

Introduction

The feature of disc degeneration most closely associated with pain is a large fissure in the annulus fibrosus. Nerves and blood vessels are excluded from normal discs by high matrix stresses and by high proteoglycan (PG) content. However, they appear to grow into annulus fissures in surgically-removed degenerated discs. We hypothesize that anulus fissures provide a micro-environment that is mechanically and chemically conducive to the in-growth of nerves and blood vessels.

Background

In the annulus fibrosus of degenerated intervertebral discs, disruption to inter-lamellar cross-ties appears to lead to delamination, and the development of anulus fissures. We hypothesise that such internal disruption is likely to be driven by high gradients of compressive stress (i.e. large differences in stress from the nucleus to the mid anulus).

Treatment of syndesmotic injuries is a subject of ongoing controversy. Locking plates have been shown to provide both angular and axial stability and therefore could potentially control both shear forces and resist widening of the syndesmosis. The aim of this study is to determine whether a two-hole locking plate has biomechanical advantages over conventional screw stabilisation of the syndesmosis in this pattern of injury. Six pairs of fresh-frozen human cadaver lower legs were prepared to simulate an unstable Maisonneuve fracture. The limbs were then mounted on a servo-hydraulic testing rig and axially loaded to a peak load of 800N for 12000 cycles. Each limb was compared with its pair; one receiving stabilisation of the syndesmosis with two 4.5mm quadricortical cortical screws, the other a two-hole locking plate with 3.2mm locking screws (Smith and Nephew). Each limb was then externally rotated until failure occurred. Failure was defined as fracture of bone or metalwork, syndesmotic widening or axial migration >2mm. Both constructs effectively stabilised the syndesmosis during the cyclical loading within 1mm of movement. However the locking plate group demonstrated superior resistance to torque compared to quadricortical screw fixation (40.6Nm vs 21.2Nm respectively, p value <0.03).

Osteoporotic vertebral deformities are conventionally attributed to fracture, although deformity is often insidious, and bone is known to “creep” under constant load. We hypothesise that deformity can arise from creep that is accelerated by minor injury.

Thirty-nine thoracolumbar “motion segments” were tested from cadavers aged 42-92 yrs. Vertebral body BMD was measured using DXA. A 1.0 kN compressive force was applied for 30 mins, while the height of each vertebral body was measured using a MacReflex optical tracking system. After 30 mins recovery, one vertebral body from each specimen was subjected to controlled micro-damage (<5mm height loss) by compressive overload, and the creep test was repeated. Load-sharing between the vertebral body and neural arch was evaluated from stress measurements made by pulling a pressure transducer through the intervertebral disc.

Creep was inversely proportional to BMD below a threshold BMD of 0.5 g/cm² (R²=0.30, P<0.01) and did not recover substantially after unloading. Creep was greater in the anterior cortex compared to the posterior (p=0.01) so that anterior wedge deformity occurred. Vertebral micro-damage usually affected a single endplate, causing creep of that vertebra to increase in proportion to the severity of damage. Anterior wedging of vertebral bodies during creep increased by 0.10^o (STD 0.20^o) for intact vertebrae, and by 0.68^o (STD 1.34^o) for damaged vertebrae.

Creep is substantial in elderly vertebrae with low BMD, and is accelerated by micro-damage. Preferential loss of trabeculae from the anterior vertebral body could explain greater anterior creep and vertebral wedging.

Background: Neck muscles stabilise the head, but muscle tension imposes high compressive forces on the cervical spine. Little is known about which structures resist these high forces.

Purpose: To quantify compressive load-sharing within the cervical spine.

Methods: Seventeen cervical “motion segments” from cadavers aged 54–92 yr (mean 72 yr), were subjected to 200 N compression while positioned in simulated flexed and extended postures. Up to 5 Nm of bending was applied in various planes. Vertebral movements were recorded at 50 Hz using an optical MacReflex system. Tangent stiffness was calculated in compression and in bending. Load-sharing was evaluated from compressive stress measurements obtained by pulling a pressure transducer through the intervertebral disc. All measurements were repeated after 2 hr of creep loading at 150 N, and following sequential removal of the spinous process, apophyseal joints and uncovertebral joints.

Results: Most compression was resisted by the disc. However, creep increased compressive load-bearing by the neural arch, from 21% to 28% in flexed posture, and from 27% to 45% in extended posture, with most of this loading being resisted by the apophyseal joints. Uncovertebral joints resisted 10% of compression in extended posture, and 20% in flexed posture. Flexion and extension movements were resisted primarily by ligaments of the neural arch, and by the apophyseal joints, respectively, whereas lateral bending was resisted mostly by the apophyseal and uncovertebral joints.

