Morphometric measurements can improve prediction of progressive vertebral deformity following vertebral damage.

PURPOSE: A damaged vertebral body can exhibit accelerated 'creep' under constant load, leading to progressive vertebral deformity. However, the risk of this happening is not easy to predict in clinical practice. The present cadaveric study aimed to identify morphometric measurements in a damaged vertebral body that can predict a susceptibility to accelerated creep. METHODS: A total of 27 vertebral trabeculae samples cored from five cadaveric spines (3 male, 2 female, aged 36 to 73 (mean 57) years) were mechanically tested to establish the relationship between bone damage and residual strain. Compression testing of 28 human spinal motion segments (three vertebrae and intervening soft tissues) dissected from 14 cadaveric spines (10 male, 4 female, aged 67 to 92 (mean 80) years) showed how the rate of creep of a damaged vertebral body increases with increasing "damage intensity" in its trabecular bone. Damage intensity was calculated from vertebral body residual strain following initial compressive overload using the relationship established in the compression test of trabecular bone samples. RESULTS: Calculations from trabecular bone samples showed a strong nonlinear relationship between residual strain and trabecular bone damage intensity (R2 = 0.78, P < 0.001). In damaged vertebral bodies, damage intensity was then related to vertebral creep rate (R2 = 0.39, P = 0.001). This procedure enabled accelerated vertebral body creep to be predicted from morphological changes (residual strains) in the damaged vertebra. CONCLUSION: These findings suggest that morphometric measurements obtained from fractured vertebrae can be used to quantify vertebral damage and hence to predict progressive vertebral deformity.

Importance of the epiphyseal ring in OLIF stand-alone surgery: a biomechanical study on cadaveric spines.

PURPOSES: To explore the function of endplate epiphyseal ring in OLIF stand-alone surgery using a biomechanical model to reduce the complications of endplate collapse and cage subsidence. METHODS: In total, 24 human cadaveric lumbar function units (L1-2 and L3-4 segments) were randomly assigned to two groups. The first group was implanted with long fusion cages which engaged with both inner and outer regions of epiphyseal ring (Complete Span-Epiphyseal Ring, CSER). Those engaged with only the inner half of epiphyseal ring were the second group (Half Span-Epiphyseal Ring, HSER). Each group was divided into two subgroups [higher cage-height (HH) and normal cage-height (NH)]. Specimens were fixed in testing cups and compressed at approximately 2.5 mm/s, until the first sign of structural failure. Trabecular structural damage was analyzed by Micro-CT, as well as the difference of bone volume fraction (BV/TV), trabecular thickness (Tb.Th) et al. in different regions. RESULTS: Endplate collapse was mainly evident in the inner region of epiphyseal ring, where trabecular injury of sub-endplate bone was most concentrated. Endplate collapse incidence was significantly higher in HSER than CSER specimens (P = 0.017). A structural failure occurred at a lower force in HSER (1.41 ± 0.34 KN) compared with CSER (2.44 ± 0.59 KN). HH subgroups failed at a lower average force than NH subgroups. Micro-CT results showed a more extensive trabecular fracture in HSER specimens compared to CSER specimens, especially in HH subgroup. CONCLUSIONS: Endplate collapse is more likely to occur with short half span cages than complete span cages, and taller cages compared with normal height cages. During OLIF surgery, we should choose cages matching intervertebral disc space height and place the cages spanning over the whole epiphyseal ring to improve support strength.

Nerves and blood vessels in degenerated intervertebral discs are confined to physically disrupted tissue.

