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Chapter 5 The Intervertebral Disc: Normal, Aging, and Pathologic 83
age-related changes be classied as early degenerative discs,
whereas the term degenerative disc disease should be applied
if the disc is also painful.
28
Although the exact mechanism of disc degeneration has
not been determined, it is known to involve a complex interaction of factors, including ECM macromolecule changes,
decreased water content, altered enzyme activity, decreased
endplate permeability, impaired metabolite transport, structural failure, and cell senescence and death. ese biologic
and biomechanical factors cause extensive histomorphologic
changes of the disc, leading to disorganization of the anulus,
solidication of the nucleus, and thinning and calcication of
the cartilaginous endplates. Recently, it has also been suggested
that several general types of degeneration may exist—namely,
endplate driven and anulus driven—that potentially aect
dierent areas of the spine at dierent ages.
29
Matrix Macromolecule Changes
e most physiologically important changes of disc degeneration start in the nucleus.23 Early changes include increased
proteolytic degradation of aggrecan and other aggregating
proteoglycans coupled with an increased concentration of
nonaggregating proteoglycans. e accumulation of degraded
proteoglycans further impairs diusion of nutrients and oxygen
through the disc. A change in the proportions of the GAGs
chondroitan sulfate, heparan sulfate, and keratan sulfate also
occurs, with increasing amounts of heparan sulfate and keratan
sulfate as degeneration progresses. ese changes diminish
the hydroscopic properties of the ECM further, resulting in
decreased water content and decreased ability to imbibe water.
Loss of proteoglycans and hydration leads to decreased swelling pressure27 and loss of disc height. e changes result in
altered responses to applied biomechanical loads, ultimately
leading to the structural features of degeneration.
Intervertebral disc degeneration also results in disorganization and destruction of the collagen network.30 As the
overall proteoglycan and water content decreases, there is a
corresponding increase in collagen content. Collagen type I
replaces collagen type II in the inner anulus and nucleus, and
there is a tendency for collagen type I brils throughout the
disc to become coarser. e highly organized collagen ber
arrangements of the anulus are also disrupted, and collagen
and elastin networks become more disorganized. When the
collagen network has been damaged, disc biomechanics are
markedly altered, and the potential for structural damage
increases.
Increased levels of proinammatory cytokines lead to
increased production of proteinases, causing breakdown of
collagens such as types VI, IX, and X. Collagen type IX is
degraded in the pericellular microenvironment, allowing for
local alteration of this microenvironment during degeneration.
With disc degeneration, collagen type IX decreases similarly
to collagen type II, implying advanced stages of degeneration
and brosis of the nucleus. e synthesis of collagen type VI,
a matrix protein with relatively low cross-linking, increases as
degeneration progresses and functions to hold proliferating
cells together.
e overall ECM content in the nucleus is a well-controlled
equilibrium between degradative and synthetic pathways
involving numerous proteins. In disc degeneration, there is
an imbalance between degradative and synthetic pathways
whereby the latter overtake the former with a predominance
of catabolic enzyme activity. Proteinases of the matrix metalloproteinase (MMP) and “a disintegrin and metalloproteinase
with thrombospondin motifs” (ADAMTS) families cleave
proteoglycans, collagens, and other macromolecules and
have been implicated in the breakdown of the ECM.31 e
degradative enzymes MMP-3 and MMP-13 (also known as
stromelysin-1 and collagenase 3, respectively) have been
found at increased levels in degenerated human discs.
e regulation of MMP and ADAMTS production and
ECM macromolecule production is achieved by numerous
cytokines and growth factors. Of particular importance in disc
ECM homeostasis are members of the interleukin (IL) family
(catabolism) and transforming growth factor-β (anabolism)
superfamily.
32,33
Mediators of inammation such as nitric
oxide and prostaglandin E2 and the cytokines IL-1 and IL-6
are found at increased levels in degenerated discs.
