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- •The Lumbar Spine
- •Contents
- •Contributing Authors
- •Preface
- •Acknowledgments
- •Epidemiology and the Economics of Low Back Pain
- •Pathophysiology of Nerve Root Pain in Disc Herniation and Spinal Stenosis
- •Biomechanical Considerations of Disc Degeneration
- •Clinical Spinal Instability Resulting from Injury and Degeneration
- •Morphologic Changes of End Plates in Degenerative Disc Disease
- •Spinal Instrumentation
- •Fracture and Repair of Lumbar Vertebrae
- •Genetic Transmission of Common Spinal Disorders
- •Genetic Applications to Lumbar Disc Disease
- •Clinical Neurophysiologic and Electrodiagnostic Testing in Disorders of the Lumbar Spine
- •Sensorimotor Control of the Lumbar Spine
- •Outcomes Assessment: Overview and Specific Tools
- •The Role of Outcomes and How to Integrate Them into Your Practice
- •Manual Therapy in Patients with Low Back Pain
- •Acupuncture and Reflexology
- •Returning Workers to Gainful Employment
- •Occupational Ergonomics
- •Preparation for Surgery
- •Surgical Approaches to the Thoracolumbar Spine
- •Surgical Approaches to the Lumbar Spine: Anterior and Posterior
- •Posterior and Anterior Surgical Approaches to the Lumbosacral Junction
- •Endoscopic Anterior Lumbar Procedures
- •Biology of Bone Grafting: Autograft and Allograft
- •Bone Graft Substitutes in Spinal Surgery
- •Spinal Instrumentation Overview in Lumbar Degenerative Disorders: Cages
- •Translaminar Screw Fixation
- •Lumbar Disc Disorders
- •Facet Joint Denervation: A Minimally Invasive Treatment for Low Back Pain in Selected Patients
- •Intradiscal Electrothermal Therapy
- •Operative Management of the Degenerative Disc: Posterior and Posterolateral Procedures
- •Posterior Lumbar Interbody Fusion
- •Operative Treatment of Anterior Procedures
- •Operative Treatment of Anterior and Posterior Fusion
- •Degenerative Disc Disease: Fusion Cages and Dowels
- •Minimally Invasive Procedures for Anterior Column Fusion and Reconstruction
- •Degenerative Disc Disease: Complications of Surgery
- •Dynamic Stabilization in the Treatment of Low Back Pain Due to Degenerative Disorders
- •Lumbar Artificial Disc Replacement: Rationale and Biomechanics
- •Lumbar Disc Replacement: Current Model, Results, and the Future
- •Disc Herniation: Definition and Types
- •Disc Herniation: Imaging
- •Disc Herniation: Nonoperative Treatment
- •Operative Treatment of Disc Herniation: Natural History and Indications for Surgery
- •Operative Treatment of Disc Herniation: Laminotomy
- •Chymopapain and Chemonucleolysis
- •Microscopic Lumbar Discectomy
- •Classification, Natural History, and Clinical Evaluation
- •Imaging of Spinal Stenosis and Degenerative Lumbar Spondylolisthesis with Stenosis

CHAPTER 6/SPINAL INSTRUMENTATION / 83
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72. Hitchon PW, Goel VK, Rogge T, et al. Biomechanical studies of a
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CHAPTER 7
Fracture and Repair of Lumbar Vertebrae
Tony S. Keller, Victor Kosmopoulos, and Thomas Steffen
The lumbar spine, located between the sacrum and thoracic regions of the vertebral column (the lower back),
typically consists of five vertebrae. These five vertebrae
generally increase in size from the superior to the inferior lumbar spine and are larger than both the cervical
and thoracic vertebrae. Similar to size, the weight-bearing ability of lumbar vertebrae is often greater, resulting
in a higher incidence of pain following injury. From a
mechanical point of view, the weight-bearing or structural capacity (force at failure) of the vertebrae depends
on both material properties (bone mineral content, trabecular bone tissue density, and apparent density) and
geometric properties (size, orientation, and connectivity
of bone elements). A close association between bone
mineral loss due to osteoporosis and the risk of fracture
has been clearly established. Skeletal structures such as
the vertebral bodies, which are comprised primarily of
trabecular bone, are particularly at risk. The purpose of
this chapter is to discuss the mechanics of vertebral
compression fractures and trabecular bone damage. An
understanding of microdamage and microfracture of
vertebrae is used to facilitate discussions of cement
repair strategies.