Nerves and blood vessels are found in the peripheral annulus and endplates of healthy adult intervertebral discs. Degenerative changes can allow these vessels to grow inwards and become associated with discogenic pain, but it is not yet clear how far, and why, they grow in. Previously we have shown that physical disruption of the disc matrix, which is a defining feature of disc degeneration, creates free surfaces which lose proteoglycans and water, and so become physically and chemically conducive to cell migration. We now hypothesise that blood vessels and nerves in degenerated discs are confined to such disrupted tissue. Whole lumbar discs were obtained from 40 patients (aged 37-75 years) undergoing surgery for disc herniation, disc degeneration with spondylolisthesis or adolescent scoliosis ('non-degenerated' controls). Thin (5-µm) sections were stained with H&E and toluidine blue for semi-quantitative assessment of blood vessels, fissures and proteoglycan loss. Ten thick (30-µm) frozen sections from each disc were immunostained for CD31 (an endothelial cell marker), PGP 9.5 and Substance P (general and nociceptive nerve markers, respectively) and examined by confocal microscopy. Volocity image analysis software was used to calculate the cross-sectional area of each labelled structure, and its distance from the nearest free surface (disc periphery or internal fissure). Results showed that nerves and blood vessels were confined to proteoglycan-depleted regions of disrupted annulus. The maximum distance of any blood vessel or nerve from the nearest free surface was 888 and 247 µm, respectively. Blood vessels were greater in number, grew deeper, and occupied more area than nerves. The density of labelled blood vessels and nerves increased significantly with Pfirrmann grade of disc degeneration and with local proteoglycan loss. Analysing multiple thick sections with fluorescent markers on a confocal microscope allows reliable detection of thin filamentous structures, even within a dense matrix. We conclude that, in degenerated and herniated discs, blood vessels and nerves are confined to proteoglycan-depleted regions of disrupted tissue, especially within annulus fissures.

Why do some intervertebral discs degenerate, when others (in the same spine) do not?

This review suggests why some discs degenerate rather than age normally. Intervertebral discs are avascular pads of fibrocartilage that allow movement between vertebral bodies. Human discs have a low cell density and a limited ability to adapt to mechanical demands. With increasing age, the matrix becomes yellowed, fibrous, and brittle, but if disc structure remains intact, there is little impairment in function, and minimal ingrowth of blood vessels or nerves. Approximately half of old lumbar discs degenerate in the sense of becoming physically disrupted. The posterior annulus and lower lumbar discs are most affected, presumably because they are most heavily loaded. Age and genetic inheritance can weaken discs to such an extent that they are physically disrupted during everyday activities. Damage to the endplate or annulus typically decompresses the nucleus, concentrates stress within the annulus, and allows ingrowth of nerves and blood vessels. Matrix disruption progresses by mechanical and biological means. The site of initial damage leads to two disc degeneration "phenotypes": endplate-driven degeneration is common in the upper lumbar and thoracic spine, and annulus-driven degeneration is common at L4-S1. Discogenic back pain can be initiated by tissue disruption, and amplified by inflammation and infection. Healing is possible in the outer annulus only, where cell density is highest. We conclude that some discs degenerate because they are disrupted by excessive mechanical loading. This can occur without trauma if tissues are weakened by age and genetic inheritance. Moderate mechanical loading, in contrast, strengthens all spinal tissues, including discs.

Significance of cartilage endplate within herniated disc tissue.

PURPOSE: Disc herniations sometimes contain hyaline cartilage fragments, but their origins and significance are uncertain. METHODS: Herniations were removed surgically from 21 patients (aged 35-74 years) whose main symptom was sciatica (10 patients) or back pain (11 patients). Frozen sections, 5 µm thick, were examined histologically, and antibodies were used to label the matrix-degrading enzyme MMP 1, pro-inflammatory mediator TNFα, and cell proliferation marker Ki-67. Proportions of each tissue type were quantified by image analysis. Cartilage and bone components of the endplate were examined in 7-µm frozen sections from 16 cadaveric spines, aged 61-98 years. RESULTS: Cartilage fragments were found in 10/21 herniations. They averaged 5.0 mm in length, comprised 25 % of the herniation area, and two had some bone attached. Hyaline cartilage was more common in herniations from patients with sciatica (7/10) than with back pain (3/11, P = 0.050), and the area (%) of the herniation occupied by the cartilage was greater in sciatica patients (P < 0.05). Cartilage fragments showed little evidence of swelling, proteoglycan loss or inflammatory cell invasion, although cell clustering was common, and TNFα was sometimes expressed. Each cartilage fragment showed at least one straight edge, as if it had been peeled off the bony endplate, and this mechanism of failure was demonstrated in preliminary mechanical experiments. CONCLUSION: Disc herniations often include hyaline cartilage pulled from the vertebral endplates. Cartilage fragments show little swelling or proteoglycan loss, and may be slow to resorb, increasing the risk of persisting sciatica. Loss of cartilage will increase endplate permeability, facilitating endplate inflammation and disc infection.

