Abstract

The study aim was to simulate oblique spinous process abutment (SPA) in cadaveric spines and determine how this affects coupled motion in the coronal plane.

L4-S1 spinal segments from thirteen cadavers were loaded on a materials testing machine in pure compression at 1kN for 10 minutes. Reflective markers on the vertebral bodies were used to assess coronal motion using a motion analysis system. Oblique SPA was simulated by attaching moulded oblique aluminium strips to the L4 and L5 spinous processes. In each specimen, both a right- and left-sided SPA was simulated, in random order, and compression at 1kN was again applied. All tests were then repeated after endplate fracture. Coronal plane motion at baseline was compared with values following simulated SPA using Mann Whitney U-tests.

Pre-fracture, SPA increased coronal motion by 0.28° and 0.34° on right and left sides respectively, compared to baseline, only the former was significant (P=0.03). Post-fracture, SPA decreased coronal motion by 0.36° and 0.46° on right and left sides respectively, only the latter was significant (P=0.03). Simulated oblique SPA in the intact spine initiated an increase in coronal motion during pure axial loading. These findings provide limited evidence that oblique SPA may be causative in DLS.

Aim:

To determine if patients with coronal plane deformity in the lumbar spine have a higher grade of lumbar spine subtype compared to controls.

Introduction

Herniated disc tissue removed at surgery is mostly nucleus pulposus, with varying proportions of annulus fibrosus, cartilage endplate, and bone. Herniated nucleus swells and loses proteoglycans, and herniated annulus is invaded by blood vessels and inflammatory cells. However, little is known about the significance of endplate cartilage and bone within a herniation.

Introduction

Disc degeneration is often scored using macroscopic and microscopic scoring systems. Although reproducible, these scores may not accurately reflect declining function in a degenerated disc. Accordingly, we compared macroscopic and microscopic degeneration scores with measurements of disc function.

Introduction

Physical disruption of the extracellular matrix influences the mechanical and chemical environment of intervertebral disc cells. We hypothesise that this can explain degenerative changes such as focal proteoglycan loss, impaired cell-matrix binding, cell clustering, and increased activity of matrix-degrading enzymes.

Introduction

Decreasing endplate porosity has been proposed as a risk factor for intervertebral disc degeneration, because it interferes with disc metabolite transport. However, endplate porosity has recently been shown to increase with age and disc degeneration. We hypothesise that this increase reflects adaptive remodelling in response to altered loading from adjacent discs.

Introduction

Discogenic pain is associated with ingrowth of blood vessels and nerves, but uncertainty over the extent of ingrowth is hindering development of appropriate treatments. We hypothesise that adult human annulus fibrosus is such a dense crosslinked tissue that ingrowth via the annulus is confined to a) peripheral regions, and b) fissures extending into the annulus.

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

Herniated disc tissue removed at surgery usually appears degenerated, and MRI often reveals degenerative changes in adjacent discs and vertebrae. This has fostered the belief that a disc must be degenerated before it can herniate, which has medicolegal significance. We hypothesise that degenerative changes in herniated disc tissues differ from those found in tissues that have degenerated in-situ, and are consistent with being consequences rather than causes of herniation.

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

Vertebroplasty helps to restore mechanical function to a fractured vertebra. We investigated how the distribution of injected cement benefits both fractured and neighbouring vertebrae.

Introduction

Risk factors for disc degeneration depend on how the condition is defined, i.e. on the specific disc degeneration “phenotype”. We present evidence that there are two major and largely-distinct types of disc degeneration.

Introduction

Delamination of the annulus fibrosus is an early feature of disc degeneration, and it allows individual lamellae to collapse into the nucleus, or to bulge radially outwards. We hypothesise that delamination is driven by high gradients of compressive stress in the annulus.

Introduction

Severe ‘discogenic’ back pain may be related to the ingrowth of nerves and blood vessels, although this is controversial. We hypothesise that ingrowth is greater in painful discs, and is facilitated in the region of annulus fissures.

Background

Fracture of an osteoporotic vertebral body reduces vertebral stiffness and decompresses the nucleus in the adjacent intervertebral disc. This leads to high compressive stresses acting on the annulus and neural arch. Altered load-sharing at the fractured level may influence loading of neighbouring vertebrae, increasing the risk of a fracture ‘cascade’. Vertebroplasty has been shown to normalise load-bearing by fractured vertebrae but it may increase the risk of adjacent level fracture. The aim of this study was to determine the effects of fracture and subsequent vertebroplasty on the loading of neighbouring (non-augmented) vertebrae.