32–34
e
synthetic capabilities of nucleus cells are unable to sustain
appropriate levels of aggrecan and collagen production in the
face of this increased catabolism, which contributes to further
degeneration of the disc.
Cellular Changes
It has long been recognized that there is a gradual progressive
loss of cells during disc degeneration,35 leading to further loss
of the ECM due to synthesis deciency. An increasing body
of literature has shown that apoptosis, or programmed cell
death, and cellular senescence may be responsible for many
of the features of degeneration.
also shown an increase in lacunae containing cell clusters,
36–38
More recent literature has
39,40
possibly causing an overall increased number of cells at the
site of injury. is increased cell proliferation may be an
attempt to oset the progressive destruction and loss of the
ECM. One reason for increased cellularity may be the focal
increase in nutrient supply owing to the ingrowth of blood
vessels in degenerating discs, as discussed elsewhere in this
chapter.
Cell clusters have been discovered in areas adjacent to the
newly formed blood vessels within degenerated discs. Cells in
these areas have access to nutrient supply and growth factors,
and undergo proliferation. e cellular changes in degenerated discs resemble osteoarthritis, in which remodeling of the
pericellular microenvironment with chondrocyte proliferation
and cluster formation have also been found. Ultimately, cellular attempts at repair become ineective as disc degeneration
progresses due to the abnormal local mechanical environment
of the cells.
Structural Changes
As disc hydration decreases, the distinction between anulus
and nucleus becomes less dened and disc height decreases
(Fig. 5.4).41 In later stages, gross tissue changes become
SECTION
I
84 BASIC SCIENCE
A
FIG. 5.4 Transverse sections of lumbar discs and apophyseal joints showing decrease in nucleus hydration, loss
of demarcation between anulus and nucleus with age, and appearance of circumferential ssures by the third
decade. (A) Adolescent. (B) At age 28 years. (Courtesy Bullough PG, Vigorita VJ. Bullough’s and Vigorita’s Atlas of
Orthopaedic Pathology. Baltimore, MD: University Park Press–Gower Medical Publishing; 1995.)
increasingly apparent, including loss of lamellae organization,
ssuring of the anulus,42 and discoloration and solidication
of the nucleus.
35,43
Radial and circumferential annular tears
are oen evident, sometimes extending to the disc periphery.42
ese changes are accompanied by ingrowth of nerves and
blood vessels into the disc, as well as deposition of granulation
tissue and calcication within the endplates. Endplate sclerosis
is thought to impede nutrient transport to the disc by occluding both nutrient channels and blood vessels. ese structural
changes ultimately lead to altered, abnormal biomechanical
properties of the disc. Damage to one area of the disc increases
load bearing by adjacent tissues, making it more likely for
damage to spread throughout the disc eventually. While a
healthy intervertebral disc equalizes pressure within it, the
decreased shock-absorbing capacity of the decompressed
nucleus leads to high compressive stresses in the anulus.44
Other gross morphologic changes of degeneration include
disc bulging, disc space narrowing, endplate irregularities, and
osteophyte formation.
Neovascularization and Sensory Nerve Innervation
As stated previously, the disc is largely avascular in adults with
blood vessels normally restricted to only the outermost layers
of the anulus. Likewise, only the outer 1 to 2 mm of the anulus
is innervated in the normal human disc. e ingrowth of
blood vessels and sensory nerves is an important feature of
degenerated discs and seems to be associated with pain.45
Ingrowth of capillaries may be facilitated by the loss of
B
hydrostatic pressure in the inner regions of the disc, which
would normally collapse small vessels. ese newly formed
microvessels release neurotrophic growth factors, such as
nerve growth factor, allowing the ingrowth of small, nonmyelinated nerve bers.
46–48
It has been hypothesized that discogenic pain arises because these nociceptive nerve bers grow
into areas of the disc that previously had no neurons.