Intervertebral disc degeneration: evidence for two distinct phenotypes.

We review the evidence that there are two types of disc degeneration. 'Endplate-driven' disc degeneration involves endplate defects and inwards collapse of the annulus, has a high heritability, mostly affects discs in the upper lumbar and thoracic spine, often starts to develop before age 30 years, usually leads to moderate back pain, and is associated with compressive injuries such as a fall on the buttocks. 'Annulus-driven' disc degeneration involves a radial fissure and/or a disc prolapse, has a low heritability, mostly affects discs in the lower lumbar spine, develops progressively after age 30 years, usually leads to severe back pain and sciatica, and is associated with repetitive bending and lifting. The structural defects which initiate the two processes both act to decompress the disc nucleus, making it less likely that the other defect could occur subsequently, and in this sense the two disc degeneration phenotypes can be viewed as distinct.

Vertebral deformity arising from an accelerated "creep" mechanism.

INTRODUCTION: Vertebral deformities often occur in patients who recall no trauma, and display no evident fracture on radiographs. We hypothesise that vertebral deformity can occur by a gradual creep mechanism which is accelerated following minor damage. "Creep" is continuous deformation under constant load. MATERIALS AND METHODS: Forty-five thoracolumbar spine motion segments were tested from cadavers aged 42-92 years. Vertebral body areal BMD was measured using DXA. Specimens were compressed at 1 kN for 30 min, while creep in each vertebral body was measured using an optical MacReflex system. After 30 min recovery, each specimen was subjected to a controlled overload event which caused minor damage to one of its vertebrae. The creep test was then repeated. RESULTS: Vertebral body creep was measurable in specimens with BMD <0.5 g/cm(2). Creep was greater anteriorly than posteriorly (p < 0.001), so that vertebrae gradually developed a wedge deformity. Compressive overload reduced specimen height by 2.24 mm (STD 0.77 mm), and increased vertebral body creep by 800 % (anteriorly), 1,000 % (centrally) and 600 % (posteriorly). In 34 vertebrae with complete before-and-after data, anterior wedging occurring during the 1st creep test averaged 0.07° (STD 0.17°), and in the 2nd test (after minor damage) it averaged 0.79° (STD 1.03°). The increase was highly significant (P < 0.001). Vertebral body wedging during the 2nd creep test was proportional to the severity of damage, as quantified by specimen height loss during the overload event (r (2) = 0.51, p < 0.001, n = 34). CONCLUSIONS: Minor damage to an old vertebral body, even if it is barely discernible on radiographs, can accelerate creep to such an extent that it makes a substantial contribution to vertebral deformity.

Biomechanics of vertebral compression fractures and clinical application.

Local biomechanical factors in the etiology of vertebral compression fractures are reviewed. The vertebral body is particularly vulnerable to compression fracture when its bone mineral density (BMD) falls with age. However, the risk of fracture, and the type of fracture produced, does not depend simply on BMD. Equally important is the state of degeneration of the adjacent intervertebral discs, which largely determines how compressive forces are distributed over the vertebral body. Disc height also influences load-sharing between the vertebral body and neural arch, and hence by Wolff's Law can influence regional variations in trabecular density within the vertebral body. Vertebral deformity is not entirely attributable to trauma: it can result from the gradual accumulation of fatigue damage, and can progress by a quasi-continuous process of "creep". Cement injection techniques such as vertebroplasty and kyphoplasty are valuable in the treatment of these fractures. Both techniques can stiffen a fractured vertebral body, and kyphoplasty may contribute towards restoring its height. The presence of cement can limit endplate deformation, and thereby partially reverse the adverse changes in load-sharing which follow vertebral fracture. Cement also reduces time-dependent "creep" deformation of damaged vertebrae.

A predictive model for creep deformation following vertebral compression fractures.