STRUCTURAL AND MECHANICAL BEHAVIOR
OF LUMBAR VER TEBRAE
Mechanical properties not only vary from vertebra to
vertebra or level to level, but also can vary dramatically
within a given vertebral body. Trabeculae tend to be
denser, rodlike structures in the inferior and superior
sections in contrast to the less dense, platelike trabeculae that are associated with the central region of the
lumbar vertebral centrum (1). Studies that have examined the physical and mechanical properties of lumbar
vertebral trabecular bone have also shown that trabecular bone underlying the normal intervertebral disc
nucleus is significantly stronger, stiffer, and denser in
comparison to trabecular bone underlying the disc annu-
bone properties have been attributed, in part, to adaptation to the heterogeneous pressure distribution within
the normal intervertebral disc (4). Namely, the pressurized disc nucleus exerts higher stresses on the underlying end plate and trabecular bone compared to pressure
transmitted by the disc annulus. Keller et al. (2,4) also
noted that disc degeneration reduces intravertebral variations in trabecular bone-apparent stiffness, strength,
and density in regions adjacent to the end plate, which
presumably reflects a more uniform or homogeneous
distribution of pressure and stress within the degenerated disc.
The architectural design or structure of bone in human
vertebrae and elsewhere in the body is very complex
ranging from a very porous solid (trabecular bone) to a
very dense solid (compact bone). The anterior column, or
centrum, of human vertebrae is comprised of only a very
thin cortical shell (less than 2 mm), which is virtually
indistinguishable from the trabeculae that comprise the
bulk of the vertebral centrum (Fig. 7-1). Silva et al. (5)
performed a f inite element analysis of an idealized lumbar vertebrae, and reported that the cortical shell’s contribution was only 10% of the total vertebral strength, thus
making the trabecular centrum the main load-bearing
structure. Using anatomically accurate microstructural
finite element simulations, the authors estimate that
removal of the trabecular centrum, leaving only the vertebral shell, results in ov er an eightfold decrease in apparent stiffness compared to the intact vertebrae (having
both the vertebral shell and centrum) (Fig. 7-2). Finite
element analysis of vertebral mechanics is covered in
more detail in later sections of this chapter.
Given the porous nature of bone, the relati ve amount of
bone tissue is described histologically using apparent
density (ρ
bone tissue present within a given volume. Clinically,
estimates of bone mass are most commonly obtained
using dual energy X-ray absorptiometry (DEXA). This
). Apparent density is defined as the mass of
a
85

86 /SECTION I/BASIC SCIENCE
FIG. 7-1. Volume rendering of microcomputed tomography
scan image of T10 osteopenic ver tebral body (1.8-mm thick
section). (From Keller TS, Kosmopoulos V, Liebschner MAK.
Modeling of bone loss and fracture in osteoporosis.In: Gunzburg R, Szpalski M, eds.Vertebral osteoporotic compression
fractures. Philadelphia: Lippincott Williams & Wilkins, 2002:
35–50.)
low-radiation method provides measures of the bone
mineral content (BMC, g/cm) and bone mineral density
2
(BMD, g/cm
) distributions within the body (6).
Although BMC and BMD are not true volumetric measures of tissue mass or apparent density, both have been
shown to be useful predictors of bone fragility (2,7–9).
Hansson (8) performed in vitro mechanical compression
tests on 109 intact L1-L4 vertebral centrum specimens
from subjects spanning five decades in age (31 to 79
years). In this test series, the BMC ranged from 1.44 g/cm
to 6.39 g/cm (mean 3.33 g/cm), and the compressive
force at failure F
ranged from 1,520 Newtons (N) to
ult
10,987 N (mean 3,850 N). From this data the following
linear correlations are obtained (10):
F
= 1,535 BMC − 1,258 (R2= 0.74)
ult
= − 75 AGE + 8,199 (R2= 0.30)
F
ult
Examination of these relationships indicates that the
compressive strength of the lumbar vertebral centrum is
strongly and positively correlated to BMC, but is
weakly and negatively correlated to subject age. After
age 30, lumbar vertebral compressive strength is predicted to decrease 750 N per decade, declining to 1,500
N at 89 years of age. When the lumbar vertebral
strength decreases to 1,500 N or lower, failure of the
vertebral structures can occur under postural loads
imposed by the weight of the body above the vertebrae
(10,11).