Conclusion: Cervical apophyseal joints play a major role in compressive load-bearing, and also offer strong resistance to backwards and lateral bending. Uncovertebral joints primarily resist lateral bending.

Conflicts of Interest: None

Source of Funding: Scholarship from the Greek Government

Background: Continuous bone “creep” under constant load can cause measurable deformity in cadaveric vertebrae, but the phenomenon is extremely variable.

Purpose: We test the hypothesis that vertebral micro-damage accelerates creep deformity.

Methods: Twenty-six thoracolumbar “motion segments” were tested from cadavers aged 42–92 yrs. Bone mineral density (BMD) of each vertebral body was measured using DXA. A 1.0 kN compressive force was applied for 30 mins, while the height of each vertebral body was measured using a MacReflex optical tracking system. After 30 mins recovery, one vertebral body from each specimen was subjected to controlled micro-damage (< 5mm height loss) by compressive overload, and the creep test was repeated. Load-sharing between the vertebral body and neural arch was evaluated from stress measurements made by pulling a pressure transducer through the intervertebral disc.

Results: Creep was inversely proportional to BMD (P=0.041) and did not recover substantially after unloading. Creep was greater in the anterior vertebral body cortex compared to the posterior (p=0.002). Vertebral micro-damage usually affected a single endplate, causing creep of that vertebra to increase in proportion to the severity of damage. Anterior wedging of the vertebral bodies during creep increased by 0.10o (STD 0.20o) for intact vertebrae, and by 0.68o (STD 1.34o) for damaged vertebrae.

Conclusion: Creep is substantial in elderly vertebrae with low BMD, and is accelerated by micro-damage. Preferential loss of trabeculae from the anterior vertebral body could explain why creep is greater there, and so causes wedging deformity, even in the absence of fracture.

Conflicts of Interest: none

Source of Funding: Action Medical Research

Background: Intervertebral discs and vertebrae deform under load, narrowing the intervertebral foramen and increasing the risk of nerve entrapment. Little is known about these deformations in elderly spines.

Purpose: To test the hypothesis that, in ageing spines, vertebrae deform more than discs, and contribute to time-dependent creep.

Methods: 117 thoracolumbar motion segments, mean age 69 yr, were compressed at 1 kN for 0.5, 1 or 2 hr. Immediate “elastic” deformations were followed by “creep”. A three-parameter model was fitted to experimental data to characterise their viscous modulus E1, elastic modulus E2 (initial stiffness), and viscosity η (resistance to fluid flow). Intradiscal pressure (IDP) was measured using a miniature needle-mounted transducer. In 17 specimens loaded for 0.5 hr, an optical MacReflex system measured compressive deformations separately in the disc and each vertebral body.

Results: On average, the disc contributed 28% of the spine’s elastic deformation, and 51% of the creep. Elastic, creep, and total deformations of 84 motion segments over 2 hrs averaged 0.87mm, 1.37mm and 2.24mm respectively. Measured deformations were predicted accurately by the model, but E1, E2 and η depended on loading duration. E1 and η decreased with advancing age and degeneration, in proportion to falling IDP (p< 0.001). Total compressive deformation increased with age, but rarely exceeded 3mm.

Conclusions: In ageing spines, vertebral bodies show greater elastic deformations than intervertebral discs, and a similar amount of creep. Deformations depend largely on IDP, but appear to be limited by impaction of adjacent neural arches. Total deformations are sufficient to cause foraminal stenosis in some individuals.

Conflicts of Interest: none

Source of Funding: Action Medical Research

Background: Intrauterine protein restriction in rodent models is associated with low bone mass which persists into adulthood. This study examined how early nutritional compromise affects the mechanical and structural properties of spinal tissues in sheep throughout the lifecourse.

Methods: Lumbar spines were removed from 19 sheep; 5 control animals and 14 that received a restricted diet in-utero. Eight animals (2 control/6 diet) were sacrificed at a mean age of 2.7 years and eleven at a mean age of 4.4 yrs. Two motion segments from each spine were tested on a hydraulically-controlled materials testing machine to determine their mechanical properties. Vertebral bodies were assessed for a number of structural parameters including cortical thickness and area, and regional trabecular density.