Etiology of Intervertebral Disc Degeneration
Multiple risk factors have been hypothesized as the underlying
cause, including aging, genetic predisposition, mechanical
overload, and numerous environmental factors. Biomechanical studies have shown that excessive mechanical loading
causes disruption of disc structure, including endplate defects,
ssures, bulging, disc prolapse, and annular collapse.49 Further
experiments have conrmed that structural damage precipitates a cascade of cell-mediated responses, leading to further
damage. Although mechanical loading may precipitate degeneration, the most important cause may be age-related biologic
processes that impair the healing response and/or weaken the
disc before structural damage. However, recent studies have
shown that low-impact, cyclic loading increases trans-endplate
nutrient diusion in both healthy and degenerated discs, sug-
gesting a complex interaction of host and environmental
factors.50 e combined eects of aging, unfavorable genetics,
altered nutrition and metabolite transport, and excessive or
repetitive loading all have been implicated in contributing to
the process of degeneration.
Chapter 5 The Intervertebral Disc: Normal, Aging, and Pathologic 85
Aging
e incidence of intervertebral disc degeneration increases with
age and is most common in the lumbar spine.
intervertebral discs undergo very early aging and degeneration,
resulting in histomorphologic and functional changes (Fig. 5.5).41
Endplate permeability and vascular supply decrease throughout
growth and aging, leading to altered metabolite transport.41
Proteoglycans begin to fragment during childhood, and the
overall proteoglycan content decreases with age, especially in the
nucleus. ere is a corresponding increase in collagen content,
with collagen type I bers replacing collagen type II bers in the
inner anulus and nucleus. In addition, reduced matrix turnover
in older discs enables collagen brils to become increasingly
cross-linked,53 leading to retention of damaged bers and reduced
tissue strength. Synthesis of ECM components decreases steadily
throughout life, which is partly attributable to decreased cell
density, although synthesis rates per cell also decrease.
A
51,52
Human
In infants, the nucleus contains approximately 90% water
and appears translucent.23 e disc dehydrates slowly with
aging, with water content of the nucleus declining to around
80% in young adults.41 e nucleus also accumulates yellow
pigmentation and becomes less distinguishable from the surrounding anulus.
23,41
As the disc water content decreases, the
nucleus becomes smaller and decompressed, oen condensing
into several brous lumps. Dehydration of the nucleus leads
to altered biomechanical properties of the disc, forcing the
anulus to act as a brous solid to resist compression directly.
e proteoglycan content of the anulus also decreases with
aging, and the anulus becomes stier and weaker, resisting
compressive loads in a haphazard manner.
Aging also causes progressive changes in disc nutrient supply
and ECM composition. ese changes decrease tissue strength
and alter cell metabolism.54 e alterations of proteoglycans and GAGs, decreased hydration, and changes in collagen
distribution and cross-linking make the disc physically more
vulnerable to injury. Age-related alteration to the vascular
supply to the disc has been hypothesized as a primary initiator of age-dependent IDD. However, experimental endplate
damage leads to degeneration35 despite enhanced metabolite
transport into the disc, suggesting that structural damage
more strongly inuences the degenerative process. Inadequate
nutrition likely predisposes the disc to degeneration by compromising its ability to respond to increased loading or injury.
SECTION
I
B
C
D
E
FIG. 5.5 Cadaveric lumbar intervertebral discs sectioned in midsagittal
plane (anterior on left). (A) Young disc (35-year-old man). (B) Mature disc
(47-year-old man). (C) Disrupted young disc (31-year-old man). Note
endplate damage and inward collapse of inner anulus. (D) Severely
disrupted young disc (31-year-old man). Note collapse of disc height. (E)
Disc induced to prolapse in the laboratory (40-year-old man). Some nucleus
pulposus has herniated through radial ssure in posterior anulus (right).
(From Adams MA, Bogduk N, Burton K, et al. The Biomechanics of Back Pain.
Edinburgh: Churchill Livingstone; 2002.)