Many vertebral compression fractures continue to collapse over time, resulting in spinal deformity and chronic back pain. Currently, there is no adequate screening strategy to identify patients at risk of progressive vertebral collapse. This study developed a mathematical model to describe the quantitative relationship between initial bone damage and progressive ("creep") deformation in human vertebrae. The model uses creep rate before damage, and the degree of vertebral bone damage, to predict creep rate of a fractured vertebra following bone damage. Mechanical testing data were obtained from 27 vertebral trabeculae samples, and 38 motion segments, from 26 human spines. These were analysed to evaluate bone damage intensity, and creep rates before and after damage, in order to estimate the model parameter, p, which represents how bone damage affects the change of creep rate after damage. Results of the model showed that p was 1.38 (R2 = 0.72, p < 0.001) for vertebral trabeculae, and 1.48 for motion segments (R2 = 0.22, p = 0.003). These values were not significantly different from each other (P > 0.05). Further analyses revealed that p was not significantly influenced by cortical bone damage, endplate damage, disc degeneration, vertebral size, or vertebral areal bone mineral density (aBMD) (P > 0.05). The key determinant of creep deformation following vertebral compression fracture was the degree of trabecular bone damage. The proposed model could be used to identify the measures of bone damage on routine MR images that are associated with creep deformation so that a screening tool can be developed to predict progressive vertebral collapse following compression fracture.

Associations Between Intervertebral Disc Degeneration Grading Schemes and Measures of Disc Function.

Disc degeneration is a major cause of spinal dysfunction and pain, but grading schemes concentrate on tissue changes rather than altered function. The aim of this study was to compare disc degeneration grading systems with each other, and with biomechanical measures of disc function. Sixty-six motion segments (T8-9 to L5-S1) were dissected from cadavers aged 48-98 years. Disc function was assessed by measuring nucleus pressure (IDP) and maximum stresses in the annulus under 1 kN of compression. Detailed "scores" of disc degeneration were based on independent radiographic, macroscopic, and microscopic evaluations. For each evaluation, scores were used to assign a degeneration "grade" (I-IV), and functional measures were then correlated with degeneration scores and grades. Results showed that all measures were reliable (intraclass correlation coefficients: 0.82-0.99). Macroscopic and microscopic assessments were highly correlated with each other (r: 0.57-0.89, p < 0.001) but only weakly correlated with radiographic features. The overall macroscopic and microscopic scores of degeneration increased significantly with age and at lower spinal levels, although the influence of age was less marked in the case of the microscopic scores. IDP decreased with age and at lower spinal levels, but annulus stresses were more variable. Importantly, IDP and annulus stresses decreased consistently with all measures of disc degeneration, and these associations remained strong after controlling for age, gender, and spinal level. We conclude that radiographic and tissue-based assessments of disc degeneration are consistent with each other, and are more closely related to mechanical (dys)function than to age or spinal level. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:1946-1955, 2019.

Mechanical efficacy of vertebroplasty: influence of cement type, BMD, fracture severity, and disc degeneration.

INTRODUCTION: Osteoporotic vertebral fractures can be treated by injecting bone cement into the damaged vertebral body. "Vertebroplasty" is becoming popular but the procedure has yet to be optimised. This study compared the ability of two different types of cement to restore the spine's mechanical properties following fracture, and it examined how the mechanical efficacy of vertebroplasty depends on bone mineral density (BMD), fracture severity, and disc degeneration. METHODS: A pair of thoracolumbar "motion-segments" (two adjacent vertebrae with intervening soft tissue) was obtained from each of 15 cadavers, aged 51-91 years. Specimens were loaded to induce vertebral fracture; then one of each pair underwent vertebroplasty with polymethylmethacrylate (PMMA) cement, the other with another composite material (Cortoss). Specimens were creep loaded for 2 h to allow consolidation. At each stage of the experiment, motion segment stiffness in bending and compression was measured, and the distribution of compressive loading on the vertebrae was investigated by pulling a miniature pressure transducer through the intervertebral disc. Pressure measurements, repeated in flexed and extended postures, indicated the intradiscal pressure (IDP) and neural arch compressive load-bearing (F(N)). BMD was measured using DXA. Fracture severity was quantified from height loss. RESULTS: Vertebral fracture reduced motion segment stiffness in bending and compression, by 31% and 43% respectively (p<0.001). IDP fell by 43-62%, depending on posture (p<0.001), whereas F(N) increased from 14% to 37% of the applied load in flexion, and from 39% to 61% in extension (p<0.001). Vertebroplasty partially reversed all these effects, and the restoration of load-sharing was usually sustained after creep-consolidation. No differences were observed between PMMA and Cortoss. Pooled results from 30 specimens showed that low BMD was associated with increased fracture severity (in terms of height loss) and with greater changes in stiffness and load-sharing following fracture. Specimens with low BMD and more severe fractures also showed the greatest mechanical changes following vertebroplasty. CONCLUSIONS: Low vertebral BMD leads to greater changes in stiffness and spinal load-sharing following fracture. Restoration of mechanical function following vertebroplasty is little influenced by cement type but may be greater in people with low BMD who suffer more severe fractures.

