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

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

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 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.

Purpose of the study: To determine if cement type, bone mineral density (BMD), disc degeneration and fracture severity influence the restoration of spinal load-sharing following vertebroplasty.

Methods: Fifteen pairs of thoracolumbar motion-segments (51–91 yrs) were loaded to induce fracture. Vertebroplasty was performed so that one of each pair was injected with Cortoss, the other with Spineplex. Specimens were then creep loaded at 1.0kN for 2 hours. At each stage of the experiment, stress” profiles were obtained by pulling a pressure-sensitive needle through the disc whilst under 1.5kN load. From these profiles, the intradiscal pressure (IDP), posterior stress peaks (SP_P), and neural arch compressive load (F_N) were determined. BMD was measured using dual photon X-ray absorptiometry. Severity of fracture was quantified from height loss.

Results: Fracture reduced IDP (p< 0.001) but increased SP_P and F_N (p< 0.001). Following vertebroplasty, these effects were significantly reversed, and in most cases persisted after creep-loading. However, no differences were observed between PMMA- and Cortoss-injected specimens. After fracture, decreases in IDP, and increases in SP_P and F_N, were greater in specimens with lower BMD or greater height loss (p< 0.05). After vertebroplasty, specimens with lower BMD showed greater increases in IDP, and those with more degenerated discs showed greater reductions in SP_P (p< 0.05).

Conclusions: Changes in spinal load-sharing following fracture were partially restored by vertebroplasty, and this effect was independent of cement type. The effects of fracture and vertebroplasty were influenced by BMD, disc degeneration, and fracture severity. People with more severe fractures, low BMD and degenerated discs may gain most mechanical benefit from vertebroplasty.

Introduction: When the spine is subjected to compressive loading in-vivo and ex-vivo, there appears to be a predisposition for the cranial endplates to fracture before the caudal. We hypothesise that this fracture pattern arises from an underlying structural asymmetry. Endplate damage is common in elderly people, and closely related to disc degeneration and pain.

Methods: 47 human thoracolumbar motion segments aged 62–90 yrs were compressed to failure while positioned in moderate flexion. Damage was assessed from radiographs and at dissection. Two 2mm-thick slices were obtained from each vertebral body in the sagittal plane. Microradiographs were analysed to yield the following: thickness and image greyscale density (IGD) of the cranial and caudal cortex at 10 locations (94 vertebrae), and IGD of the cancellous bone in three regions adjacent to each endplate (34 vertebrae).

Results: Endplate damage occurred cranially in 39/47 vertebrae, and caudally in 4/47. Mean thickness of cranial and caudal endplates was 0.77mm (SD 0.27) and 0.90mm (SD 0.29) respectively (p=0.01). Thinnest regions were located centrally on cranial endplates. Endplate thickness increased at lower spinal levels for caudal (p< 0.01) but not cranial endplates. IGD was similar in cranial and caudal endplates, but IGD of trabecular bone adjacent to the endplate was 3–8% lower cranially than caudally (P< 0.01).

Discussion: In elderly spines, cranial endplates fracture more readily because they are thinner and supported by less dense trabecular bone. Endplate thickness may be minimised by the need to allow nutritional access to adjacent discs, and the vulnerability of cranial endplates may be associated with asymmetries in blood supply, or proximity to the pedicles.

Introduction: Osteoporotic fractures in elderly people are usually attributed to hormonal changes and inactivity. But why should the anterior vertebral body be affected so often?

Materials and Methods: Forty-one cadaveric thoraco-lumbar motion segments aged 62–94 yrs were loaded to simulate upright and flexed postures. A pressure transducer was used to measure “stress” inside the disc, and calculations showed how compressive loading was distributed between the neural arch, and the anterior and posterior halves of the vertebral body. Compressive strength was measured in flexed posture. Regional volumetric bone mineral density (BMD) and histomorpho-metric parameters were measured.

Results: Upright posture. Compressive load-bearing by the neural arch increased with grade of disc degeneration, averaging 52+25% in specimens with grade 3 or 4 discs. In these same specimens, the anterior half of the vertebral body resisted only 16+18% of the applied load. Relative unloading of the anterior vertebral body was associated with low BMD and with histomorphometric evidence of inferior bone quality. Flexed posture. Flexion always transferred loading to the anterior half of the vertebral body, so that it resisted 55+17% in specimens with grade 3/4 discs. Compressive strength measured in this posture was most closely proportional to BMD in the anterior vertebral body (r² = 0.75), and inversely proportional to neural arch load-bearing in the upright posture (r² = 0.39).

Conclusion: Disc degeneration causes the anterior vertebral body to be unloaded in habitual upright postures, reducing bone density and quality within it. This predisposes to wedge fracture when the spine is flexed.

Introduction: Vertebral bodies and intervertebral discs resist most of the compressive force acting on the spine. However, experiments on lumbar spines have shown that apophyseal joints can resist more than 50% of applied compression, and that the proportion varies with spinal level, disc narrowing, and posture. In the cervical spine, the situation is likely to be complicated by the presence of uncovertebral joints on the lateral margins of the disc. Load-sharing is important because it influences injury risk, and predisposition to degenerative changes. The present study aims to characterise compressive load-sharing in the cervical spine.

Methods: Sixteen cervical motion segments, consisting of two vertebrae and the intervening disc and ligaments, were dissected from nine cadaveric spines, aged 48-77 yrs (mean 63 yrs) which had been stored at -17degC. Specimens were subjected to 200N of compression while the distribution of compressive ‘stress’ was measured along the mid-sagittal diameter of the disc, using a pressure transducer side-mounted in a 0.9mm-diameter needle. ‘Stress profiles’ effectively were integrated over area to calculate the total compressive force acting on the disc. Experiments were performed with each specimen in flexion, extension and neutral posture. They were repeated after creep compressive loading (2 hrs at 150N) to simulate diurnal loading in life, and again following removal of the apophyseal joints. Eight specimens were re-tested following bi-lateral removal of the uncovertebral joints.

Results: Creep loading reduced disc height by an average 0.64mm (approximately 12%). Creep reduced overall computed disc loading by 14% and 25% in neutral and extended postures respectively (P< 0.005). Apophyseal joint removal increased disc loading in extension (only) by 14% (P< 0.05). Uncovertebral joint removal further increased disc loading in flexed, neutral and extended postures by 28%, 33% and 21% respectively (P< 0.05).