Genetic Predisposition
Genetic predisposition has been suggested as the greatest risk
factor for disc degeneration, accounting for approximately
50% to 70% of the variability in identical twin studies.
55–57
Individual gene polymorphisms associated with disc degeneration include aggrecan,57 cartilage intermediate layer protein,57
collagen type IX,
58,59
MMP-3,60 and vitamin D receptor.
61,62
e
products of these genes alter the ECM composition, decrease
tissue strength, impair regenerative capability, and undoubtedly inuence disc cell function. ere has also been recent
attention to the roles of microRNA molecules, 18-22 nucleotide posttranslational regulatory elements, in intervertebral
disc generation, but their roles have yet to be established.62
Age-related disc degeneration develops aer many decades,
however, and preferentially aects the lumbar spine. Since
unfavorable genetic predisposition is present throughout the
life span, this suggests that genetic inheritance and polymorphic
variations in susceptibility genes predispose the disc toward
degeneration, but further insults such as excessive loading,
structural damage, and other aging changes are necessary to
trigger the cascade of degenerative events.
Nutrition
e failure of nutrient supply is hypothesized to be a primary
cause of disc degeneration.63 In vitro studies demonstrate that
the metabolic activity of disc cells is sensitive to extracellular
oxygen and pH, with matrix synthesis rates decreasing at
acidic pH and low oxygen concentrations.
glucose supply or altered pH could negatively aect the ability
64,65
A decrease in
86 BASIC SCIENCE
of disc cells to synthesize and maintain the ECM, ultimately
leading to disc degeneration.
A relationship between loss of cell viability and a decrease
in nutrient transport in scoliotic discs has been found,66 and
there is evidence that nutrient transport is aected in disc
degeneration in vivo.
67,68
Likewise, the transport of solutes
from bone to disc was signicantly lower in degenerated discs
compared with normal discs as measured by in vitro studies.63
Other factors aecting the blood supply to the vertebral body
that may lead to an increased incidence of disc degeneration
include atherosclerosis,
69,70
sickle cell anemia, caisson disease
(decompression sickness), and Gaucher disease. In addition,
calcication of the cartilaginous endplates can cause decreased
nutritional supply even if the blood supply remains undisturbed, as seen in scoliotic discs.
63,71
All of this evidence supports the hypothesis that a decrease in nutrient supply
ultimately leads to degeneration of the disc.
Environmental Factors
Environmental risk factors hypothesized to inuence disc
degeneration include heavy or repetitive mechanical loading
(i.e., occupational physical loading and whole-body vibra-
56,72
tion),
obesity, and cigarette smoking.73 Heavy physical
loading, particularly related to occupation, was previously
suspected to be a major risk factor for degeneration and commonly viewed as a “wear and tear” phenomenon. However,
results of identical twin studies on physical loading specic
to occupation or sport suggest that repetitive physical loading
plays a relatively minor role in disc degeneration.
72
Obesity has oen been implicated as a risk factor for
degeneration, but epidemiologic studies have reported mixed
ndings. More recently, obesity was found to be a risk factor
for marked reduction of the NP magnetic resonance imaging
(MRI) signal intensity of lumbar discs. e mechanism by
which obesity contributes to degeneration is thought to be a
combination of mechanical and systemic factors. Some authors
suggest that atherosclerosis and cardiovascular disease associated with obesity parallel atherosclerosis of the spinal vessels,
with decreased blood and nutrient supply leading to increased
risk of degeneration.
e only chemical exposure associated with disc degeneration is cigarette smoking, which explains only 2% of the
variance in lumbar disc MRI changes between identical twins
with highly discordant lifetime exposures. In other studies of
monozygotic twins in whom the mean of co-twin discordance
was less, no signicant association between disc degeneration
and cigarette smoking was found. Cigarette smoke is presumed
to alter blood ow to disc capillaries and nutrient transport,
possibly as a result of the presence of muscarinic receptors in
blood vessels of the vertebral endplate.