From a mechanical point of view, ultimate force is a
structural property that is dependent upon both the size
A B
FIG. 7-2. Finite element microstr uctural models used to simulate experimental compression of (A) just
the cortical shell (without the trabecular centrum) and (B) of the complete vertebral body (cortical shell
and trabecular centrum).

CHAPTER 7/FRACTURE AND REPAIR OF LUMBAR VERTEBRAE / 87
(geometry) and composition (material) of the tissue.
Thus, one cannot directly compare the ultimate force of
vertebrae from different regions in the spine because the
size of the cervical, thoracic, and lumbar vertebrae varies
appreciably from each other and from one level to the
next. For this reason, material property measurements,
such as stress or force/area are often preferred, since they
account for geometry variations of different size structures. An estimate of the apparent stress at failure (σ
6
MPa or 10
dividing the ultimate force (F
area (mm
N/m2) can be obtained for Hansson’s data by
, N) by the cross-sectional
2
) reported for the vertebral end plate. The
ult
ult
apparent stress at failure of the lumbar vertebrae is found
to range from 0.95 to 4.95 MPa (mean 2.29 MPa). Here
apparent stress refers to the fact that we still have not
accounted for the porosity of the vertebral centrum.
Namely, two similar size vertebrae can have very different structural properties if their porosity or apparent density differs appreciably.
Keller (12) published empirical relationships from in
vitro mechanical tests that can be used to calculate the
compressive apparent strength (ρ
σa= 97.8 ρ
, MPa) of vertebral bone:
a
2.30
a
where ρais the apparent density (0.05 < ρa< 0.30 g/
3
). Note that the approximately square exponent
cm
means that a relative reduction in apparent density of
one half will produce a corresponding relative reduction
in compressive apparent strength of one fourth. In older
adults (more than 70 years), the apparent density of
human vertebral trabecular bone can be as low as 0.05
3
, which corresponds to an ultimate compressive
g/cm
strength of only 0.05 MPa. Stresses much greater than
0.05 MPa are produced in vertebrae when subjected to
compressive forces associated with weight bearing in
upright postures (10).
OSTEOPOROSIS
Osteoporosis is a skeletal disorder distinguished by
weakened skeletal architecture caused by suboptimal
bone development or a reduction in bone mass. It is a disease that weakens the structural properties of bone in
both men and women, and results in fracture when loads
applied to bone exceed the bone’s ability to support those
loads. Thus, osteoporosis is a significant risk factor for
,
fracture and its incidence increases with age. In the
United States, 10 million individuals have been diagnosed with osteoporosis and another 18 million have low
bone mass, which places them at increased risk for osteoporosis and fracture. Treatment of osteoporotic fracture is
estimated to be as high as $15 billion annually (13).
Osteoporosis is accompanied by reduced bone
strength, and has been clinically characterized using noninvasive radiographic measures such as BMD, BMC, and
apparent density (ρ
). The standard diagnosis for osteo-
a
porosis is 2.5 standard deviations or more below the
mean BMD (or BMC) for an average 30-y ear -old adult of
the same sex. Osteoporosis affects bone quality, which
refers to bone architecture, rate of adaptation/remodeling,
level of mineralization, and damage accumulation (13).
In osteoporosis perforations exist within the structure
causing increased fragility (Fig. 7-3). One reason for this
fragility increase is due to the replacement of the platelike closed cell trabecular structures by open cell rodlike
structures, resulting in an increasingly porous appearance. Mechanically, trabecular-buckling strength is dependent on the diameter, length, distance between crosslinks, and the material properties of individual
trabeculae. In osteoporosis the vertebral trabeculae
become thinner and cross-linking continuity with horizontal trabeculae is reduced without compensation by the
vertebral shell. Throughout the progression of this disease, deterioration of the trabecular structure induces the
FIG. 7-3. Volumetric rendering of a 2.56 mm × 2.56 mm × 2.56 mm region of trabecular bone from the
human lumbar vertebral centrum. The panels (from left to right) illustrate progressive and uniform
bone loss resulting in a decrease of the bone volume fraction from 15.3% to 11.1% to 7.66%. Note that
there is significant loss of trabecular connectivity following the simulated bone loss. The 20 µm voxel
(volume pixel) images were reconstructed from a histologic specimen using a quantitative serial imaging and marching cubes algorithm. (From Saxena R, Keller TS. Computer modeling for evaluating trabecular bone mechanics. In: An YH, Draughn RA, eds.Mechanical testing of bone and the bone-implant
interface. Boca Raton, FL: CRC Press, 1999:407–436.)