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).

Introduction

Vertebral osteoporotic fracture increases both elastic and time-dependent ('creep') deformations of the fractured vertebral body during subsequent loading. The accelerated rate of creep deformation is especially marked in central and anterior regions of the vertebral body where bone mineral density is lowest. In life, subsequent loading of damaged vertebrae may cause anterior wedging of the vertebral body which could contribute to the development of kyphotic deformity. The aim of this study was to determine whether gradual creep deformations of damaged vertebrae can be reduced by vertebroplasty.

Background

The Plantaris Longus Tendon (PLT) may be implicated in Achilles (AT) tendinopathy. Different mechanical characteristics may be the cause. This study is designed to measure these.

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.

To investigate whether restoration of mechanical function and spinal load-sharing following vertebroplasty depends upon cement distribution.

Fifteen pairs of cadaver motion segments (51-91 yr) were loaded to induce fracture. One from each pair underwent vertebroplasty with PMMA, the other with a resin (Cortoss). Various mechanical parameters were measured before and after vertebroplasty. Micro-CT was used to determine volumetric cement fill, and plane radiographs (sagittal, frontal, and axial) to determine areal fill, for the whole vertebral body and for several specific regions. Correlations between volumetric fill and areal fill for the whole vertebral body, and between regional volumetric fill and changes in mechanical parameters following vertebroplasty, were assessed using linear regression.

For Cortoss, areal and volumetric fills were significantly correlated (R=0.58-0.84) but cement distribution had no significant effect on any mechanical parameters following vertebroplasty. For PMMA, areal fills showed no correlation with volumetric fill, suggesting a non-uniform distribution of cement that influenced mechanical outcome. Increased filling of the vertebral body adjacent to the disc was associated with increased intradiscal pressure (R=0.56, p<0.05) in flexed posture, and reduced neural arch load bearing (F_N) in extended posture (R=0.76, p<0.01). Increased filling of the anterior vertebral body was associated with increased bending stiffness (R=0.55, p<0.05).

Cortoss tends to spread evenly within the vertebral body, and its distribution has little influence on the mechanical outcome of vertebroplasty. PMMA spreads less evenly, and its mechanical benefits are increased when cement is concentrated in the anterior vertebral body and adjacent to the intervertebral disc.

Introduction

Osteoporotic fracture reduces vertebral stiffness, and alters spinal load-sharing. Vertebroplasty partially reverses these changes at the fractured level, but is suspected to increase deformations and stress at adjacent levels. We examined this possibility.

Introduction

Vertebral osteoporotic fracture increases both elastic and time-dependent (‘creep’) deformations of the fractured vertebral body during subsequent loading. This is especially marked in central and anterior regions of the vertebral body, and could explain the development of kyphotic deformity in life. We hypothesise that vertebroplasty can reduce these creep deformations.

Background

Fissures in the anulus fibrosus are common in disc degeneration, and are associated with discogenic pain. We hypothesise that anulus fissures are conducive to the ingrowth of blood vessels and nerves.

Background: Severe and chronic back pain often originates from degenerated intervertebral discs, probably from lesions in the outer posterior anulus. Unlike the nucleus, the outer anulus has a high cell density and adequate metabolite transport. The outer annulus can heal after injury in small and young experimental animals, but little is known about the healing potential of adult human discs.

Purpose: We seek evidence that healing of the human outer anulus follows the three stages of tendon healing: inflammation, repair, remodelling. If so, then manual therapy and self-treatment techniques known to facilitate tendon healing could be adapted to treat discogenic back pain.

Methods: Anulus tissue was removed at surgery (usually posteriorly) from 14 patients with discogenic back pain. Tissue was paraffin embedded and sectioned at 5 μm for histology and immunohistochemistry. Apoptosis was detected using an antibody for caspase-3.

Results: Fissures in the peripheral posterior annulus, and herniated tissue fragments, were associated with blood vessels, inflammatory cells, and with focal loss of proteoglycans. Cell density decreased with distance from fissures from the disc periphery. Overall cell density decreased with age. Apoptosis was greater in the nucleus than in the annulus, and was particularly associated with cell clusters, and with anulus fissures.

Conclusion: These preliminary results suggest an inflammatory healing response in the outer anulus, strongly associated with radial fissures. Loss of proteoglycan from fissure margins may facilitate the ingrowth of capillaries and nerves, which then stimulate local healing in the vicinity of the fissures.