Results: Younger animals in the diet group showed a 25% reduction in forward bending stiffness (p< 0.05) and a 32% reduction in extension strength (p< 0.05) compared to controls of the same age. Furthermore, these young animals showed a 25% reduction in the thickness of the anterior cortex (p< 0.001) and an 18% reduction in the thickness of the superior cortex (p< 0.02). In older animals, no differences were observed in any of the mechanical parameters examined between diet and control groups, although animals in the diet group showed an average increase in cortical thickness of 14%, across all regions (p< 0.01).

Conclusions: These results suggest that early nutritional challenge can have detrimental effects on the mechanical and structural properties of spinal tissues in young animals but that adaptation occurs over the lifecourse to compensate for these differences in older animals.

Conflicts of Interest: None

Source of Funding: None

Introduction: Vertebroplasty is used to treat painful osteoporotic vertebral fractures, and involves transpedicular injection of bone cement into the fractured vertebral body. During injection, the fluid cement begins to “harden” to a solid, enabling it to support mechanical load. But the mechanical efficacy of vertebroplasty can be improved by using cements which disperse evenly throughout the vertebral body during injection (1). We hypothesise that a better cement dispersion is obtained with cements that have a slower viscosity increase during hardening. We test this using a numerical model.

Methods: A computer model mimicking the plate- and rod-like morphologies of cancellous bone was loaded into a commercial fluid dynamics package (CFX). During injection, viscosity increased linearly with time to simulate the hardening behaviour of the cement (2). The rate of viscosity increase was altered to mimic the hardening behaviour of 5 different cements, with the rates of increase chosen to encompass the hardening behaviour of commercial vertebroplasty cements (1). Simulations were run for 13 seconds, with cement injection at 1.5 mm/s. Cement dispersion was quantified by the proportion of marrow replaced by cement during injection. Injection pressure was also recorded.

Results: Injection pressure increased with time (p< 0.001), and maximum pressure correlated with the rate of viscosity increase (r2=0.7). The proportion of marrow replaced at the end of the experiment was inversely proportional to the rate of viscosity increase (r2=0.85). Cements with a rapidly increasing viscosity do not fully infiltrate regions of bone with plate-like morphologies, leading to a poorer cement dispersion.

Conclusion: Cements with slower hardening characteristics are dispersed more evenly throughout cancellous bone. Such cements may provide safer and more effective vertebroplasty procedures.

Conflicts of Interest: None

Source of Funding: Bupa Foundation

Introduction: Vertebroplasty is increasingly used in the treatment of painful osteoporotic vertebral fractures, and involves transpedicular injection of bone cement into the fractured vertebral body. Effective infiltration of the vertebral body cancellous bone by the cement is determined by the cement viscosity, and by the permeability of the bone. However, it is unclear how permeability is influenced by regional variations in porosity and architecture of bone within the vertebral body. The aim of the present study was to investigate how permeability is influenced by porosity and architecture of cancellous bone mimics.

Methods: Cylindrical polyamide mimics of two types of cancellous bone structures were fabricated using selective laser sintering (SLS) techniques. Structure A had the rod-like vertical and horizontal trabeculae typical of the anterior vertebral body, while structure B had oblique trabeculae typical of the posterior-lateral vertebral body. Structure B had fewer trabeculae than A. Porosities of 80 and 90% were represented for both structures. Golden syrup, which has a viscosity similar to bone cement1, was injected into the mimics at a constant speed using a ram driven by a materials testing machine. Pressure drop measurements across the mimic, made using a differential pressure transducer, were obtained at five different injection speeds. Permeability of each mimic was calculated from these measurements2. Two more repeat permeability measurements were performed on each mimic.

Results: Repeat measurements were always within 12% of the mean value. For structure A the mean permeabilities were 1.26×10-7 and 1.82×10-7m2 for the 80 and the 90% porosity mimics respectively. The corresponding mean permeabilities for structure B were 1.92×10-7 and 2.86×10-7m2.

Discussion: These preliminary results indicate that higher permeabilities occur in structures with higher porosities, and with structures containing fewer trabeculae that are arranged obliquely. Since permeability is a determinant of cement infiltration, taking into account patient-specific bone architecture parameters may improve the safety and clinical outcome of vertebroplasty. Future experiments will clarify in more detail the architectural parameters that have greatest effect on permeability.

Introduction: Endplate fractures are clinically important. They are very common, are associated with an increased risk of back pain, and can probably lead on to intervertebral disc degeneration. However, such fractures tend to damage the cranial endplate much more often than the caudal. In this study, we test the hypothesis that the vulnerability of cranial endplates arises from an underlying structural asymmetry in cortical and cancellous bone.