88 /SECTION I/BASIC SCIENCE
reduction in bone mass (and thus density) ensuring an
increased rate of fracture.
VERTEBRAL FRACTURE
Approximately 700,000 osteoporotic vertebral fractures occur per year in the United States with 230,000
resulting in chronic disabling pain (13,14). Vertebral fractures alter force transmission to the vertebral body segments, lead to vertebral body collapse, increase fracture
risk (fivefold) to neighboring vertebrae (15), and result in
progressive spinal deformity (e.g., kyphosis) (16).
Vertebral fracture may occur as a result of a traumatic
force exceeding the load-bearing capacity of the vertebral body, or by the accumulation of trabecular tissuelevel damage (microdamage) from repeated (fatigue),
uniform and nonuniform, everyday subfailure-type postural loading (no trauma) (10,11,17). A traumatic force
can result from high-impact falls to normal lifting and
bending (13).
Apparent density and its clinical counterpart BMD provide good estimates of bone mechanical properties but are
not definitive in predicting vertebral strength (12). The
load-bearing capacity of the lumbar vertebrae (structural
characteristics) coupled with the applied loads (magnitude,
duration, rate) determine fracture risk (Fig. 7-4). Vertebral
fracture is about four times more common in women than
in men, and the risk for a vertebral fracture has been found
to increase almost exponentially with age. The frequency
of osteoporotic vertebral fracture also increases during
menopause in women and continues to steadil y increase in
frequency throughout the remainder of life. Furthermore,
depending on the age groups studied (40 years to more
than 80 years), the prevalence of osteoporotic vertebral
fractures varies from around 5% to somewhat over 50%
(18–21).
Compression Fracture Classification
Vertebral compression fractures are primarily caused
by excessive axial loads that may result in vertebral body
height reductions, and in the more extreme cases, deformities. The axial failure loads for lumbar vertebrae have
been estimated and classified by age. In general, a force
of approximately 4,200 N produces fracture in individuals over the age of 60, whereas under the age of 40, an
increased load of approximately 7,600 N causes fracture
(22,23). As we noted earlier, however, the compressive
strength of lumbar vertebrae is closely dependent on the
size and quality of the segment, and, in the case of osteoporosis, can be substantially lower than 4,200 N.
Different postural loading conditions (e.g., uniform and
nonuniform) endured by the vertebral body result in different vertebral fracture geometries at failure. In the most
general case, postural loads are greatest on the anterior
aspect of the vertebral body resulting in what is known as
anterior wedge-type compression fractures. Anterior compression fractures have been classified into four subtypes
(22): (a) both end plates are damaged; (b) only the superior
end plate is damaged (most common); (c) only the inferior
end plate is damaged; and (d) both end plates are intact but
anterior cortical shell is damaged.
In the least severe case, hairline fractures to the cortical shell or the vertebral end plate may occur . These types
of hairline fractures are difficult to diagnose and may
plague the patient with pain. End-plate damage can occur
in the central regions, periphery regions, or as transverse
cracks across the end plate (22). End-plate damage has
been proposed to be the initial stage of more severe vertebral compression fractures (1,24,25). Burst fractures
are the most severe and can range from an end-plate fracture resulting in disc intrusion into the vertebral body
(22) to complete shattering of the vertebral body. Burst
fractures occur at axial loads ranging from 6,000 to
10,000 N (26).
FIG. 7-4. Vertebral material, geometry, and structure are
biomechanical determinants of fracture risk. Loading characteristics (magnitude, profile, duration, and rate) also influence fracture risk.
Clinical Definition of Vertebral Fracture
Radiographic detection of vertebral compression fractures is often the confir mation of the presence of osteoporosis or bone fragility. Without any known pathomorphologic aberrations distinguishing osteoporotic

CHAPTER 7/FRACTURE AND REPAIR OF LUMBAR VERTEBRAE / 89
bone from nonosteoporotic bone tissue, the fracture itself
defines pathology. Since the occurrence of a fracture is
not only the result of the mechanical properties of the
bone, but is also a function of the fracturing trauma, both
factors must be considered when defining osteoporosis.
In the presence of a patient with a recent fracture, knowing nothing or very little about the patient’s bone quality
or the forces involved in the trauma, the most practical
way for clarifying whether a fracture is osteoporotic or
not is Harold Frost’s criterion of the “everyday trauma.”