74
Facet Joints, Ligaments, and Vertebral Bodies
No discussion of intervertebral disc degeneration would be
complete without consideration of the other elements of the
spine. Degeneration of the spine has an impact not only on
the disc, but also the surrounding structures, such as the facet
joints, ligaments, and vertebral bodies. Degenerative changes
are thought to occur simultaneously or close in time in each of
these components, altering the ability of the spine to respond
to normal physiologic loads. In addition, degeneration of the
surrounding nondisc structures may cause pain and reduced
mobility of the spine.
Facet Joints
Degeneration of the facet joints resembles osteoarthritic
changes occurring at other synovial joints, starting with
synovitis and progressing to articular cartilage loss, capsular
redundancy, and eventually degenerative spondylolisthesis.
Hypertrophic osteophytes at the joint margins and periarticular brosis can also result in reduced mobility and pain
at the facet joint. Osteoarthritis of the facet joints parallels
degenerative changes of the disc, possibly resulting from
abnormal loading and narrowing of the disc in the early stages
of degeneration.
75
Ligaments
e anterior longitudinal ligament and posterior longitudinal
ligament contribute to the overall stability of the spine. e
strong anterior longitudinal ligament buttresses the anulus
anteriorly, whereas the posterior longitudinal ligament oers
only weak reinforcement to the posterior anulus. Information regarding degenerative changes of these ligaments is
minimal, but the anterior longitudinal ligament and the
posterior longitudinal ligament become more redundant as
disc height decreases, and ossication occurs in later stages.
ese changes may contribute to pain and reduced mobility of
the spine.
Vertebral Bodies
Osteoarthritic changes of the vertebral body are also associated with intervertebral disc degeneration.76 e cartilaginous
endplates are normally the weakest structure under compressive loads, and thinning and calcication with aging further
compromise endplate strength. e endplates accumulate
trabecular microdamage and undergo remodeling in response
to altered loads, and the nucleus bulges into the vertebral body
as degeneration progresses. Endplate damage decompresses
the nucleus further, and loss of disc height transfers forces
onto the anulus, causing it to bulge into the nucleus.
nucleus may eventually herniate through a damaged endplate;
subsequent calcication of the herniated nucleus is called a
Schmorl node. e loss of disc height and annular laxity leads
to formation of osteophytes at the vertebral body margins,
decreased separation of the posterior neural arches, and
eventual bony ankylosis (Fig. 5.6).
49,76
e
Chapter 5 The Intervertebral Disc: Normal, Aging, and Pathologic 87
FIG. 5.6 Radiograph of old cadaveric lumbar spine (anterior on left).
Radiograph depicts how severe disc narrowing can be associated with
vertebral osteophytes, sclerosis of vertebral endplates, and selective loss of
horizontal trabeculae from the vertebral body. (From Adams MA, Bogduk N,
Burton K, et al. The Biomechanics of Back Pain. Edinburgh: Churchill
Livingstone; 2002.)
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SECTION
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SECTION
6
Biomechanics of the Spinal Motion Segment
CHAPTER
In biomechanics, information from the biologic sciences and
engineering mechanics is integrated for the purpose of analyzing and quantifying the function of and forces occurring on
tissue under various conditions. With an understanding of the
natural behavior mechanics of the spinal motion segment, it
can be possible to better understand the limitations of the
system and the conditions under which tissue damage occurs
and subsequent pain would be likely. Biomechanical assessments provide a quantitative means by which to accomplish
this goal.
From a biomechanical standpoint, the spine accomplishes
three major functions.1 First, the spine provides a structure by
which loads can be transmitted through the body. Second, the
spine permits motion in multidimensional space. ird, the
spine provides a structure to protect elements of the nervous
system (spinal cord). To appreciate the ability of the spine to
accomplish these functions, we need to understand the natural
movements of the spine and its ability to withstand forces or
loads that are transmitted through its structure.