Conclusion: Creep loading of the cervical spine transfers loading to the apophyseal joints and uncus. The former effect is small, and significant only in extended postures. The latter effect is larger, and is greatest in flexed and neutral postures.

Introduction: Epidemiology suggests that an intrauterine nutrient restriction increases the likelihood of osteoporosis in later life, possibly due to differences in bone structure and strength. We hypothesise that, in an ovine model, early nutritional compromise reduces vertebral cancellous bone density and cortical thickness, and thereby reduces vertebral compressive strength.

Materials and methods: Lumbar spines were dissected from 8 sheep (6 male, 2 female: mean age 2.7 yrs). Spines were divided into different groups, based on the early diet of the sheep: group CC received a control diet, group IU received low protein in utero, and group PN received low protein both in utero and postnatally. Fifteen motion segments (consisting of two vertebrae and the intervening disc and ligaments) were prepared from the spines, and compressed to failure using a hydraulically-controlled materials testing machine to obtain yield strength. 1mm-thick bone slices were taken from the mid-sagittal and para-sagittal regions of each vertebral body and micro-radiographed. Digital images of the micro-radiographs were analysed to obtain the cancellous bone density in anterior and posterior regions, and the cortical thickness in the anterior, posterior, superior and inferior regions. Repeated measures ANOVA was used to test for differences in parameters at the different locations, and between the groups.

Results: The anterior cortex was 28% thinner for the IU group, and 23% thinner for the PN group compared to controls (both p< 0.001). In the PN group, the superior cortex was also 18% thinner than controls (p< 0.02). There was no significant difference between cancellous bone density in either region. Yield strength was 16% lower in the IU group compared to controls, but this did not reach significance.

Discussion: In the nutritionally compromised groups, cortical thickness was lower in regions of the vertebral body where fractures often occur in elderly people. However, the reduction in cortical thickness is not accompanied by a significant reduction in compressive strength in the sheep model. These findings suggest that the well-maintained cancellous bone protects the vertebra from fracture.

Introduction: We have shown that vertebroplasty increases stiffness and partly restores normal load-sharing in the human spine following vertebral fracture. The present study investigated how this restorative action is influenced by type of cement injected, bone mineral density (BMD), and fracture severity.

Methods: Fifteen pairs of thoracolumbar motion-segments (51–91 yrs) were loaded on a hydraulic materials testing machine to induce vertebral fracture. One from each pair underwent vertebroplasty with polymethyl-methacrylate (PMMA) cement, the other with a biologically- active resin (Cortoss). Specimens were then creep loaded at 1.0kN for 2 hours. At each stage of the experiment, bending and compressive stiffness were measured, and ‘stress’ profiles were obtained by pulling a pressure-sensitive needle through the disc whilst under 1.5kN load. Profiles indicated the intradiscal pressure (IDP) and neural arch compressive load (FN). BMD was measured using dual photon X-ray absorptiometry. Severity of fracture was quantified from height loss. Changes were compared using repeated measures ANOVA.

Results: Fracture reduced bending and compressive stiffness by 31% and 41% respectively (p< 0.0001), and IDP by 43%–62%, depending upon posture (p< 0.001). In contrast, FN increased from 14% to 37% of the applied load in flexion, and from 39% to 61% in extension (p< 0.001). Following vertebroplasty, these effects were significantly reversed, and in most cases persisted after creep-loading. No differences were observed between PMMA- and Cortoss-injected specimens. The decrease in IDP and increase in FN after fracture were correlated with BMD in flexion and with height loss in extension (p< 0.01). After vertebroplasty, restoration of IDP and FN in flexion were correlated with their loss after fracture (p< 0.01). The former was also related to BMD (p< 0.05).

Conclusions: Changes in spinal load-sharing following fracture were partially restored by vertebroplasty, and this effect was independent of cement type. The effects of fracture and vertebroplasty on spinal load-sharing were influenced by severity of fracture, and by BMD.

These findings suggest that people with more severe fractures and low BMD may gain most mechanical benefit from vertebroplasty.

Introduction: There are extensive differences in structure and composition between cervical and thoracolumbar discs, yet practically nothing is known about the time-dependent “creep” behaviour of cervical discs.

Methods: 41 cadaveric cervical motion segments aged 48–89 yrs were subjected to a static compressive load of 150N for 2 hrs. Specimen height was recorded by the displacement of the actuator of the testing machine. Digitized radiographs were analysed to obtain dimensions of the vertebrae and discs. A three-parameter solid viscoelastic model was fitted to experimental data using nonlinear regression. Model parameters represent compressive stiffness of the wet tissue (E₂) and of the drained solid matrix (E₁), and tissue viscosity (η₁).

Results:Model and experimental data were in good agreement (r²> 0.98) and the average absolute error was always < 2%. E₁ was 11% and 39% lower than published values for thoracic and lumbar discs, respectively, whereas E₂ was 43% and 53% higher. The ratio E₂/E₁ for cervical discs (1.63) was greater than for thoracic (1.01) and lumbar (0.66) discs. η₁ for cervical discs was 108% and 21% higher than in thoracic and lumbar discs, resulting in a creep rate (E₁/η₁) which was lower by 51% and 43% respectively. Comparisons between younger (mean age 58 yrs) and older (79 yrs) cervical discs showed that in the latter, η₁ was reduced by 32% (p=0.01), E2 reduced by 18% (p=0.06), whereas E₁/η₁ was increased by 47% (p=0.02).

Discussion: Cervical discs appear to resist water loss more than thoracolumbar discs, but this resistance falls in old age.

Introduction: To evaluate whether a biologically-active cement “Cortoss” confers any short-term mechanical advantages when compared with a polymethylmethacrylate bone cement “Spineplex” which is currently in widespread use.

Methods: Two thoracolumbar motion segments were harvested from each of six spines (51 – 82 yrs). Specimens were compressed to failure in moderate flexion to induce vertebral fracture. Pairs of specimens were randomly assigned to undergo vertebroplasty with either Cortoss or Spineplex. Compressive stiffness and compressive stress on the disc were measured before and after fracture, and after vertebroplasty. Compressive stress was measured by pulling a pressure- sensitive needle through the mid-sagittal diameter of the disc whilst under 1.5kN load. Intradiscal pressure (IDP), peak stress in the annulus and neural arch compressive load were obtained from the resulting stress profiles.

