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

Dual energy X-ray absorptiometry (DEXA) is the gold standard for assessing bone mineral density (BMD) and fracture risk in vivo. However, it has limitations in the spine because vertebrae show marked regional variations in BMD that are difficult to detect clinically. This study investigated whether micro-CT can provide improved estimates of BMD that better predict vertebral strength.

The belief that an intervertebral disc must degenerate before it can herniate has clinical and medicolegal significance, but lacks scientific validity. We hypothesised that tissue changes in herniated discs differ from those in discs that degenerate without herniation. Tissues were obtained at surgery from 21 herniated discs and 11 non-herniated discs of similar degeneration as assessed by the Pfirrmann grade. Thin sections were graded histologically, and certain features were quantified using immunofluorescence combined with confocal microscopy and image analysis. Herniated and degenerated tissues were compared separately for each tissue type: nucleus, inner annulus and outer annulus.

Herniated tissues showed significantly greater proteoglycan loss (outer annulus), neovascularisation (annulus), innervation (annulus), cellularity/inflammation (annulus) and expression of matrix-degrading enzymes (inner annulus) than degenerated discs. No significant differences were seen in the nucleus tissue from herniated and degenerated discs. Degenerative changes start in the nucleus, so it seems unlikely that advanced degeneration caused herniation in 21 of these 32 discs. On the contrary, specific changes in the annulus can be interpreted as the consequences of herniation, when disruption allows local swelling, proteoglycan loss, and the ingrowth of blood vessels, nerves and inflammatory cells.

In conclusion, it should not be assumed that degenerative changes always precede disc herniation.

Cite this article: Bone Joint J 2013;95-B:1127–33.

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.

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

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.

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: 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: Neck pain is a growing problem which is linked to occupational factors that include work above shoulder height or sustained neck flexion. These activities may induce fatigue in the neck muscles impairing the muscles’ ability to provide reflex contractions that protect against tissue injury. The aim of this study was to investigate the effect of neck muscle fatigue on reflex activation of the neck muscles.

Methods: Healthy volunteers were subjected to one of two loading protocols. Isometric contractions of neck extensors at 60% MVC were sustained to the endurance limit (n=30) to induce high level fatigue in these muscles. A similar protocol for neck flexors (n=21) was used to initiate low level contraction of the extensors which are co-activated to stabilise the cervical spine under such circumstances. Before and after each loading protocol, reflex activation of the trapezius muscle was assessed using skin surface electromyography (EMG) to measure the latency and amplitude of muscle activation in response to a sudden perturbation of the head.

Results: Reflex latencies increased from 73±17ms to 93±27ms (p=0.0041), and from 72±12ms to 97±28ms (p< 0.0001) following low and high level extensor fatigue, respectively. Time to peak EMG also increased from 122±32ms to 148±39ms (p=0.0093), and from 113±15ms to 138±25ms (p< 0.0001), respectively, although no change in peak EMG amplitude was observed.

Conclusions: Reflex activation of trapezius was substantially delayed following both loading protocols. These findings suggest that even low level postural loading in the workplace may impair neck muscle reflexes rendering the underlying tissues more vulnerable to strain injury.

Conflicts of Interest: None

Source of Funding: BBSRC (Biotechnology and Biological Sciences Research Council, UK)

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.)

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

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: Impaired muscle function due to pain or inactivity may contribute to poor outcome following disc surgery. This study investigated the effects of postoperative exercise on pain, disability and spinal function in patients undergoing microdiscectomy.

Methods: Volunteers who gave informed consent (65M/26F) were blindly randomised to Exercise and Control groups. All patients were assessed the week before surgery. Posture and range of motion were measured using the 3-Space Fastrak, and back muscle fatigue was evaluated during the Biering-Sorensen test from changes in median frequency of the electromyographic signal. In 42 patients, intra-operative muscle biopsies were obtained. Four weeks after surgery, patients underwent a second functional assessment, after which the Exercise group began a 4-week exercise programme. Further assessments were performed at 2, 6, 12, 18 and 24 months after surgery. Pain, disability and psychological status were evaluated throughout using appropriate questionnaires.

Results: Marked type II fibre atrophy was evident at surgery, and this was reflected in pre-operative measures of median frequency. At 4 weeks, both groups showed significant improvements in pain, disability and psychological status but limited improvements in function. At 2 months, the Exercise group showed further improvements in pain, disability and psychological status, increased ranges of motion, and improved fatigability. Increases in initial median frequency in the fatigue test suggested fibre hypertrophy. Further improvements in the Control group generally achieved significance 6–12 months after surgery.

Conclusions: Surgery is effective in improving pain, disability and psychological status. Recovery of muscle function after surgery is naturally slow but can be accelerated by post-operative exercise.

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: Intrauterine protein restriction in rats is associated with low bone mass which persists with development through to adulthood. However, such adverse effects are not only restricted to bone. Intervertebral discs are the largest avascular structures in the body, and are particularly sensitive to their nutritional environment. We have examined the hypothesis that changes in the intervertebral disc (or ligaments), as a result of early nutritional compromise, affect the spine’s mechanical properties.