Defects of the vertebral end plate: implications for disc degeneration depend on size.

BACKGROUND CONTEXT: Bony vertebral end plates must be porous to allow metabolite transport into the disc, and yet strong to resist high intradiscal pressure (IDP). End plate defects may therefore have nutritional and mechanical consequences for the disc, depending on their size and type. We hypothesize that broad, diffuse defects are more closely associated with disc decompression and degeneration than are focal Schmorl's node-type defects. PURPOSE: This study aimed to determine how the size and type of end plate defects are related to decompression and degeneration in the adjacent intervertebral disc. STUDY DESIGN: Mechanical, histologic, and micro-computed tomographic investigations were carried out in cadaver spines. METHODS: The study involved 40 motion segments (T8-T9 to L4-L5) dissected from 23 cadavers aged 48-98 years. Intradiscal stresses were measured, under 1 kN compression, by pulling a pressure transducer along the disc's midsagittal diameter. The resulting "stress profiles" revealed nucleus pressure (IDP) and maximum stresses in the anterior and posterior annulus. Micro-computed tomography was then used to examine all 40 discs, with 5 mm of adjacent bone on either side, so that end plate defects could be characterized at a resolution of 35 µm. Cross-sectional area (in the transverse plane), volume, location, and morphologic type were determined for all bony defects in the 80 end plates. Finally, discs from each motion segment (with hyaline cartilage and bone attached) were sectioned (undecalcified) at 7 µm for histology to allow degeneration to be assessed. RESULTS: Substantial defects were identified in 24 of 40 specimens (35 of 80 end plates). Of these, 83% was centrally located, and 17% was laterally located. Defects occurred more frequently in male than female specimens (p=.043), and were more common in thoracic than lumbar end plates (p=.002), although lumbar defects were greater in volume (p=.05). Defect area and volume increased with decreasing IDP, with decreasing peak stress in the annulus, and with increasing tissue degeneration. Stepwise multiple regression showed that average defect area depended most strongly on IDP, whereas maximum defect area and volume depended most strongly on peak stress in the anterior annulus. Multiple end plate defects were associated with lower values of IDP and higher degeneration scores when compared with erosions and Schmorl's nodes. CONCLUSIONS: Disc degeneration has a stronger association with large or multiple end plate defects than with small or single defects (of any type). Large end plate defects probably allow greater volume changes within the disc, leading to greater nucleus decompression.

How are adjacent spinal levels affected by vertebral fracture and by vertebroplasty? A biomechanical study on cadaveric spines.

BACKGROUND CONTEXT: Spinal injuries and surgery may have important effects on neighboring spinal levels, but previous investigations of adjacent-level biomechanics have produced conflicting results. We use "stress profilometry" and noncontact strain measurements to investigate thoroughly this long-standing problem. PURPOSE: This study aimed to determine how vertebral fracture and vertebroplasty affect compressive load-sharing and vertebral deformations at adjacent spinal levels. STUDY DESIGN: We conducted mechanical experiments on cadaver spines. METHODS: Twenty-eight cadaveric spine specimens, comprising three thoracolumbar vertebrae and the intervening discs and ligaments, were dissected from fourteen cadavers aged 67-92 years. A needle-mounted pressure transducer was used to measure the distribution of compressive stress across the anteroposterior diameter of both intervertebral discs. "Stress profiles" were analyzed to quantify intradiscal pressure (IDP) and concentrations of compressive stress in the anterior and posterior annulus. Summation of stresses over discrete areas yielded the compressive force acting on the anterior and posterior halves of each vertebral body, and the compressive force resisted by the neural arch. Creep deformations of vertebral bodies under load were measured using an optical MacReflex system. All measurements were repeated following compressive injury to one of the three vertebrae, and again after the injury had been treated by vertebroplasty. The study was funded by a grant from Action Medical Research, UK ($143,230). Authors of this study have no conflicts of interest to disclose. RESULTS: Injury usually involved endplate fracture, often combined with deformation of the anterior cortex, so that the affected vertebral body developed slight anterior wedging. Injury reduced IDP at the affected level, to an average 47% of pre-fracture values (p<.001), and transferred compressive load-bearing from nucleus to annulus, and also from disc to neural arch. Similar but reduced effects were seen at adjacent (non-fractured) levels, where mean IDP was reduced to 73% of baseline values (p<.001). Vertebroplasty partially reversed these changes, increasing mean IDP to 76% and 81% of baseline values at fractured and adjacent levels, respectively. Injury also increased creep deformation of the vertebral body under load, especially in the anterior region where a 14-fold increase was observed at the fractured level and a threefold increase was observed at the adjacent level. Vertebroplasty also reversed these changes, reducing deformation of the anterior vertebral body (compared with post-fracture values) by 62% at the fractured level, and by 52% at the adjacent level. CONCLUSIONS: Vertebral fracture adversely affects compressive load-sharing and increases vertebral deformations at both fractured and adjacent levels. All effects can be partially reversed by vertebroplasty.