Results: No differences in IDP, annulus stress, neural arch load bearing and compressive stiffness were observed between the groups before fracture, after fracture or after vertebroplasty (p> 0.05). After fracture, IDP decreased from 1.02 to 0.68 MPa in flexion and from 0.75 to 0.34 MPa in extension (p< 0.05), neural arch load bearing increased from 13% to 37% of the applied load in flexion (p< 0.05), and compressive stiffness decreased from 2441 to 1478 N/mm (p< 0.05). After vertebroplasty, these changes were largely reversed: IDP increased to 0.45 MPa in extension (p< 0.05), neural arch load bearing fell to 20% in flexion (p=0.1), and compressive stiffness increased to 1799 N/mm (p< 0.05).

Conclusion: Vertebroplasty using either Cortoss or Spineplex was equally effective in reversing fracture-induced changes in motion segment mechanics.

Introduction: The cervical spine can be severely loaded in bending during sporting injuries and ‘whiplash’. Compressive loading could also be high if some advanced warning of impact stimulated vigorous (‘protective’) contraction of the neck muscles. Combined bending and compression can cause some lumbar discs to herniate in-vitro (1) but the outcome depends on spinal level, and may not be applicable to cervical discs. We test the hypotheses: a) that cervical discs can prolapse in-vitro, and b) that prolapse leads to irregular stress distributions inside the disc.

Material and methods: Human cervical ‘motion segments’ (two vertebrae and intervening soft tissues) were obtained from cadavers aged 51–88yrs. Specimens were secured in cups of dental stone and subjected to static compressive loading (150N) for 20s. During this time, the distribution of vertically-acting compressive ‘stress’ was recorded along the postero-anterior diameter of the disc by pulling a 0.9mm-diameter pressure transducer through it (2). Injury was induced by compressing each specimen at 1mm/s while positioned in 20 deg of flexion, 15 deg of extension, or 8 deg of lateral bending. The distribution of compressive stress within the disc was then re-measured. Specimens were sectioned at 2mm intervals in order to ascertain soft tissue disruption.

Results: In all six specimens tested to date, one or both of the apophyseal joint capsules were ruptured by the complex loading. Intervertebral disc prolapse also occurred in all six specimens, with the herniated nucleus appearing on the anterior, posterior and postero-lateral disc surface in extension, flexion and lateral bending respectively. All modes of failure affected intradiscal stresses: on average, nucleus pressure decreased by 75% (STD 7%), while stress concentrations in the annulus increased by 130% (STD 21%).

Discussion: These preliminary results confirm that severe complex loading can cause cervical discs to prolapse. No particular state of disc degeneration is required, provided the loading is sufficiently severe. Indeed, the altered stress distributions suggest that cell-mediated changes would probably follow prolapse.

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.

Introduction: ‘Stress profilometry’ involves pulling a pressure transducer through a loaded intervertebral discs in order to characterise the intensity of loading within it. The technique has been used to explore how stress distributions vary with age, spinal level, degeneration, creep loading, and injury. However, can the output of the strain-gauged transducer (which is calibrated in a fluid) really quantify stress perpendicular to its membrane when inserted into the fibrous matrix of degenerated discs?

Methods: Thirteen full-depth cylinders, 7mm in diameter, were cut from inner, middle and outer regions of the anterior and lateral annulus of two human upper-lumbar discs aged 74 and 82 yrs. Specimens were confined within a metal cylinder of internal diameter 7 mm. Two vertical slots on opposite sides of the metal cylinder allowed a pressure transducer, side-mounted near the tip of a 0.9 mm-diameter needle, to be pulled through the annulus sample. Constant compressive loading was applied for 20s to the top of the annulus sample, using a plane-ended 6.9 mm-diameter indenter, while the transducer was pulled through the sample. Transducer output was sampled at 25Hz. ‘Stress profiles’ were repeated with the transducer orientated vertically and horizontally, and with 6-21 values of compressive load, corresponding to stresses up to 3MPa. Average values of measured ‘stress’ were compared to applied stress (compressive force/indenter area).

Results: Measured (average) vertical compressive stress was linearly related to applied stress, with Rsq values averaging 0.97. The gradient of the line averaged 0.98 (range 0.77 – 1.28) indicating that measured stress values approximated to applied stress, and were not merely proportional to it. For horizontal measurements, the Rsq and gradient averaged 0.97 and 0.92 respectively. Abnormal results in 3/13 specimens appeared to be affected by transducer damage and were disregarded.

Conclusion: Stress profilometry can quantify compressive stress within the annulus of degenerated intervertebral discs. This fibrous tissue appears to be sufficiently deformable to allow efficient coupling of stress between the matrix and transducer membrane.

Introduction: Cement augmentation of osteoporotic vertebral fractures by vertebroplasty can alleviate pain, possibly by restoring normal load-sharing to the affected motion segment. Fracture is known to decrease vertebral compressive stiffness (1), and also affects the compressive stress distribution acting on the vertebral body, causing stress concentrations to appear in the adjoining intervertebral discs (2). We hypothesise that vertebro-plasty can reverse these fracture-induced changes.

Methods: Nineteen cadaver thoraco-lumbar motion segments (64–90 yrs) were used. Each was mounted on a hydraulic materials testing machine and induced to fracture by compressive overload in moderate flexion. Vertebroplasty was performed by injecting 7 cc of poly-methylmethacrylate cement (Simplex P, Stryker Howmedica, NJ) into the fractured vertebral body. Specimens were then creep loaded at 1.5 kN for 1 hour to allow consolidation. Before and after each procedure, profiles of the compressive stress distribution were obtained by pulling a miniature pressure transducer along the mid-sagittal diameter of the intervertebral disc whilst it was compressed at 1.5kN. Using these profiles, stress peaks in the anterior and posterior annulus were measured by subtracting the nucleus pressure from the peak stress in each region (2). Compressive stiffness of the motion segment was also measured before and after vertebroplasty from the tangent of the load-displacement curve at 1 kN. Changes were compared using ANOVA.