Material and methods: Lumbar spines were removed from 8 sheep (6 male, 2 female: mean age 2.7 yrs) that had received different diets early in their development: two animals received a control diet, three received low protein in utero (IU), and three received low protein both in utero and postnatally (PN). Fifteen motion segments (consisting of two vertebrae and the intervening disc and ligaments) were dissected from the spines and tested on a hydraulically-controlled materials testing machine. Compressive stiffness and bending stiffness were measured before and after creep loading, in both flexion and extension. Reflective markers attached to the specimens were tracked during loading, enabling intervertebral angles to be calculated. Bending moment-angular rotation curves were used to calculate bending stiffness. Repeated measures ANOVA was used to test for differences in stiffness with posture and creep, and between the dietary groups.

Results: Compressive stiffness increased after creep loading (p=0.002) but was unaffected by posture or dietary group. In contrast, bending stiffness was unaffected by creep but differed significantly between groups and with posture. When compared to controls, bending stiffness in the IU group was reduced by 35% in flexion and 26% in extension (p< 0.02). In the PN group, reductions of 28% in flexion and 15% in extension were observed (p=0.056).

Discussion: These results indicate that early protein restriction can affect the mechanical properties of the spine. These effects were evident in bending but not in compression, and tended to be greater in flexion than extension. These preliminary findings suggest that early protein restriction may affect the composition and mechanical function of the annulus fibrosus and the intervertebral ligaments which are the structures most involved in resisting flexion movements.

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: 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: Neck pain often arises without any evident trauma suggesting that everyday loading may cause fatigue damage to spinal tissues. However, little is known about the forces acting on the cervical spine in everyday life. The purpose of this study was to determine spinal compressive forces using an electromyo-graphic (EMG) technique.

Methods: Eight subjects performed a number of tasks while cervical flexion/extension and surface EMG activity of upper trapezius and sternocleidomastoid were measured. Dynamic EMG signals were corrected for contraction speed, using a correction factor obtained from lumbar muscles, and were then compared with isometric calibrations in order to predict moment generation. Calibrations were performed in different amounts of cervical flexion/extension by each subject to account for changes in the EMG-moment relationship with muscle length. Compressive force on the C7-T1 intervertebral disc was determined by dividing the generated moments by the resultant lever arm of flexor or extensor muscles obtained from MRI scans on the same subjects.

Results: Peak values (mean ± SD) of extensor and flexor moments increased from 1.9±1.6Nm and 1.4±1.0Nm respectively in standing to 52.7±32.2Nm and 4.2±1.8Nm when lifting above the head. Resultant muscle lever arms ranged between 3.0–5.2cm and 1.6–3.5cm for extensor and flexor muscles respectively. Therefore, peak compressive forces on the C7–T1 disc were 110±74N in standing and 1570±940N during overhead lifting.

Conclusion: Neck muscles generate high forces in activities such as overhead lifting. If applied on a repetitive basis, such forces could lead to the accumulation of fatigue damage in life.

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: 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: 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: 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.

Study design: To investigate the effects of muscle atrophy on back muscle fatigue:

Objective: To assess fibre type atrophy in patients undergoing surgery for pro-lapsed lumbar intervertebral disc, and to determine its effect upon EMG measures of fatigue.

Methods: Intra-operative biopsies were obtained from the erector spinae muscles of patients undergoing microdiscectomy. Mean fibre area of type I and II fibres were determined after myosin ATPase staining. Prior to surgery, EMG activity of the erector spinae muscles was recorded bilaterally at T10 and L3 whilst subjects performed the Biering-Sorensen fatigue test. Power spectral analysis indicated the initial median frequency and its rate of decline (median frequency gradient) at each recording site. Fibre type area was compared with the median frequency measures.

Subjects: 34 subjects (20 male) with intervertebral disc prolapse.

Results: Mean fibre area of type I and II fibres was 5890 ± 1947μm² and 3461 ± 1946μm² in men, and 5144 ± 1692μm² and 1945 ± 1039μm² in women, indicating marked type II fibre atrophy. Type II MFA was positively correlated with initial median frequency at L3 on the operated side (R=0.445) and negatively correlated with the maximum median frequency gradient of the four recording sites (R= −0.430).

Conclusion: Type II fibre atrophy influences EMG measures of fatigue. The decrease in initial median frequency with type II fibre atrophy probably reflects a reduced conduction velocity in these small fibres. The less negative median frequency gradient with decreased type II fibre size indicates a lower rate of fatigue which may be explained by an increased contribution to force generation from type I fibres which occupy a greater proportion of the muscle.

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: 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: 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.

During forward bending activities, the collagenous tissues of the spine are protected from injury by reflex contractions of the back muscles which prevent excessive spinal flexion. Animal experiments have shown that this reflex response is diminished when spinal ligaments are subjected to creep ( 1). This study examined the effects of creep on the latency and amplitude of reflex activation of the back muscles in living people.

