Abstract

Abstract

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

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

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

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

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

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

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

Conflicts of Interest: None

Source of Funding: Scholarship from the Greek Government

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

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

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

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

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

Conflicts of Interest: none

Source of Funding: Action Medical Research

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

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

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

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

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

Conflicts of Interest: none

Source of Funding: Action Medical Research

Purpose: To determine how cement volume during vertebroplasty influences:

stress distributions on fractured and adjacent vertebral bodies,

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

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

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

Conflicts of Interest: None

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

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: 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.