Results: Following fracture, motion segment compressive stiffness was reduced by 37% from 2478 N/mm, STD 966N/mm, to 1583 N/mm, STD 585 N/mm (p = 0.0001), stress peaks in the posterior annulus were increased by 139% from 0.24 MPa, STD 0.24 MPa, to 0.57 MPa, STD 0.47 MPa (p = 0.016), and stress peaks in the anterior annulus showed no significant change. The decrease in compressive stiffness was significantly correlated with the increase in the size of the posterior stress peak (Rsq = 0.65, p< 0.001). Following vertebroplasty and subsequent creep loading, compressive stiffness was increased to 2156 N/mm, STD 718 N/mm, and stress peaks in the posterior annulus were reduced to 0.31 MPa, STD 0.43 MPa. These changes were again highly correlated with each other (Rsq = 0.68, p< 0.001). Both compressive stiffness and the size of posterior stress peaks after vertebroplasty showed no significant difference when compared to pre-fracture values.

Discussion: Fracture reduces the ability of vertebrae to resist deformation, thereby decreasing compressive stiffness. These changes impair the disc’s ability to press evenly on the vertebral body, giving rise to increased stress peaks in the posterior annulus. Vertebroplasty can reverse these fracture induced changes by increasing vertebral compressive stiffness which acts to restore pressure in the nucleus. This enables the disc to press more evenly on the vertebral body and thereby reduces the size of stress peaks in the posterior annulus. This restoration of normal load-sharing may possibly contribute to pain relief in patients undergoing this procedure.

Introduction: Age-related hormonal changes and inactivity lead to systemic bone loss and osteoporotic fractures. However, it is not clear why the vertebral body should be affected so often, or why its anterior region should characteristically sustain a “wedge” deformity. We hypothesise that intervertebral disc degeneration in elderly spines leads to altered spinal load-sharing in such a manner that the anterior region of the vertebral body becomes vulnerable to injury.

Methods: Forty thoraco-lumbar “motion segments”, consisting of two vertebrae and the intervening disc and ligaments, were obtained from cadaver spines aged 62–94 yrs. Volumetric bone mineral density (BMD) was measured for various regions of each vertebra using a Lunar Piximus DXA scanner. The distribution of the applied compressive force (1.5 kN) between the anterior and posterior halves of the vertebral body was calculated by pulling a needle-mounted pressure transducer along the sagittal midline of the adjacent disc. Pressure measurements were integrated over area to give force. Anterior and posterior disc forces were subtracted from the applied 1.5 kN to indicate loading of the neural arch. Measurements were repeated with the specimens positioned to simulate various postures in life. The strength of each motion segment was determined by compressing it to failure while positioned in a forward stooped posture. Disc and vertebral morphology were assessed from radiographs, and from digital photographs of tissue sections.

Results: Load-bearing by the neural arch in erect posture increased in the presence of intervertebral disc degeneration, and was inversely proportional to the average height of the disc (P< 0.01). High neural arch load-bearing was associated with relatively low BMD in the anterior vertebral body (P< 0.01), and with low compressive strength (P< 0.0001). BMD in the anterior region of the vertebral body was the best univariate predictor of compressive strength (R² = 0.78). Stepwise multiple linear regression showed that 86% of the variance in compressive strength could be explained by the following: anterior vertebral body BMD, vertebral body X-sectional area, and neural arch load-bearing (% of applied load). Forcing age, gender and spinal level into the model did little to improve the prediction.

Discussion and Conclusions: Results strongly support our hypothesis. Evidently, intervertebral disc degeneration and narrowing cause the neural arch to “stress shield” the anterior vertebral body whenever the spine is held erect. This leads to reduced BMD in the anterior vertebral body, weakening the spine when it is loaded in a stooped posture. The small age-dependence of results can be attributed to the relatively narrow age range of specimens tested. Vertebral fracture risk can best be assessed from BMD measured in the anterior half of the vertebral body.

Introduction: Back pain can be associated with erratic and/or excessive movements between adjacent vertebrae. Such movements are normally resisted by intervertebral ligaments, and yet few back pain patients report traumatic rupture of ligaments prior to their onset of symptoms. We suggest that two other mechanisms can lead to ligamentous slack and therefore to spinal instability. The first of these is the age-related dehydration of intervertebral discs, which reduces disc volume and height, bringing the vertebrae closer together. The second mechanism is disc decompression following vertebral endplate fracture, which is a common injury but one which is difficult to detect. Decompression allows the disc to bulge and lose height, increasing ligamentous laxity. In the present experiment, we simulated disc dehydration and endplate injury in cadaveric spines, and compared their effects on spinal (in)stability.

Methods: Cadaveric thoraco-lumbar motion segments were subjected to complex, continuous loading using a hydraulic materials testing machine (Zwick-Roell, Leominster, UK) to simulate full flexion and extension movements in vivo. Vertebral movements were recorded at 50 Hz using the optical “MacReflex” video capture system (Qualisys AB, Sweden). Experiments were repeated following 2 hours of compressive “creep” loading at 1500 N, which reduced disc water content by an amount similar to the aging process, and again following compressive overload sufficient to fracture a vertebral endplate. Bending moment-rotation curves were used to quantify the “neutral-zone” (NZ), range of motion (ROM), and bending stiffness (BS).

Results: Preliminary results (10 motion segments) showed that specimen height was reduced by 1.0 mm (STD 0.3 mm) following creep, and by a further 1.5 mm (STD 0.5 mm) following endplate fracture. Mean ROM in flexion increased from 6.5 deg initially, to 8.9 deg after creep and 12.6 deg after fracture. Corresponding values for NZ in flexion were 4.6 deg, 6.6 deg and 9.5 deg. BS decreased from 28.9 to 23.0 to 15.2 Nm/deg. All changes were statistically significant (p< 0.03). NZ, ROM and BS values in extension were initially 1.6 deg, 4.0 deg and 32.7 Nm, respectively, but no significant changes were noted following creep and endplate fracture. Total ROM (flexion + extension) increased from 10.5 deg to 16.7 deg degrees following both interventions.

Discussion: Results suggest that disc dehydration, which is a normal feature of aging, increases NZ and ROM in flexion, presumably because accompanying disc height loss allows more slack to the posterior intervertebral ligaments. Endplate fracture, which can occur under physiological loads in osteoporotic elderly spines, has an even greater effect. Extension movements were little affected, presumably because loss of disc height also increases the risk of impaction between neural arches.

Conclusion: We conclude that age-related disc dehydration, and relatively minor endplate injury, can increase segmental motion and cause substantial mechanical instability to the thoraco-lumbar spine.