Frost stated that a fracture occurring because of an everyday trauma indicates that the patient has osteoporosis or
bone fragility. Even if current technology allows us to
determine, for example, the amount of bone mineral in
different parts of the human skeleton, we still lack practical techniques for measuring the fracture-generating
forces. Therefore the “e veryday trauma” definition is still
a practical measure for estimating bone fragility (27).
Hence, development of models that can simulate both the
loading and structural (trabecular) damage behavior of
vertebral bodies are important for understanding clinical
pathologies (e.g., osteoporosis) and for predicting bone
fragility and its risk for fracture.
TRABECULAR BONE DAMAGE
Trabecular bone is a porous structure (Figs. 7-1 to 7-4),
which behaves similarly to typical engineering materials
(and cortical bone) in compression until the ultimate
stress is reached. The mechanical behavior in trabecular
bone shows a relatively linear or elastic response for
deformations less than 1% (Fig. 7-5). The point at which
the mechanical behavior becomes nonlinear (strain
increasing at a greater rate than the stress) is def ined as
the yield strain and permanent or inelastic deformation
and damage occurs beyond yield. The yield point of ver-
tebral trabecular bone is similar for both compression and
tension: 0.84% and 0.78% indicate compressive and tensile yield strain, respectively, for vertebral trabecular
bone specimens (28). However, beyond yield the compressive load capacity of trabecular bone does not go to
zero as would be expected. Instead the load is maintained
or may even show a slight increase compared to the previously recorded ultimate load (Fig. 7-5B.).
Physically this behavior can be explained by understanding the compressive mechanics of porous structures.
As the pore spaces begin to collapse, the trabeculae collide and compress into each other increasing the trabecular bone-volume fraction (bone volume/combined bone
and pore space volume) of the specimen. This reduction
in pore space and consequent increase in volume fraction
results in a temporary load tolerance by the trabecular
structure. Thus, the load-carrying capacity of trabecular
bone is still quite substantial following compression fracture, and results in a large post-yield stress-strain response (28). This behavior is similar to elastoplastic
materials having large post-yield regions and therefore
can be modeled as such. In contrast, during tensile loading the load-carrying capacity of trabecular bone is minimal resulting in a smaller post-yield region and abrupt
failure. Note that in studying the mechanics of porous
structures it is often useful to clarify between whole specimen properties (e.g., vertebral body) by referring to
them as “apparent” and site-specific properties of the
individual constituents (e.g., trabeculae) by referring to
them as “tissue.”
Stress-Strain Behavior
The inelastic stress-strain behavior of bone is mainly a
result of cracks, plasticity, and viscous creep. Cracks
degrade stiffness, strength, and other material properties
A
FIG. 7-5. Experimental stress-strain cur ve displaying the load-unload-reload mechanical behavior (A)
and post-yield mechanical behavior (B) of an osteoporotic ver tebral body.
B

90 /SECTION I/BASIC SCIENCE
because of the imposed material discontinuities. The
complex strain behavior of vertebral trabecular bone and
other porous materials is a result of the cumulative ef fects
of the elastic strain, inelastic strain due to damage accumulation, plastic strain, and anelastic (viscous) strain
(29). Such strain behavior can be differentiated using a
load-unload-reload protocol. After unloading from a
damaging event, the stress-strain behavior of bone (trabecular and compact) is similar to that of composites
(30). Namely, bone recovers approximately three-fourths
of the total inelastic strains (29). Damaged bone shows
relativel y small changes in its elastic modulus or stiffness
during the initial onset (at low strain levels) of a reload.
As loads are increased (relativel y high strain levels) however, cracks propagate, and residual stresses are relieved
resulting in a curvilinear stress-strain behavior (Fig. 7-5)
(31). This c yclic load-unload-reload beha vior in time produces bone fatigue, which in turn reduces bone strength
and stiffness (32–36). Bone damage resulting from fatigue or creep can occur under elastic conditions (preyield loading) and has been accepted as a normal physiologic process (37–39).