Development and validation of a subject-specific finite element model of the functional spinal unit to predict vertebral strength.

Finite element models of an isolated vertebral body cannot accurately predict compressive strength of the spinal column because, in life, compressive load is variably distributed across the vertebral body and neural arch. The purpose of this study was to develop and validate a patient-specific finite element model of a functional spinal unit, and then use the model to predict vertebral strength from medical images. A total of 16 cadaveric functional spinal units were scanned and then tested mechanically in bending and compression to generate a vertebral wedge fracture. Before testing, an image processing and finite element analysis framework (SpineVox-Pro), developed previously in MATLAB using ANSYS APDL, was used to generate a subject-specific finite element model with eight-node hexahedral elements. Transversely isotropic linear-elastic material properties were assigned to vertebrae, and simple homogeneous linear-elastic properties were assigned to the intervertebral disc. Forward bending loading conditions were applied to simulate manual handling. Results showed that vertebral strengths measured by experiment were positively correlated with strengths predicted by the functional spinal unit finite element model with von Mises or Drucker-Prager failure criteria ( R2 = 0.80-0.87), with areal bone mineral density measured by dual-energy X-ray absorptiometry ( R2 = 0.54) and with volumetric bone mineral density from quantitative computed tomography ( R2 = 0.79). Large-displacement non-linear analyses on all specimens did not improve predictions. We conclude that subject-specific finite element models of a functional spinal unit have potential to estimate the vertebral strength better than bone mineral density alone.

Intervertebral disc degeneration can predispose to anterior vertebral fractures in the thoracolumbar spine.

UNLABELLED: Mechanical experiments on cadaveric thoracolumbar spine specimens showed that intervertebral disc degeneration was associated with reduced loading of the anterior vertebral body in upright postures. Reduced load bearing corresponded to locally reduced BMD and inferior trabecular architecture as measured by histomorphometry. Flexed postures concentrated loading on the weakened anterior vertebral body, leading to compressive failure at reduced load. INTRODUCTION: Osteoporotic fractures are usually attributed to age-related hormonal changes and inactivity. However, why should the anterior vertebral body be affected so often? We hypothesized that degenerative changes in the adjacent intervertebral discs can alter load bearing by the anterior vertebral body in a manner that makes it vulnerable to fracture. MATERIALS AND METHODS: Forty-one thoracolumbar spine "motion segments" (two vertebrae and the intervertebral disc) were obtained from cadavers 62-94 years of age. Specimens were loaded to simulate upright standing and flexed postures. A pressure transducer was used to measure the distribution of compressive "stress" inside the disc, and stress data were used to calculate how compressive loading was distributed between the anterior and posterior halves of the vertebral body and the neural arch. The compressive strength of each specimen was measured in flexed posture. Regional volumetric BMD and histomorphometric parameters were measured. RESULTS: In the upright posture, compressive load bearing by the neural arch increased with disc degeneration, averaging 63 +/- 22% (SD) of applied load in specimens with severely degenerated discs. In these specimens, the anterior half of the vertebral body resisted only 10 +/- 8%. The anterior third of the vertebral body had a 20% lower trabecular volume fraction, 16% fewer trabeculae, and 28% greater intertrabecular spacing compared with the posterior third (p < 0.001). In the flexed posture, flexion transferred 53-59% of compressive load bearing to the anterior half of the vertebral body, regardless of disc degeneration. Compressive strength measured in this posture was proportional to BMD in the anterior vertebral body (r2 = 0.51, p < 0.001) and inversely proportional to neural arch load bearing in the upright posture (r2 = 0.28, p < 0.001). CONCLUSIONS: Disc degeneration transfers compressive load bearing from the anterior vertebral body to the neural arch in upright postures, reducing BMD and trabecular architecture anteriorly. This predisposes to anterior fracture when the spine is flexed.