Cortical porosity is a useful evaluator of bone since it is sensitive to changes in bone turnover. The aim of this study was to evaluate cortical bone porosity of human vertebrae samples using Scanning Acoustic Microscopy (SAM). Currently the common techniques used to determine bone porosity are histomorphometry or scanning electronmicrosopy images. Both methods require extensive preparation of the bone samples. SAM represents a new technique with the great advantage of minimal sample interference since the bone is imaged in water, or saturated, and requires just one flat surface which is scanned (but not contacted) by the transducer. 46 specimens between the ages of 64–90 years were randomly selected and ground before SAM imaging of was carried out using a 400 MHz transducer. For each sample posterior and anterior sections of the cortical bone were scanned several times, and the porosity measured using Scion image software to process the images. It was possible to image the entire anterior or posterior cortex in a single image with 4 mm spatial resolution. Measured porosity was in the region 5 % – 21 %, and showed a significant increase with age for the female specimens but no age dependence in the male specimens. At low porosity (< 6 %) vertebral compressive strength was uncorrelated with porosity. However, at higher porosities strength was highly correlated with porosity. (As would be expected, strength decreased with increasing porosity). High frequency SAM has potential for future bone characterisation, particularly where it is desirable to correlate local measurements of material properties such as nanohardness or microhardness, with microstructure.

Introduction : We have shown previously that, in the presence of severe disc degeneration, the neural arch can resist up to 80% of the compressive force acting on the spine. We hypothesise that the inferior articular processes can then act as a “pivot” during backward and lateral bending movements.

Materials and Methods: Twenty-one motion segments (T8–9 to L4–5) were obtained from spines aged 48–90yrs. Specimens were loaded rapidly to simulate flexion, extension and lateral bending, while vertebral movements were tracked using an optical MacReflex system. The varying position of the centre of rotation (CoR) during these movements was calculated. Experiments were repeated after a treatment designed to simulate two effects of severe disc degeneration: creep loading to dehydrate the disc, and compressive overload to fracture a vertebral endplate and decompress the nucleus.

Results: In flexion, the CoR was usually located just below the inferior endplate of the disc, close to the antero-posterior midline, and in extension it moved an average 4.6 mm posteriorly. The additional “disc degeneration” treatment increased the variability of the CoR within and between specimens. It also moved the CoR an average 10.7mm posteriorly during extension movements (P< 0.001), so that in some specimens it was near the tip of the inferior articular processes.

Discussion: Severe disc decompression and narrowing increase translational (gliding) movements between adjacent vertebrae so that the effective CoR becomes more variable. During extension movements, the CoR can move so far posteriorly that the vertebrae can effectively “pivot” about the inferior articular processes.

Introduction: We hypothesise that disc degeneration is a major cause of segmental instability in elderly spines. Accordingly, we simulated two mechanical features of disc degeneration on cadaveric spines, and measured their effects on spinal movements.

Methods: Twenty-one motion segments (T8–9 to L4–5) were obtained from spines aged 48–90yrs. Specimens were loaded rapidly to simulate full spinal bending movements in vivo, while vertebral movements were tracked using an optical MacReflex system. Intradiscal stresses were investigated using “stress profilometry”. Experiments were repeated following compressive creep loading (which reduced disc water content by an amount similar to the aging process) and again following a compressive overload cycle which fractured a vertebral endplate and decompressed the nucleus. MacReflex data were used to quantify the neutral-zone (NZ), the range of motion (ROM), and the range of translational (gliding) movements.

Results Creep and endplate fracture both reduced disc height, and generated stress concentrations within the posterior annulus. Both treatments increased NZ, ROM and translational movements in flexion and lateral bending, but not in extension. Endplate fracture markedly increased the “instability index” (NZ/ROM) in flexion.

Discussion Disc “degeneration” increased all measures of spinal instability during flexion and lateral bending. Disc decompression in particular created a large NZ in which the spine had negligible resistance to bending. In life, muscle action would prevent the spine “wobbling” within this range of movement. Results in extension suggest impaction between the neural arches. Back pain associated with spinal instability could arise from stress concentrations in the annulus and neural arches, or from abnormal muscle activity.

Introduction Vertebral fractures in the elderly frequently involve the anterior and superior regions of the vertebral body. We hypothesise that vertebral fracture patterns reflect regional variations in bone mineral density (BMD).

Methods Nineteen motion segments (aged 48–90 yrs) were obtained from thoracic and lumbar regions of cadaver spines. Specimens were compressed to failure while positioned in moderate flexion (to simulate someone lifting in a stooped posture). Superior and inferior vertebrae were dissected and the site of fracture identified by visual inspection. The volume of each vertebral body was measured by water immersion, and BMD was measured using dual X-ray absorptiometry (DXA). BMD was also calculated for the following regions: superior and inferior end-plates; upper, middle and lower thirds of the vertebral body between the end-plates; anterior, middle and posterior thirds of the vertebral body.

Results In 16 of the 19 specimens, an obvious fracture was located in the anterior or central region of the superior end-plate of the inferior vertebral body, accompanied by collapse of supporting trabeculae. BMD of the superior end-plate was significantly lower than that of the inferior end-plate. Similarly, BMD of the upper third of the vertebral body was less than that of the lower third, and BMD increased significantly from anterior to posterior regions in the vertebral body.

Discussion Low BMD in the superior and anterior regions of old vertebral bodies predisposes them to fracture. Altered load-sharing in old spines secondary to disc degeneration may explain these regions of low BMD.

Introduction: Intradiscal electrothermal therapy (IDET) is a novel minimally invasive treatment for discogenic back pain. It involves inserting a catheter into discs which are suspected of being symptomatic in order to heat certain regions of the disc matrix and thereby influence the pain process. The clinical efficacy of IDET appears to be variable, and the scientific evidence suggests that the heating effect on disc tissues is very local to the catheter. We test the hypothesis that IDET can affect the internal mechanical functioning of lumbar intervertebral discs.

Methods: Eighteen cadaveric lumbar “motion segments” (aged 64–97 yrs) were used, 16 of which had degenerated intervertebral discs. Following incubation at 37°C, a miniature pressure transducer, side mounted in a 1.3mm diameter needle, was used to measure the distribution of compressive “stress” along the mid-sagittal diameter of each disc while it was compressed at 1.5 kN. Measurements were repeated in three simulated postures. IDET was then performed, using biplanar radiography to confirm placement of the heating element, and an independent thermocouple to measure temperature in the inner lateral annulus. Stress profilometry was repeated immediately after IDET.