Conflicts of Interest: None

Source of Funding: BackCare

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

Purpose: To determine how cement volume during vertebroplasty influences:

stress distributions on fractured and adjacent vertebral bodies,

Methods: Nineteen thoracolumbar motion segments from 13 cadavers (42–91 yrs) were loaded to induce fracture. Fractured vertebrae received two sequential injections (VP1 and VP2) of 3.5cm3 of polymethylmethacrylate cement. Before and after each injection, motion segment stiffness was measured in compression and in bending, and the distribution of compressive “stress” in the intervertebral disc was measured in flexed and extended postures. Stress profiles yielded the intradiscal pressure (IDP), stress peaks in the posterior (SPP) annulus, and the % of the applied compressive force resisted by the neural arch (FN). Cement leakage and vertebral body volume were quantified by water-immersion, and % cement fill was estimated.

Results: Bending and compressive stiffness fell by 37% and 50% respectively following fracture, and were restored only after VP2. Depending on posture, IDP fell by 59%–85% after fracture whereas SPP increased by 107%–362%. VP1 restored IDP and SPP to prefracture values, and VP2 produced no further changes. Fracture increased FN from 11% to 39% in flexion, and from 33% to 59% in extension. FN was restored towards pre-fracture values only after VP2. Cement leakage, IDP and compressive stiffness all increased with %fill.

Conclusions: 3.5cm3 of cement largely restored normal stress distributions to fractured and adjacent vertebral bodies, but 7cm3 were required to restore load-sharing between the vertebral bodies and neural arch. Risks of cement leakage increased with %fill.

Conflicts of Interest: None

Source of Funding: This work was funded by Action Medical Research and The Hospital Saving Association Charitable Trust. Vertebroplasty materials were provided by Stryker.

Background: Sensorimotor mechanisms that control activation of neck and trunk muscles are important in preventing injury to spinal tissues. People with back pain often show delayed reflex activation of trunk muscles, and such impairment increases the risk of future back pain. The aim of this study was to investigate whether sensorimotor impairment is evident in patients with neck pain.

Methods: Measures of sensorimotor function were assessed in fourteen patients with chronic, non-traumatic neck pain and forty healthy controls. Position sense was evaluated using the Fastrak electromagnetic tracking device to assess angular errors during head repositioning tasks. Movement sense was assessed using a KinCom dynamometer to determine the time taken to detect head motion at 1°s-1 and 10°s-1. Reflex responses were assessed using surface electromyography to determine the onset of muscle activation (reflex latency) in trapezius and sternocleidomastoid muscles, following perturbations of the head.

Results: Neck pain patients showed increased angular errors in reproducing upright postures, compared to controls (2.24±1.21° vs 1.85±1.06° respectively; p=0.01), and faster movement detection times (385±98ms vs 540±182ms respectively; p=0.0052). Reflex activation of trapezius was delayed in patients, indicated by a 20ms increase in reflex latency (89±19ms vs 69±21ms in controls; p=0.0039).

Conclusions: Sensorimotor function is altered in patients with neck pain. Enhanced movement detection suggests some afferents become hypersensitive in response to pain. However, impaired position sense and reflex activation suggest that some proprioceptors, including muscle spindles, develop a reduced sensitivity to mechanical stimuli. These changes may impair reflexive muscle protection and expose the cervical spine to repetitive minor injuries.

Conflicts of Interest: None

Source of Funding: BBSRC (Biotechnology and Biological Sciences Research Council, U.K.)

Purpose of Study: The neck is the most mobile region of the spine, so neck muscles must provide stability, and control spinal movements. This action requires effective sensory and motor control mechanisms which, if impaired, may increase the risk of injury and pain. The aim of this study was to investigate sensorimotor function of neck muscles in healthy volunteers in order to provide normative data for comparative studies on neck pain patients.

Methods: Thirty-one healthy volunteers participated. Position sense was evaluated using an electromagnetic tracking device (3-Space FASTRAK) to assess errors in repositioning the head in upright and flexed postures. Movement sense was assessed as time to detect head motion at 1°s-1 and 10°s-1, using a KinCom dynamometer. Latency of reflex muscle activation following rapid perturbation of the head was assessed bilaterally in trapezius and sternocleidomastoid muscles using surface electromyography.