[The feature of experimental endplate fracture in lumbar spine and its related factors].

OBJECTIVE: To evaluate the feature of experimental endplate fracture in lumbar spine and its related factors. METHODS: Nineteen cadaveric lumbar motion segments aged 48 - 77 years were compressed by overload to fracture the endplate and dissected into isolated vertebrae to evaluate feature of their endplate failure. Before and after failure of endplate, radiographic tests were taken on every motion segment. The bone mineral density (BMD), bone mineral content (BMC) of the vertebral body and endplate were tested respectively before endplate fracture. RESULTS: Among 19 motion segments, 16 were fractured and accounted for 84.2% of all and fracture featured as stellate, step, depression and intrusion. Fracture concentrated on the center or anterior of superior endplate of the inferior vertebrae in one motion segment. Failure load of endplate was positively correlated with BMD, BMC of vertebral endplate. Within one vertebral body, the BMD and BMC of its superior endplate was markedly less than that of inferior endplate, on the other hand, the difference of BMD and BMC of endplate around one disc was opposite. CONCLUSIONS: Fractures usually concentrate on the center or anterior part of superior endplate of one vertebrae and are hard to be identified by conventional radiographic examination. Failure load of endplate is positively correlated with BMD, BMC of vertebral body and endplate. There might be certain relationship between feature of fracture and severity of disc degeneration.

Spine biomechanics.

Current trends in spine research are reviewed in order to suggest future opportunities for biomechanics. Recent studies show that psychosocial factors influence back pain behaviour but are not important causes of pain itself. Severe back pain most often arises from intervertebral discs, apophyseal joints and sacroiliac joints, and physical disruption of these structures is strongly but variably linked to pain. Typical forms of structural disruption can be reproduced by severe mechanical loading in-vitro, with genetic and age-related weakening sometimes leading to injury under moderate loading. Biomechanics can be used to quantify spinal loading and movements, to analyse load distributions and injury mechanisms, and to develop therapeutic interventions. The authors suggest that techniques for quantifying spinal loading should be capable of measurement "in the field" so that they can be used in epidemiological surveys and ergonomic interventions. Great accuracy is not required for this task, because injury risk depends on tissue weakness as much as peak loading. Biomechanical tissue testing and finite-element modelling should complement each other, with experiments establishing proof of concept, and models supplying detail and optimising designs. Suggested priority areas for future research include: understanding interactions between intervertebral discs and adjacent vertebrae; developing prosthetic and tissue-engineered discs; and quantifying spinal function during rehabilitation. "Mechanobiology" has perhaps the greatest future potential, because spinal degeneration and healing are both mediated by the activity of cells which are acutely sensitive to their local mechanical environment. Precise characterisation and manipulation of this environment will be a major challenge for spine biomechanics.

Sensorimotor function of the cervical spine in healthy volunteers.