Results: Peak temperatures in the inner lateral annulus during IDET averaged 40°C (STD 2.3°). Differences between stress measurements repeated before IDET never exceeded 8% (NS), and a sham IDET procedure produced no consistent changes. After IDET, pressure in the nucleus fell significantly by 6–13%, and stress peaks in the annulus were reduced (P< 0.008). In 12/18 specimens, annulus stress peaks were reduced by more than 8%, and in these “responders”, the mean reduction was 78%. Stress concentrations were increased by more than 8% in two specimens.

Conclusion: IDET has a significant but inconsistent affect on compressive stresses within intervertebral discs. These results may partly explain the variable clinical success of IDET.

Introduction: Peripheral rim tears in the annulus fibrosus are a common finding in autopsy specimens, and animal experiments suggest that they lead eventually to degenerative changes throughout the disc. We test the hypothesis that injury to the outer annulus decompresses the nucleus, thereby providing a progressive stimulus for disc degeneration.

Methods: Seven human cadaveric lumbar “motion segments” aged 49–70 yrs were compressed at 2 kN while the distribution of compressive stress was measured in each disc by pulling a 1.3 mm-diameter pressure transducer along its mid-sagittal diameter. Measurements were repeated after “rim tears” were simulated by 10 mm-deep scalpel cuts into the anterior annulus, as follows. 1st cut: horizontal, 15 mm right lateral; 2nd cut: vertical, 15 mm left lateral; 3rd cut: horizontal, midline (through the transducer needle track). Stress measurements were repeated a final time following compressive overload sufficient to fracture the endplate.

Results: “Rim tears” had negligible effect on compressive stress distributions more than 15mm from the scalpel cut, and nucleus pressure fell by only 1.0% (STD 1.3%, NS). However, compressive stresses in the outer annulus adjacent to the cut were greatly reduced, and a steep stress gradient appeared in the middle annulus. The effective decrease in the A-P diameter of the disc was 7.1% (STD 1.7%, P< 0.01). Endplate fracture reduced nucleus pressure by 36.1% (STD 16.7%, P< 0.001).

Discussion: Stress gradients generated in the middle annulus could cause the “rim tear” to progress inwards until it reached the nucleus, at which point it might decompress it. However, the present results suggest that injuries to the outer annulus are unlikely to have any direct effect on the pressure in, or metabolism of, the nucleus pulposus. This is in contrast to injuries to the vertebral endplate, which do affect the nucleus directly.

Introduction: Little is known about how the cervical spine resists the high complex loading to which it is often subjected in life. In this study, such loading was applied to cadaveric cervical motion segments in order to a) measure their strength in forward and backwards bending, b) indicate which structures resist bending most strongly, and c) indicate how compressive injury influences the bending properties.

Methods: Ten human cervical spines aged 65–88yrs were obtained post-mortem, dissected into 14 motion segments, and stored at −20°C. Subsequently, motion segments were defrosted and secured in dental plaster for testing on a hydraulic materials testing machine. An optical motion capture system recorded specimen movement simultaneously. Specimens were loaded in 2.5sec in combined bending and compression to reach their elastic limit in flexion, and then extension. Experiments were repeated following creep loading, removal of spinous processes, removal of apophyseal joints, and vertebral body compressive damage.

Results: On average, full flexion was reached at an angle of 7.2° and a bending moment of 6.8Nm. Full extension occurred at 9.2° and 9.0Nm. Creep loading reduced specimen height by 0.37mm, increased flexion by 1.5° (P< 0.01) but had little effect on extension. After creep, resistance to flexion came from the spinous processes and related ligaments (46%), apophyseal joints (30%), and disc (24%). Resistance to extension came from spinous processes (23%), apophyseal joints (45%), and disc (32%). The compressive strength of discvertebral body specimens was 1.87kN (STD 0.63kN). Compressive damage reduced specimen height by 0.83mm (STD 0.29mm). This reduced the disc’s resistance to flexion by 44% and extension by 18%.

Conclusion: Cervical motion segments have approximately 20% of the bending strength, and 45% of the compressive strength, of lumbar specimens of similar age. The relative weakness of the cervical spine in bending may influence the patterns of injury seen in “whiplash”.

Introduction: Cement augmentation of osteoporotic vertebral fractures by vertebroplasty can alleviate pain, although the mechanism remains unknown. We hypothesise that vertebral fracture reduces loading by the vertebral body, and that vertebroplasty reverses this effect.

Methods: Nineteen thoracolumbar motion segments (64 – 90 yrs) were used. Specimens were compressed at 1.5kN in moderate flexion and extension while intradis-cal stress profiles were obtained by pulling a miniature pressure transducer along the mid-sagittal diameter of the disc (1). Vertebral fracture was induced by compressive overload in moderate flexion. Vertebroplasty was then performed by injecting polymethylmethacry-late cement into the anterior vertebral body. Stress profiles were repeated after fracture, and after vertebroplasty.

Stress concentration in the annulus was calculated by subtracting the nuclear pressure from the maximum stress in the annulus. Neural arch compressive load was obtained by subtracting the disc compressive force, calculated by integrating intradiscal stress over area, from the applied 1.5kN (1).

Results: Fracture increased the stress concentration in the annulus from 0.21 to 0.58MPa in flexion (p< 0.01) and from 0.02 to 0.20MPa in extension (p< 0.05). It also increased neural arch load bearing from 9% to 27% of the applied load in flexion (p< 0.01), and from 53% to 70% in extension (p< 0.01). Following vertebroplasty, these changes were largely reversed: in flexion, stress concentrations in the annulus decreased to 0.36MPa and neural arch load-bearing fell to 5% (p< 0.01). Similar, non-significant trends were observed in extension.

Discussion: Vertebral fracture reduces load-bearing by the vertebral body, and increased compressive loading of the neural arch. Vertebroplasty goes some way to reversing these effects, and significantly decreased stress concentration in the annulus and loading of the neural arch in flexion. This could contribute to pain relief in patients undergoing this procedure.

Introduction: Osteoporotic fractures affect certain bones more than others, suggesting that systemic bone loss is not the only underlying cause. We have shown that age-related intervertebral disc degeneration causes the anterior vertebral body (VB) to be stress-shielded in erect postures, and yet severely loaded when the spine is flexed (1). We hypothesise that this unequal loading causes exaggerated bone loss from the anterior vertebral body, making it vulnerable to fracture when the spine is heavily loaded in a forward stooping (flexed) posture.