Ten healthy volunteers (4M/6F) consented to participate in the study. Subjects underwent two flexion treatments: i) prolonged sitting in a low chair for 2 hours, ii) 100 toe-touching exercises, each on a separate day. Before and after each treatment, subjects performed a standardised forward bending task during which simultaneous measurements were made of lumbar flexion, using the 3-Space Fastrak, and surface EMG activity of the erector spinae muscles at T10 and L3 ( 2). The latency of the reflex response was measured by recording the amount of lumbar flexion that occurred prior to the onset of muscle activation at each site. The amplitude of the reflex was measured by determining the peak EMG activity during the bending task. Each subject’s range of lumbar flexion was also measured independently before and after each treatment to determine the extent of any creep.

Both treatments caused creep, as indicated by a significant increase in the range of lumbar flexion. The treatments also brought about a significant delay in the reflex activation of the back muscles in the standardised bending task: after prolonged sitting, lumbar flexion during the bending task increased by 9.2 ± 7.4° and 5.7 ± 4.6° before the onset of EMG activity at T10 and L3 respectively; following the toe-touches, the equivalent increases in lumbar flexion were 5.4 ± 3.9° and 3.1 ± 4.4°. The amplitude of the reflex response was unchanged following prolonged sitting, but after the toe-touches, a 50% increase in peak EMG activity was observed at L3.

Creep in spinal tissues as a result of prolonged or repetitive flexion was associated with delayed reflex activation of the back muscles. There was no associated reduction in the amplitude of the reflex. The increase in peak EMG activity following the toe touches may reflect increased activation as a result of muscle fatigue. These results suggest that creep in spinal tissues may allow increased lumbar flexion and hence increased bending stresses to be applied to the intervertebral disc.

We investigated the distribution of compressive ‘stress’ within cadaver intervertebral discs, using a pressure transducer mounted in a 1.3 mm diameter needle. The needle was pulled along the midsagittal diameter of a lumbar disc with the face of the transducer either vertical or horizontal while the disc was subjected to a constant compressive force. The resulting ‘stress profiles’ were analysed in order to characterise the distribution of vertical and horizontal compressive stress within each disc. A total of 87 discs from subjects aged between 16 and 87 years was examined.

Our results showed that age-related degenerative changes reduced the diameter of the central hydrostatic region of each disc (the ‘functional nucleus’) by approximately 50%, and the pressure within this region fell by 30%. The width of the functional annulus increased by 80% and the height of compressive ‘stress peaks’ within it by 160%. The effects of age and degeneration were greater at L4/L5 than at L2/L3, and the posterior annulus was affected more than the anterior. Age and degeneration were themselves closely related, but the stage of degeneration had the greater effect on stress distributions.

We suggest that structural changes within the annulus and endplate lead to a transfer of load from the nucleus to the posterior annulus. High ‘stress’ concentrations within the annulus may cause pain, and lead to further disruption.

Diurnal changes in the loads acting on the spine affect the water content and height of the intervertebral discs. We have reviewed the effects of these changes on spinal mechanics, and their possible clinical significance. Cadaveric lumbar spines subjected to periods of creep loading show a disc height change similar to the physiological change. As a result intervertebral discs bulge more, become stiffer in compression and more flexible in bending. Disc tissue becomes more elastic as its water content falls, and its affinity for water increases. Disc prolapse becomes more difficult. The neural arch and associated ligaments resist an increasing proportion of the compressive and bending stresses acting on the spine. Observations on living people show that these changes are not fully compensated for by modified muscle activity. We conclude that different spinal structures are more heavily loaded at different times of the day. Therefore, the time of onset of symptoms and signs, and any diurnal variation in their severity, may help us understand more about the pathophysiology of low back pain and sciatica.

Cadaveric lumbar discs were injected with chymopapain and subjected to a series of mechanical tests over a period of up to 19 hours. Discs from the same spine injected with saline were used as controls. The results showed that chymopapain had no measurable effect on the mechanical properties of the disc apart from the increased height and stiffening caused by fluid injection. Another series of tests on isolated pieces of disc material showed that chymopapain could reduce the size of prolapsed nuclear material by 24% in one hour and by 80% in 48 hours. It is concluded that, in the short-term, chymopapain has a negligible effect on the mechanics of a disc but it can reduce the size of any prolapsed nuclear material with which it comes in contact.

One hundred and thirty-nine discs from cadaveric lumbar spines were injected with a mixture of radio-opaque fluid and dye. Discograms were taken and the discs were then sectioned in the sagittal plane. Examination of the sections revealed that injected fluid did not at first mix with the disc matrix but pushed it aside to form pools of injected fluid. The location of these pools, and hence the appearance of a discogram, depended on the stage of degeneration of the disc. It is concluded that useful clinical information can be obtained from discograms.