Methods: Sixty-two “motion segments” (two vertebrae and the intervening disc and ligaments) were obtained post-mortem from human spines aged 48–92 yrs. All levels were represented, from T8–9 to L4–L5. Specimens were compressed to failure while positioned in 2–6o of flexion, and the resulting damage characterised from radiographs and at dissection. 2mm-thick slices of 94 vertebral bodies (at least one from each motion segment) were cut in the mid-sagittal plane, and in a para-sagittal plane through the pedicles. Microradiographs of the slices were subjected to image analysis to determine the thickness of each endplate at 10 locations, and to measure the optical density of the endplates and adjacent trabecular bone. Comparisons between measurements obtained in cranial and caudal regions, and in mid-sagittal and pedicle slices, were made using repeated measures ANOVA, with age, level and gender as between-subject factors. Linear regression was used to determine significant predictors of compressive strength (yield stress).

Results: Fracture affected the cranial endplate in 55 specimens and caudal endplate in 2 specimens. Endplate thickness was low centrally and higher towards the periphery. Cranial endplates were thinner than caudal, by 14% and 11% in mid-sagittal and pedicle slices respectively (p=0.003). Differences were greater in central and posterior regions. Cranial endplates were supported by trabecular bone with 6% less optical density (p=0.004) with this difference also being greatest posteriorly. Caudal but not cranial endplates were thicker at lower spinal levels (p=0.01). Vertebral yield stress (mean 2.21 MPa, SD 0.78 MPa) was best predicted by the density of trabecular bone underlying the cranial endplate in the mid-sagittal slices of the fractured vertebral bodies (r2 = 0.67, p=0.0006).

Conclusions: When vertebrae are compressed by adjacent discs, cranial endplates usually fail before caudal endplates because they are thinner and supported by less dense trabecular bone. These asymmetries in vertebral structure may be explained by the location of back muscle attachments to vertebrae, and by the nutritional requirements of adjacent intervertebral discs.

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.

Introduction: Vertebral body osteophytes are common in elderly spines, but their mechanical function is unclear. Do they act primarily to reduce compressive stress on the vertebral body, or to stabilise the spine in bending? How do they influence estimates of vertebral strength based on bone mineral density (BMD)?

Methods: Spines were obtained from cadavers aged 51–92 yrs (mean 77 yrs) with radiographic evidence of vertebral osteophytes (mostly antero-lateral). Twenty motion segments, from T5-T6 to L3–L4, were dissected and loaded a) in compression to 1.5 kN, and b) in bending to 10–25 Nm. Vertebral movements were tracked at 50 Hz using an optical MacReflex system. Bending tests were performed in random order, in flexion, extension, and lateral bending. Resistance to bending and compression was measured before and after surgical excision of all osteophytes. The bone mineral content (BMC) and density (BMD) of each vertebra was measured in the antero-posterior direction, using DXA. Density measurements were repeated after excision of all osteophytes. ANOVA was used to detect changes after osteophyte excision, and regression was used to examine the influence of osteophyte size and BMC.

Results: Removal of osteophytes reduced-vertebral BMD by 9% (SD 13%). Compressive stiffness was affected rather more, being reduced by an average 17% (p< 0.05). Bending stiffness was reduced in flexion and extension by 50% and 39% respectively (p< 0.01), and in left and right lateral bending by 41% and 49% respectively (p< 0.01). Osteophyte removal increased the neutral zone and range of motion in each mode of bending. Most mechanical changes were proportional to osteophyte mass, and to changes in BMC (p< 0.01).

Conclusions: Vertebral body osteophytes primarily stabilise the spine in bending, and do not play a major role in resisting compression. Animal models show that osteophytes grow in response to experimentally-induced instability, so their formation can be seen as mechanically-adaptive (restoring stability) rather than degenerative. The influence of typical osteophytes on compressive stiffness is greater than their influence on vertebral BMD (17% vs 9%) so predictions of vertebral compressive strength based on BMD measurements are likely to be under-estimates if osteophytes are present.

Introduction: Osteoarthritis (OA) of the apophyseal (facet) joints often appears to follow degenerative changes in the adjacent intervertebral discs. We test the hypothesis that facet joint OA is directly related to high compressive load-bearing resulting from disc degeneration.