Materials and Methods: Regional volumetric bone mineral density (BMD) was measured in 35 thoracolumbar motion segments (aged 64–92 yrs) using dual-energy x-ray absorptiometry. The distribution of compressive stress was measured along the mid-sagittal diameter of each intervertebral disc using a miniature pressure transducer. Stresses were integrated over area to give the compressive force acting on the anterior and posterior halves of the VB (1). Motion segment compressive strength was measured in moderate flexion.

Results: BMD of the anterior half of the VB was 26% (STD 13%) lower than that of the posterior half (p< 0.0001), was correlated with % load on the anterior VB in erect posture (r²=0.48, p< 0.0001), and was a better predictor of motion segment compressive strength (in flexion) than was BMD of the whole vertebral body (r² = 0.79 compared to r² = 0.59).

Conclusion: These results clearly support our hypothesis. It appears that intervertebral disc degeneration leads to exaggerated bone loss from the anterior VB, leaving it more vulnerable to fracture when the spine is flexed. Future work aims to confirm this important result on a larger number of specimens, and to compare the relative importance of disc degeneration and overall bone loss on vertebral compressive strength.

Pollintine P et al (2001). SBPR Annual Meeting, Bristol. Backcare Research Award 2002.

Numerous studies have examined the biomechanical properties of the vertebral body following PMMA cement augmentation for the treatment of osteoporotic vertebral body fractures. To date there is no published literature reporting the effects of Vertebroplasty on internal intervertebral disc biomechanics which in turn have been shown to reflect loading patterns of the vertebral column.

To study effects of PMMA cement augmentation of vertebral body fractures on intervertebral disc biomechanics using stress prolifometry to assess differential anterior and posterior vertebral column loading.

Eight cadaveric motion segments were individually loaded on a hydraulically powered materials testing machine under 1.5kN of axial compression. Following fracture induction the lower vertebral body underwent Vertebroplasty.

Profiles of the vertically acting compressive stress were obtained by pulling a pressure sensitive transducer along the mid-sagittal diameter of the intervertebral disc. “Stress profile” measurements were obtained before fracture, following fracture, and after vertebro-plasty both in extension and flexion.

Stress profiles were integrated over area to calculate the compressive force across the disc. The compressive load acting on the neural arch was calculated by subtracting the disc force from the applied 1.5kN load.

In flexed postures posterior column loading increased from 17.1% to 42.2% following fracture (p< 0.01) and then decreased significantly from 42.2% to 23.68% following vertebroplasty (p< 0.03). There was no significant difference between pre-fracture and post-vertebroplasty status (p=0.11). In extended posture, fracture produced increased posterior column loading 72.9% vs 51.8% (p< 0.005) and following vertebroplasty there was no significant change (p=0.2).

In moderate degrees of flexion, vertebroplasty produces normalisation of load bearing through the anterior vertebral column and hence offloads the posterior elements to a significant degree. This could be postulated, to partly account for the analgesic effect seen following vertebroplasty in the clinical setting.

Introduction. : Measurements of overall vertebral bone mineral density (BMD_v) do not adequately explain the observed patterns of osteoporotic vertebral fracture. Perhaps bone loss from specific regions of the vertebra has a more important effect on vertebral strength, and risk of fracture, than overall bone loss? We hypothesise that ‘stress shielding’ of the anterior vertebral body by the neural arch in erect standing postures can reduce BMD_v in the anterior vertebral body and thereby reduce vertebral compressive strength.

Materials and Methods: A compressive force of 1.5kN was applied to lumbar ‘motion segments’. positioned to simulate erect standing posture. Compressive stresses within the intervertebral disc were measured by pulling a miniature pressure transducer through it. ‘Stress profiles’ were integrated over area to calculate the total compressive force on the disc¹. This was subtracted from the 1.5kN to calculate the force resisted by the neural arch. Motion segments were then compressed to failure in moderate flexion (to simulate heavy lifting) and their compressive strength obtained. After disarticulation, the BMD_v, of the whole and the anterior half of each vertebral body was measured by dual energy x-ray absorptiometry (DXA). We report preliminary results from 9 specimens, aged 72–92 yrs.

Results: Vertebral strength (in flexion) was inversely related to load-bearing by the neural arch in erect posture (r²=0.42, p=0.05). Strength was directly related to the BMD_v of the whole (r²=0.65, p=0.06) and the anterior (r²=0.8, p=0.005) vertebral body.

Conclusions: These results suggest that habitual load-bearing by the neural arch in erect postures can lead to stress shielding of the anterior vertebral body so that the latter losesBMD_v, and the vertebra is weakened in the anterior vertebral body appears to be a BMD_v better predictor of vertebral strength than BMD_v, of the whole vertebra.

Introduction: Intradiscal electrothermal therapy (IDET) is a novel treatment for discogenic back pain. A heating element is inserted percutaneously into a disc in order to denature the collagen of the posterior annulus. Clinical success is claimed, although laboratory studies indicate that temperature increases may be insufficient to cause widespread collagen denaturation, or denervation, and that IDET has little effect on gross mechanical properties. We report on changes in internal disc mechanics following IDET.

Methods: Ten cadaveric lumbar ‘motion segments’ (aged 72–79 yrs) were stored at −17°C. Subsequently, each was equilibrated at 37°C. A miniature pressure transducer was used to measure the distribution of compressive stress along the mid-sagittal diameter of each disc while it was compressed at 1.5kN. IDET was performed, using bi-planar radiography to confirm placement of the heating element, and an independent thermocouple to measure temperature in the inner lateral annulus. Stress profilometry was repeated irnmediately after IDET.

Results: Before IDET, all discs exhibited stress concentrations typical of mild degeneration. Accurate placement of the element was confirmed in all discs. Temperatures in the inner lateral annulus during IDET reached only 40.9°C (STD 2.3°C). Differences between stress measurements repeated before IDET never exceeded 8% (NS). After IDET, peak stresses (above nucleus pressure) were reduced by more than 8% in 6/10 specimens (mean reduction 55%), increased in 2/10, and were unchanged in 2/10. Nucleus pressure fell by 13% (n=10 0, P=0.05).