Damage Mechanics
A microstructural reduction in tissue mechanical properties (e.g., strength, stiffness) is often referred to as
microdamage. The accumulation of microdamage,
microfracture, leads to local tissue discontinuities within
a single trabecula and a decrease in apparent vertebral
bone strength. Both microdamage and microfracture are
load-dependent, although bone microdamage occurs at a
higher incidence than microfracture (40). Microdamage
or microfracture may act as a precursor for bone remodeling (41–44). The resorption phase of bone remodeling
can in turn induce further microdamage (45,46) by
increasing pore size. This increase in pore size (decrease
in apparent density and volume fraction) consequentially
reduces the apparent modulus, increases the tissue strain,
and results in a temporary increase in bone fragility and
osteoporotic fracture risk (39,47–50). Gross vertebral
fracture can be a result of extensive microdamage or
microfracture accumulation to the trabecular structure
(47,51,52).
Continuum damage mechanics (CDM) is a rapidly
developing area in the study of bone fracture. For a simple isotropic or axisymmetric material, the presence of
cracks or damage (D) can be expressed as a simple scalar
representing the loss of load-carrying area (Fig. 7-6) (53).
An effective modulus (E
scaling the elastic modulus (E) by the damage parameter
(D):
where D is continuous between zero (fractured material)
and 1 (undamaged material).
) can then be determined by
EFF
E
= (E)(D)
EFF
FIG. 7-6. Schematic illustration of the isotropic damage concept defined by continuum damage mechanics.
To study vertebral trabecular bone damage a quasicontinuum CDM approach has been developed based on
an empirical nonlinear stress-strain relationship (generalized tangent hyperbolic law) (54,55) and an elastoplastic modulus reduction (EPMR) scheme (56,57). The
latter assumes that the evolution of trabecular bone
microdamage (D) can be modeled as a change in bone
elastic modulus or stiffness, wherein the elastic modulus of bone is assumed to be proportional to the apparent density cubed (discussed earlier) (12,58). The
EPMR scheme is easily implemented using the finite
element method and can therefore be used to model the
damage evolution behavior of complex material geometries. The following sections illustrate the use of CDM
and the finite element method to study vertebral damage
and cement repair.
Finite Element Damage Simulations
The finite element method is a numerical technique that
provides approximations to theory. Finite element analysis
is an efficient method used to solve differential equations
over complex domains or structures. The structure is discretized and represented by finite elements formed by
nodes. Finite element modeling is especially attractive in
the analysis of heterogeneous and anisotropic structures,
such as trabecular bone, for which a closed form solution
using analytic methods will be impossible. In recent y ears,
anatomically accurate models of trabecular bone can and
have been investigated (59–61). These microstructural
finite element models are usually constructed from microcomputed tomography raster arrays at spatial resolutions
of 150 µm or less for large volumes and 50 µm or less for
3
small volumes of bone (less than 50 mm
). Microstructural

CHAPTER 7/FRACTURE AND REPAIR OF LUMBAR VERTEBRAE / 91
finite element models enable calculation and visualization
of internal tissue stresses and strains.
Damage simulations of complex structures, such as
that of trabecular bone in the vertebral body, can be studied using microstructural f inite element models. Continuum damage and EPMR approaches have been inte grated
within the finite element numerical framework and used
as a research tool to investigate existing or potential bone
damage (56,57,62–65). Furthermore, finite element bone
damage models can be used to study the mechanics of
surgical repair. To date however, only a few studies have
used finite element damage models to study the f ailure
mechanisms (56,57,64–67) and surgical repair (vertebroplasty) efficacy (56,64,67) of the vertebral body. Simulation of vertebral body damage using the finite element
approach is presented in the following section, and repair
simulations will be discussed later in this chapter.
Kosmopoulos and Keller (64) coupled the EPMR damage approach with an anatomically accurate two-dimensional (2D) microstructural finite element model of a
midsagittal vertebral body section. Two vertebral loading
postures were simulated by using a uniform loading profile and a nonuniform (ramped) loading profile. Compressive loads were applied incrementally over a stress
range of 0 to 3 MPa. The experimentally validated (65)
EPMR scheme and iterative finite element analysis
resulted in a nonlinear stress-strain response (Fig. 7-5A)
and a decrease in the apparent modulus of the vertebral
body. At the highest stress the uniformly loaded model
resulted in a total vertebral body apparent modulus
reduction of 32%, while the ramp-loaded model resulted
in a 95% apparent modulus reduction, compared to the
initial undamaged vertebral body apparent modulus (E
0
444 MPa). Microdamage initiation (modulus reduction of
5%) was first apparent at an applied stress level of 1.5
MPa for both the uniform-loaded and ramped-loaded
cases. At the maximum applied stress there was a trabecular bone modulus reduction of 40% or more in 10.4%
and 15.9% of the total bone elements for the uniformloaded and ramped-loaded microdamage models, respectively (Fig. 7-7). For the uniform-loaded vertebral body
the distribution of highly stressed elements followed a
column-wise (superior-inferior) pattern within the cortical shell and more centrally located trabeculae, in contrast to the ramped-loaded case where the highly stressed
elements were located on the posterior vertebral shell.