Methods: Thirty six cadaveric thoraco-lumbar “motion segments” consisting of two vertebrae and the intervening disc and ligaments, were obtained from 22 human cadavers aged 64–92 yrs (mean 77 yrs). Each was subjected to a constant compressive load of 1.5 kN while the distribution of compressive stress was measured along the mid-sagittal diameter of the intervertebral disc, using a miniature pressure transducer, side-mounted in a 1.3 mm-diameter needle. Measurements of compressive “stress” were summed over area to give the compressive force resisted by the disc. This was subtracted from the applied 1.5 kN to indicate compressive load-bearing by the neural arch, including the apophyseal joints. After mechanical testing, the cartilage of each apophyseal joint surface was graded for degree of degeneration. Joints were then macerated, and each bony joint surface was scored for the following four degenerative changes, according to established criteria: marginal osteophytes, pitting, bony contour change, and eburnation. The four bone scores were summed and used to represent the severity of OA for that joint surface, and values were then averaged for the two facet joints (four surfaces) of each motion segment.

Results: Cartilage degeneration and summed bone scores both increased with age, and with each other (P< 0.01). Neural arch load-bearing ranged from 5%–96% (mean 45%) of the applied 1.5 kN compressive force, with values over 50% being found only in specimens with degenerated intervertebral discs. Facet joint summed bone score increased with neural arch load-bearing (P< 0.01), especially when the latter exceeded 50%.

Conclusion: High apophyseal joint load loading, equivalent to neural arch compressive load-bearing above 50%, is strongly associated with severe OA changes in the apophyseal joints. Associations were stronger for bone rather than cartilage changes, possibly because pathological load-bearing by the facet joints can occur between the tip of the inferior articular process and the adjacent lamina, substantially by-passing the articular (cartilage) surfaces.

Introduction: Vertebral body osteophytes are common in elderly spines, but their mechanical function is unclear. Do they act primarily to reduce compressive stress on the vertebral body, or to stabilise the spine in bending?

Methods: Spines were obtained from cadavers aged 51–92yrs (mean 77yrs) with radiographic evidence of vertebral osteophytes (mostly antero-lateral). Twenty motion segments, from T5-T6 to L3-L4, were dissected and loaded a) in compression to 1.5kN, and b) in bending to 10–25Nm. Vertebral movements were tracked at 50Hz using an optical MacReflex system. Bending tests were performed in random order, in flexion, extension, and lateral bending. Resistance to bending and compression was measured before and after surgical excision of all osteophytes. Bone mineral content (BMC) of osteophytes was measured using DXA. ANOVA was used to detect changes after osteophyte excision, and regression was used to examine the influence of osteophyte size.

Results: Compressive stiffness was reduced by an average 17% following osteophyte removal (p< 0.05). In flexion and extension, bending stiffness was reduced by 60% and 79% respectively (p< 0.01). In left and right lateral bending, stiffness was reduced by 42% and 49% respectively. Osteophyte removal increased the neutral zone and range of motion in each mode of bending, and changes were proportional to osteophyte mass and BMC (p< 0.01).

Conclusion: Vertebral body osteophytes primarily stabilise the spine in bending, and do little to resist compression, despite their considerable BMC. Predictions of vertebral compressive strength based on BMC measurements are likely to be over-estimates if large osteophytes are present.

Introduction: Kyphoplasty is a modification of the basic vertebroplasty technique used to treat osteoporotic vertebral fracture. This study evaluated whether kyphoplasty conferred any short-term mechanical advantage when compared with vertebroplasty.

Methods: Pairs of thoracolumbar “motion segments” were harvested from nine spines (42–84 yrs). Specimens were compressed to failure in moderate flexion to induce vertebral fracture. One of each pair underwent vertebroplasty, the other kyphoplasty. Specimens were then creep loaded at 1.0kN for 2 hours to allow consolidation. At each stage of the experiment, motion segment stiffness in bending and compression was determined, and the distribution of compressive “stress” was measured in flexed and extended postures by pulling a pressure- sensitive needle through the mid-sagittal diameter of the disc whilst under 1.5kN load. Stress profiles indicated the intradiscal pressure (IDP), stress peaks in the posterior annulus (SPP), and neural arch compressive load-bearing (FN).

Results: Vertebral fracture reduced bending and compressive stiffness by 37% and 55% respectively (p< 0.0001), and IDP by 55%–83%, depending upon posture (p< 0.001). SPP increased from 0.188 to 1.864 MPa in flexion, and from 1.139 to 3.079 MPa in extension (p< 0.05). FN increased from 13% to 37% of the applied load in flexion, and from 29% to 54% in extension (p< 0.001). Vertebroplasty and kyphoplasty partially reversed these changes, and their immediate mechanical effects were mostly sustained after creep-loading. No differences were found between vertebroplasty and kyphoplasty.

Conclusion: Kyphoplasty and vertebroplasty are equally effective in reversing fracture-induced changes in motion segment mechanics. In the short-term, there is no mechanical advantage associated with kyphoplasty.

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.