Results: Mean repositioning errors were 2.20±1.46° and 2.54±1.69° for upright and flexed postures respectively. Time to detect head motion was greater at 1°s-1 (739±349ms and 556±213ms, in extension and flexion respectively) compared to 10°s-1 (375±89ms and 377±66ms). Mean reflex latencies were shorter for trapezius (left: 77.9±43.4ms, right: 72.3±35.1ms) than for sternocledomastoid (left: 106.1±29.2ms, right: 102.7±35.9ms).

Conclusion: Position sense in the cervical spine is superior to that reported in thoracolumbar regions, especially in flexed postures. Detection of head movement is velocity-dependent suggesting input occurs from both phasic and tonic mechanoreceptors. Reflex latencies were shorter for trapezius than for sternocledomastoid suggesting that stretch reflexes in trapezius play a predominant role in preventing excessive flexion of the cervical spine.

Introduction: Vertebroplasty increases stiffness and partly restores normal load-sharing in the human spine following vertebral fracture. The present study investigated whether the mechanical effects of vertebroplasty are influenced by the distribution of injected cement.

Methods: Ten pairs of cadaver motion segments (58–88 yr) were loaded to induce fracture, after which one from each pair underwent vertebroplasty with polymethyl-methacrylate cement, the other with a resin (Cortoss). Various mechanical parameters were measured before fracture, after fracture and following subsequent vertebroplasty. Micro-computed tomography scans and plane radiographs (sagittal, frontal, and axial) obtained from each augmented vertebral body were analysed to determine percentage cement fill in the whole vertebral body and in selected regions. The relationship between volumetric fill obtained by micro-CT and areal fill obtained by radiography was investigated using linear regression analysis. Regression analysis also indicated whether changes in mechanical parameters following vertebroplasty were dependent upon cement distribution.

Results: Cement type had no significant influence upon regional fill patterns, so data from both cements were pooled for all subsequent analyses. Volumetric fill of the whole vertebral body was predicted best by areal fill in the sagittal plane (R2=0.366, P=0.0047). Restoration of intradiscal pressure and compressive stiffness following vertebroplasty were dependent upon volumetric cement fill both in the whole vertebral body (R2=0.304, P=0.0118 and R2=0.197, P=0.0499 respectively), and in the anterior half (R2=0.293, P=0.0137 and R2=0.358, P=0.0053).

Conclusion: Cement fill patterns can best be assessed radiographically from sagittal plane views. Placement of cement in the anterior vertebral body may help to improve mechanical outcome following vertebroplasty.

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: The aim of this cadaver study was to examine how cement volume used in vertebroplasty influences the restoration of normal load-sharing and stiffness to fractured vertebrae.

Methods: Nineteen thoracolumbar motion segments obtained from 13 spines (42–91 yrs) were compressed to failure in moderate flexion to induce vertebral fracture. Fractured vertebrae underwent two sequential vertebroplasty treatments (VP1 and VP2) each of which involved unipedicular injection of 3.5ml of polymethyl-methacrylate cement. During each injection, the volume of any cement leakage was recorded. At each stage of the experiment (pre-fracture, post-fracture, post-VP1 and post-VP2) measurements were made of motion segment stiffness, in bending and compression, and the distribution of compressive stress across the disc. The latter was measured in flexed and extended postures by pulling a pressure transducer 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). Measurements obtained after VP1 and VP2 were compared with pre-fracture and post-fracture values using repeated measures ANOVA to examine the effect of cement volume (3.5 ml vs. 7 ml) on the restoration of mechanical function.

Results: Fracture reduced compressive and bending stiffness by 50% and 37% respectively (p< 0.001) and IDP by 59%–85%, depending on posture (p< 0.001). SPP increased from 0.53 to 2.46 MPa in flexion, and from 1.37 to 2.83 MPa in extension (p< 0.01). FN increased from 11% to 39% of the applied load in flexion, and from 33% to 59% in extension (p< 0.001). VP1 partially reversed the changes in IDP and SPP towards pre-fracture values but no further restoration of these parameters was found after VP2. Bending and compressive stiffness and FN showed no significant change after VP1, but were restored towards pre-fracture values by VP2. Cement leakage occurred in 3 specimens during VP1, and in 7 specimens during VP2. Leakage volumes ranged from 0.5–3.0 ml, and were larger during VP2 than VP1.

Conclusions: Unipedicular injection of 3.5 ml of cement reversed fractured induced changes in IDP and SPP, but did not affect stiffness and neural arch load-bearing. Larger injection volumes may provide some extra mechanical benefit in terms of restoring stiffness and reducing neural arch loading, but these extra mechanical benefits can be at the cost of increased risk of cement leakage.

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: 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: 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: 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.