BACKGROUND: Sensorimotor mechanisms are important for controlling head motion. However, relatively little is known about sensorimotor function in the cervical spine. This study investigated how age, gender and variations in the test conditions affect measures of position sense, movement sense and reflex activation in cervical muscles. METHODS: Forty healthy volunteers (19M/21F, aged 19-59 years) participated. Position sense was assessed by determining repositioning errors in upright and flexed neck postures during tests performed in 25%, 50% and 75% cervical flexion. Movement sense was assessed by detecting thresholds to passive flexion and extension at velocities between 1 and 25°s(-1). Reflexes were assessed by determining the latency and amplitude of reflex activation in trapezius and sternocleidomastoid muscles. Reliability was evaluated from intraclass correlation coefficients. FINDINGS: Mean repositioning errors ranged from 1.5° to 2.6°, were greater in flexed than upright postures (P=0.006) and in people aged over 25 years (P=0.05). Time to detect head motion decreased with increasing velocity (P<0.001) and was lower during flexion than extension movements (P=0.002). Reflexes demonstrated shorter latency (P<0.001) and greater amplitude (P=0.009) in trapezius compared to sternocleidomastoid, and became slower and weaker with age. None of the measures were influenced by gender. Reliability was good for movement sense measures, but was influenced by the test conditions when assessing position sense. INTERPRETATION: Increased repositioning errors and slower reflexes in older subjects suggest that sensorimotor function in the cervical spine becomes impaired with age. In position sense tests, reliability was influenced by the test conditions with mid-range flexion movements, performed in standing, providing the most reliable measurements.

Annulus Fibrosus Can Strip Hyaline Cartilage End Plate from Subchondral Bone: A Study of the Intervertebral Disk in Tension.

Study Design Biomechanical study on cadaveric spines. Objective Spinal bending causes the annulus to pull vertically (axially) on the end plate, but failure mechanisms in response to this type of loading are poorly understood. Therefore, the objective of this study was to identify the weak point of the intervertebral disk in tension. Methods Cadaveric motion segments (aged 79 to 88 years) were dissected to create midsagittal blocks of tissue, with ∼10 mm of bone superior and inferior to the disk. From these blocks, 14 bone-disk-bone slices (average 4.8 mm thick) were cut in the frontal plane. Each slice was gripped by its bony ends and stretched to failure at 1 mm/s. Mode of failure was recorded using a digital camera. Results Of the 14 slices, 10 failed by the hyaline cartilage being peeled off the subchondral bone, with the failure starting opposite the lateral annulus and proceeding medially. Two slices failed by rupturing of the trabecular bone, and a further two failed in the annulus. Conclusions The hyaline cartilage-bone junction is the disk's weak link in tension. These findings provide a plausible mechanism for the appearance of bone and cartilage fragments in herniated material. Stripping cartilage from the bony end plate would result in the herniated mass containing relatively stiff cartilage that does not easily resorb.

Porosity and Thickness of the Vertebral Endplate Depend on Local Mechanical Loading.

STUDY DESIGN: Mechanical and microcomputed tomography (micro-CT) study of cadaver spines. OBJECTIVE: To compare porosity and thickness of vertebral endplates with (1) compressive stresses measured in adjacent intervertebral discs and (2) grade of disc degeneration. SUMMARY OF BACKGROUND DATA: Endplate porosity is important for disc metabolite transport, and yet porosity increases with age and disc degeneration. We hypothesize that porosity is largely determined by mechanical loading from adjacent discs. METHODS: Forty motion segments (T8-9 to L4-5) were dissected from 23 cadavers aged 48 to 98 years. Each was subjected to 1 kN compression during which time intradiscal stresses were measured by pulling a pressure transducer along the disc's midsagittal diameter. "Stress profiles" revealed the average pressure in the nucleus, and the maximum stress in the anterior and posterior annulus. Specimens were further dissected to obtain discs with endplates (and 5 mm of bone) on either side. Microcomputed tomography scans (resolution 35 µm) were analyzed to calculate thickness and porosity in the midsagittal regions of all 80 endplates. Average values for the anterior, central, and posterior regions of each endplate were obtained. Disc degeneration was assessed macroscopically and microscopically. RESULTS: Endplate porosity was inversely related to its thickness, being greatest in the central region opposite the nucleus, and least near the periphery. Superior endplates (relative to the disc) were 14% thicker (P < 0.001) and 4% less porous (P = 0.008) than inferior. In each of the 3 endplate regions (anterior, central, and posterior), porosity was inversely and significantly related to mechanical loading (pressure or maximum stress) in the adjacent disc region (P < 0.01 in all cases). Disc degeneration was best predicted by (reduced) nucleus pressure (R = 0.46, P < 0.001) and (reduced) maximum stress in the anterior annulus (R = 0.31, P < 0.001). CONCLUSION: Mechanical loading is a major determinant of endplate thickness and porosity. Disc degeneration is more closely related to reduced disc stresses than to endplate thickness or porosity. LEVEL OF EVIDENCE: N/A.