With these goals in mind, this chapter (1) considers the
physical characteristics of the spinal tissues that could inuence
function, (2) assesses the motion characteristics (kinematics)
of the dierent portions of the spine, and (3) summarizes
the ability of the spine to withstand forces that it is supporting (load tolerance). Collectively, this chapter shows, from a
biomechanical perspective, how the spine functions and how
it breaks down. Box 6.1 is a glossary of terms to facilitate better
understanding of the content of this chapter.
Assessing the Biomechanics of the Spinal Motion Segment
I
William S. Marras
Prasath Mageswaran
Safdar N. Khan
Ehud Mendel
spine in vivo are rare and currently dicult in humans. Much
of the biomechanical information about the human spinal
motion segment is based on in vitro studies. is information
must be considered with caution because the properties of
the spine derived from cadaveric studies are understood to
be dierent in many respects from those of a live individual.
An alternative to direct measurement of spine tissue
loading is the prediction of tissue loads based on in silico or
biomechanical models. A biomechanical model is a conceptual
representation and prediction of how the forces within the
biomechanical system interact ultimately to impose force on
a particular tissue of interest. Biomechanical analyses assume
that the body behaves according to the laws of newtonian
mechanics that must govern the distribution of forces within
the musculoskeletal system. e object of interest in spinal
biomechanics is a precise quantitative assessment of the movement behavior and mechanical loading occurring within the
tissue of the musculoskeletal system. Biomechanical modeling
permits estimation of the direction and magnitude of forces
acting on the spinal motion segment and allows estimation of
when natural motion tolerances have been exceeded and when
damage or degeneration would be expected to occur. Biomechanical assessments help one understand potential pathways
of low back disorders and can potentially help surgeons
understand how contemplated surgical interventions might
aect the health of the spine.
Ultimately, biomechanical assessments are intended to
determine how much loading of the tissues within the spinal
motion segment is too much loading. is high degree of
precision and quantication is the characteristic that distin-
guishes biomechanical analyses from other types of analyses.
Ideally, it would be desirable to measure directly the forces
imposed on the various tissues within the spine. With current
technology, invasive measures would be required, however, to
understand the loading imposed on the various spinal tissues.
Such invasive measures would disrupt the tissues of interest
and would most likely alter the very factors that one is attempting to measure. Direct biomechanical measurements of the
Physical Charcteristics of the Spine Structures
e spine is composed of four types of vertebrae classied
according to their regional location along the spinal column—
cervical, thoracic, lumbar, and sacral. ere are 7 cervical
vertebrae, 12 thoracic vertebrae, and 5 lumbar vertebrae.
In addition, the sacrum consists of ve immobile— or
91
92 BASIC SCIENCE
BOX 6.1 Glossary
Acceleration. The rate of change of velocity. In body angular motion, dened
in degrees per second.
Acute trauma. Load applied to a structure with enough force to result in
damage in one application.
Axis of rotation. The point about which two vertebrae move relative to
one another.
Bending. Load applied to a structure at a point where it is not directly
supported, causing it to deform.
Biomechanical model. A theoretical representation of how forces behave
and interact in a biomechanical system.
Cortical bone. Compact bone forming a protective outer shell for a bone.
It has high resistance to bending and torsion, and provides strength where
bending would be undesirable.
Forms the interior scaolding of the structure and helps maintain bone
shape during force application.
Central coordinate system. A reference system that denes the positions
and motions of the body in space.
Compression. Force that pushes together the materials of a structure.
Contact pressure. The force per unit area distributed over a contact area.
Coupling. Movements in which one motion is accompanied by the
motion in a dierent plane.
Cumulative trauma. Repetitive load applied to a structure that weakens
the structure and results in damage.
Degree of freedom. The number of directions and motions in which a
body is able to move.
Dynamics. The study of forces applied to a structure in motion.
Force . An action that changes the state of rest or motion of a body.
Kinematics. The study of the motion of a structure that considers posi-
tion, velocity, and acceleration without taking into account the force that
produces the motion.