The ramp-loaded model resulted in a substantially greater
number of highly stressed bone elements (20.9% of bone
elements with stress concentrations greater than 3) compared to the uniform-loaded model (4.2% of bone elements with stress concentrations greater than 3).
VERTEBRAL REPAIR
Most compressive fractures do not affect the spinal
cord, are relati v ely stab le, and are therefore asymptomatic
in nature. These types of fractures rarely require surgical
intervention (68,69) and are treated using conservative
nonsurgical approaches. These treatments often involve a
short period of postural reduction (bed rest) directly after
incidence, followed by external immobilization, and
finally by gradual ambulation (16,70). Bed rest is usually
recommended for the first 4 to 6 weeks followed by 6 to
12 weeks of bracing using a rigid orthosis. In severe cases
of burst fractures, tissue fragments may enter the spinal
canal and cause myelopathy (71). Fractures may lead to
progressive deformity and instability, spinal stenosis,
neurologic deficit, and pain requiring surgical intervention. The probability of fracture healing without surgery
decreases as the severity or amount of tissue involved in
the fracture increases (72).
Bone Cement Augmentation
Vertebroplasty and kyphoplasty are two recently de veloped minimally invasive repair techniques for the treatment of vertebral compressive fractures. Unlike traditional treatments, these bone cement augmentation repair
procedures help to restore spinal alignment and decrease
chronic pain (73).
Vertebroplasty involves the forced injection, usually
using either a parapedicular or transpedicular approach, of
bone cement, usually polymethylmethacrylate (PMMA),
through one (unipedicular) or two bone (bipedicular)
biopsy needles into the closed space of a collapsed vertebral body (16,73). The injections are performed under
continuous fluoroscopic guidance, and for high-risk cases,
computed tomography is also used (74,75). This technique
=
provides pain relief and stabilization, but typically does
not restore the height of the collapsed vertebral body.
Kyphoplasty involves the insertion of a bone balloon
into the vertebral body using biplanar fluoroscopic image
guidance. The balloon is inflated causing the trabecular
bone to compact, resulting in a suitable cavity to reexpand the vertebral body. In kyphoplasty, bone cement
is injected with more control and with less pressure than
during vertebroplasty. Another advantage of kyphoplasty
is the restoration of vertebral body height and reduction
of spinal deformity (16,73).
The main complication with each of these cement
repair techniques is associated with the use of PMMA. In
vertebroplasty cement, extravasation may occur since the
PMMA is injected at much higher pressures. The rates of
this occurrence have been reported to be as high as 40%
when PMMA cement is used in the treatment of osteoporotic compression fractures (15), and is greater when
using higher injection volumes or less viscous cement
(76). Another concern with PMMA is its high polymerization temperature. Polymerization has been reported to
produce average peak cement core temperatures of 87°C
and 108°C for small (approximately 14.9 cm
3
(approximately 27.6 cm
) cement volume fills (77).
3
) and larger

92 /SECTION I/BASIC SCIENCE
A
C
B
FIG. 7-7. Numer ical simulation of vertebral trabecular bone microdamage using the elastoplastic modulus reduction finite element scheme. Four-node isoparametric elements were used to represent the
vertebral body structure, which was assumed to have isotropic material properties. The applied compressive stress (3 MPa) corresponds to upright posture loads acting on the lumbar spine (10).Two vertebral loading postures were simulated by using a uniform (A, B) and a nonuniform or ramped (C, D)
loading profile. In (A) and (C) the bone and marrow tissues are depicted as white and black elements,
respectively, whereas bone tissue damage (modulus reduction of 40% or greater) is depicted by the
dark gray elements. In (B) and (D), the gray scale intensity plots show the resulting stress concentrations (element axial stress/apparent stress, σ
respectively. Highly stressed elements are depicted as lighter gray (max σ
stressed elements as darker gray to black (min σ
) following the uniform and ramp loading profiles,
y/σa
y/σa
> 0).
< 6) and less severely
y/σa
D
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