Discussion: IDET had a variable effect on these 10 degenerated discs. In six of them, stress concentrations in the annulus were reduced, suggesting that IDET can cause disc material to resist compression in a more coherent fashion, possibly by ‘bonding’ fragmented tissue together, and thereby distributing load more evenly across the endplate. Reduction in nucleus pressure following IDET suggests load transfer to the neural arch, although this could not be confirmed. Reducing annulus stress concentrations could conceivably reduce pain in some individuals.

Introduction: Pathological changes in the elderly spine include intervertebral disc degeneration, apophyseal joint arthritis and osteoporotic fracture of the vertebral body. Such changes are likely to be inter-related through alterations in the sharing of load between the apophyseal joints and the intervertebral disc unit. We describe an accurate, non-destructive method for calculating the load sharing based on measurements of the distribution of stress within the intervertebral disc.

Materials and Methods: Twenty three motion segments, consisting of two vertebrae and the intervening disc and ligaments, were dissected from 17 human lumbar spines. A preliminary “creep” test was used to reduce disc height and water content by an amount equivalent to the diurnal variation seen in vivo. Then, a constant load was applied to each motion segment, using a computer-controlled hydraulic materials testing machine, for a period of 20s while a pressure-transducer, sensitive to spatial variations in compressive stress, was pulled through the disc along its mid-sagittal diameter. Profiles of vertically-acting compressive stress were obtained in each disc positioned in 2° of extension (appropriate for an erect standing posture). The total compressive force acting on the intervertebral disc was calculated by modelling the disc using approximately 20 elliptical rings of known cross-sectional area. The force acting on each ring was given by the product of area and the average compressive stress acting on it, which was obtained from the appropriate region of the stress profile. The total force acting through the disc was obtained by summing up the force contribution from each ring. The force acting on the apophyseal joints was calculated from the difference between applied (known) load and the calculated load acting on the disc. A correction factor was obtained separately for each disc to account for deviations in the cross-section from the elliptical, and variations in the sensitivity of the transducer in disc tissues of different ages. The correction factor was obtained by comparing the applied force with the force calculated from a stress profile measured before creep loading while the disc was in a neutral position, when the load passing through the apophyseal joints is negligible.

Results: The proportion of load passing through the apophyseal joints increased significantly with age (r²=0.48, p< 0.01), from 7% at age 27 yrs to 42% at 82yrs. Similarly, the proportion of load passing through the apophyseal joints increased with degree of disc degeneration (r²=0.5, p< 0.05 Pearson, Chi-square) from 8% in “grade 1” discs to 40% in “grade 4” discs.

Discussion: The compressive load passing through the apophyseal joints is higher than that predicted by previous, inaccurate, methods, or by experiments which failed to reduce the height and water content of the intervertebral disc. Increased load-bearing may be a contributing factor in apophyseal joint degeneration. Also, in lordotic postures, “stress shielding” by the apophyseal joints could contribute to bone loss in the vertebral body, leaving it vulnerable to osteoporotic fracture when the spine is loaded in flexion.

Osteoporotic fractures are associated with bone loss following hormonal changes and reduced physical activity in middle age. But these systemic changes do not explain why the anterior vertebral body should be such a common site of fracture. We hypothesise that age-related degenerative changes in the intervertebral discs can lead to abnormal load-bearing by the anterior vertebral body.

Cadaveric lumbar motion segments (mean age 50 ± 19 yrs, n = 33) were subjected to 2 kN of compressive loading while the distribution of compressive stress was measured along the antero-posterior diameter of the intervertebral disc, using a miniature pressure-transducer. “Stress profiles” were obtained with each motion segment positioned to simulate a) the erect standing posture, and b) a forward stooping posture. Stress measurements were effectively integrated over area in order to calculate the force acting on the anterior and posterior halves of the disc ( 1). These two forces were subtracted from the applied 2 kN to determine the compressive force resisted by the neural arch. Discs were sectioned and their degree of disc degeneration assessed visually on a scale of 1–4.

In motion segments with non-degenerated (grade 1) discs, less than 5% of the compressive force was resisted by the neural arch, and forces on the disc were distributed evenly in both postures. However, in the presence of severe disc degeneration, neural arch load-bearing increased to 40% in the erect posture, and the compressive force exerted by the disc on the vertebral body was concentrated anteriorly in flexion, and posteriorly in erect posture. In severely degenerated discs, the proportion of the 2 kN resisted by the anterior disc increased from 18% in the erect posture to 58% in the forward stooped posture.

Disc degeneration causes the disc to lose height, so that in erect postures, substantial compressive force is transferred to the neural arch. In addition, the disc loses its ability to distribute stress evenly on the vertebral body, so that the anterior vertebral body is heavily loaded in flexion. These two effects combine to ensure that the anterior vertebral body is stress-shielded in erect postures, and yet severely loaded in flexed postures. This could explain why anterior vertebral body fractures are so common in elderly people with degenerated discs, and why forward bending movements often precipitate the injury.

Osteoporotic vertebral fractures are normally attributed to weakening of the vertebral body. However, the compressive strength of the spine also depends on the manner in which the intervertebral disc presses on the vertebral body, and on load-bearing by the neural arch. We present preliminary results from a large-scale investigation into the relative importance of these three influences on vertebral compressive strength.

Lumbar motion segments from elderly cadavers were subjected to 1.5 kN of compressive loading while the distribution of compressive stress was measured along the antero-posterior diameter of the intervertebral disc, using a miniature pressure-transducer. The overall compressive force on the disc, obtained by integrating the stress profile ( 1), was subtracted from the 1.5 kN applied load to give the force resisted by the neural arch. Stress profilometry was performed with each motion segment positioned to simulate the erect standing posture, and a forward stooping posture. Vertebral strength was measured by compressing the motion segments to failure in the forward stooping posture. In life, the spine is usually compressed most severely in this posture.

A univariate analysis of results from the first 9 motion segments (aged 72–92 yrs) showed that vertebral strength increased from 2.0 kN to 4.6 kN as the compressive force resisted by the neural arch in erect postures decreased from 1.1 kN to 0.4 kN (r² = 0.42, p = 0.05). Updated results from this on-going study will be presented at the meeting.

Preliminary results suggest that habitual load-bearing by the neural arch in erect postures can lead to progressive weakening of the vertebral body, which is effectively “stress-shielded” by the neural arch. This weakening is exposed when the spine is loaded severely in a forward stooped posture, when it has a reduced compressive strength. This mechanism could explain some features of osteoporotic vertebral fractures in old people.