Kinetics. The study of the relationship between the force acting on a
body and the change in motion produced
Load. The application of force or moment (torque) to a structure.
Loading cycle. The number of repetitions of a load application.
Local coordinate system. A reference system that denes the positions
and motions of vertebrae relative to one another.
Microfracture. Small cracks in a structure.
Moment. A force applied about an axis. A force multiplied by a distance.
Also known as torque.
Neutral zone. The amount of displacement between the neutral position
of the vertebrae and point at which resistance to physiologic motion is
experienced.
Pressure. Force per unit area.
Range of motion. The two points that dene the extremes of physiologic
motion.
Rotations. Movement about a point, as when bending.
Shear. A force applied parallel to the surface upon which it acts.
Stability. The ability of a system to respond to a perturbation and rees-
tablish a state of equilibrium.
Statics. The study of forces occurring within a structure when they are
not in motion.
Strain. The change in unit length or angle of a material that is subjected
to load.
Stress. A measure of the intensity of force represented in force per unit
area.
Tolerance. The point at which a structure can no longer resist a load
without suering damage.
Torsion. A twisting load applied about the long axis of a structure.
Translations. Straight line movements in any direction.
Velocity. The rate of change of position. In angular body motion, dened
in degrees per second.
“fused”—vertebrae, and the coccyx (oen referred to as the
tailbone) is a fusion of four coccygeal vertebrae at the base of
the spine. Each vertebra is referenced according to a nomenclature system in which the spine region (e.g., cervical, thoracic) is followed by a numbering system that refers to the
vertical position of the vertebral body along the spine (beginning with the vertebra closest to the head) (e.g., rst cervical
vertebra, or C1). Disc levels are referenced relative to the
vertebral levels surrounding the disc. e lowest lumbar vertebra (h lumbar vertebra, or L5) is adjacent to the rst sacral
vertebra (S1), and the disc between these vertebrae is referred
to as L5–S1.
e shape of the vertebrae changes from level to level in
the spine. e vertebral body shape and the orientation of the
posterior elements change. In particular, the orientation of the
bony structures that compose the posterior elements change
in their shapes and contact angles. ese subtle changes permit
or restrict motions in dierent directions along the human
spine.
Several physiologic curves are also characteristic of the
upright spine (Fig. 6.1A). e curves within the cervical and
lumbar regions of the spine are referred to as cervical lordosis
and lumbar lordosis, whereas the thoracic and sacral curves
are referred to as thoracic kyphosis and sacral kyphosis because
these curves bow in the opposite direction of the lordotic
curves. ese curves work collectively to accommodate pelvic
orientation under dierent conditions. When sitting, the pelvis
rotates backward and the lumbar curve attens. When the
pelvis is rotated forward, the lumbar curve is accentuated.
Collectively, the spinal curves balance each other and form a
stable system that maintains the center of gravity in a balanced
state. However, this normal balance can change with age and
a number of other factors such as degeneration, osteoporosis,
and trauma.
e “building blocks” of the spine are the spinal motion
segments (Fig. 6.1B), also known as the functional spinal unit.
is unit consists of two vertebrae and the disc in between
them. is unit represents the central focus of biomechanical
functioning and clinical assessment. is chapter explores the
spinal motion segment from a biomechanical perspective with
the intent of understanding the signicance of features that
may inuence status.
Support Structures
e spine is constructed of a series of vertebral bones that are
stacked on one another to form the spinal column that runs
from the pelvis to the head. A vertebral bone, or vertebra, is
shown in Fig. 6.2. e large, round portion of the bone is the
vertebral body, which is the major load-bearing structure of
the spinal column. e outer portion of this bone is composed
of a thin, yet very strong, layer of cortical bone. Cortical bone,
also known as compact bone, forms a protective outer shell,
has a high resistance to bending and torsion, and provides
strength in situations in which bending would be undesirable.
e inner portion of the bone consists of a spongy matrix of