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44 /SECTION I/BASIC SCIENCE
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CHAPTER 4
Morphologic Changes of End Plates in Degenerative Disc Disease
Robert J. Moore
The vertebral bodies of the axial skeleton are separated
by intervertebral discs, which are highly specialized
structures that enable a range of physiologic and mechanical functions associated with motion. The discs have
three main structural components—a central nucleus pulposus surrounded by the annulus fibrosus and the end
plates, which are located at the cranial and caudal interfaces with the vertebrae. While the structure and function
of the annulus and nucleus are well characterized, much
less is known about the end plates. P erhaps this is because
their constitution has not yet been consistently defined, or
because structural changes to the end plates are more
subtle than changes to other disc components, and therefore easily overlooked.
In some early anatomical studies the end plates were
described as the transitional zone between the vertebral
body and the adjacent disc because they possessed both
an osseous and a hyaline cartilage component (1,2).
Other authors, however, proposed a more limited situation, and described the end plates as the thin layer of hyaline cartilage interposed between the vertebral body and
the disc (3,4). For w hatever reason, this latter concept has
survived and they are now more commonly known as the
“cartilage end plates” or simply the “end plates.”
Volumes of literature have been devoted to the normal
development of the end plates that are recognizable from
an early embryologic stage and retain their cartilaginous
nature during normal maturation while the adjacent vertebrae undergo ossification (5). The cartilaginous component of the mature end plate is essentially an aqueous gel
containing large proteoglycan molecules within a dense
mesh of collagen fibrils that are aligned along the longitudinal axis (horizontally in the human). Although it has
been suggested that there is no direct physical connection
between the end plates and the underlying bone (6), their
juxtaposition almost certainly contributes to the strong
bond that is essential for the normal function of the end
plate (7). When the epiphyses fuse in the young adult
spine, only the outer rim of the end plates is ossified,
leaving a broad central cartilaginous plate. The lamellae
of the outer annulus attach directly to the adjacent bone,
while the fibers of the inner annulus connect the end
plates directly with the disc.
The end plates are thin, particularly in the center of the
disc, measuring no more than 1 mm at maturity (8), but
there can be considerable variation from one side to the
other (9). In the lower lumbar spine the end plates are
roughly cardioid to elliptical in shape (10). While this
fact in itself may seem to have little relevance, shape is
the only one of several parameters investigated by computed tomography-myelography that is claimed to be significantly related to the development of disc herniation
(11). The most abundant cell type in the end plate is the
chondrocyte, distributed more uniformly than the clearly
defined layers of cells within articular cartilage. Otherwise the end plate bears a close similarity to the articular
cartilage of synovial joints.
The biochemical characteristics of the end plates, from
normality through the spectrum of degenerative conditions, are well documented (12,13). The two most abundant families of molecules in the disc are the collagens
and the proteoglycans that are found in varying proportions in the annulus, the nucleus, and the end plates. Of
the several species of collagen, type X is probably the
most important in the end plates because it is a marker of
hypertrophic chondrocytes and is thought to be involved
in cartilage calcification (14). It has been detected mainly
in the central region (15).
Proteoglycan molecules are essential for the maintenance of the water content and overall integrity of the
nucleus (16). It is known that altered tissue levels of proteoglycans can adversely influence disc function (17).
The proteoglycans of the end plate have not been studied
extensively, but suff ice to say loss of proteoglycans from
46
CHAPTER 4/ MORPHOLOGIC CHANGES OF END PLATES / 47
the end plate is implicated in loss of proteoglycans from
the nucleus (18). It follows that disc degeneration invariably is preceded by widespread degradation of disc proteoglycans (19). It has long been suspected that alterations to the biochemical composition of the end plate,
particularly during the growth phase, may be involved in
the development of scoliosis (20–22).
Heterozygous inactivation of the Col2a1 gene allele in
1-month old mice has been shown to lead to lower glycosaminoglycan concentration in the end plates and
thicker and more irregular end plates that become calcified prematurely (23).
The developing discs receive essential nourishment
from two sources. From the embryonic stage, a network
of blood vessels penetrates the annulus no deeper than
about one-third of its total thickness (24). Most of these
vessels do not persist beyond maturity and by adulthood
they can be seen in only the outer two or three lamellae.
Blood vessels also penetrate the end plates from the vertebral body margins (5) and arise from ramifications of a
large primary nutrient artery on the dorsal surface of each
vertebral body. With maturation however, these small
vessels also disappear, leaving only a limited blood supply in the form of capillary buds that perforate the
osseous component of the end plate (25). It is curious that
mammalian discs have evolved in this way, since the central nucleus pulposus in the adult human can be up to
20 mm from the nearest blood vessels and is therefore
totally reliant on diffusion of solutes across the end plates
and the annulus for nutrition. No other tissue in the body
is so distanced from a blood supply, and presumably
therefore so susceptible to deterioration.
Extensive in vitro study of the transport of solutes, disc
nutrition, and metabolism using small dye molecules has
shown that the lateral end plate at the vertebral rim is relatively impermeable compared with the central portion,
and even the entire annulus fibrosus (26). The contribution of the periannular blood supply was well accepted,
but the permeability of the capillary network immediately
beneath the end plate attracted new attention. Quantitative analysis of human autopsy specimens that had been
injected with dye solution subsequently confirmed that
there were significantly more marrow contacts along the
central end plate adjacent to the nucleus than there were
in the lateral margins (27,28).
While determining the signif icance of these vessels to
disc nutrition and cell metabolism, diffusion was shown
to be the principal mechanism for transporting small dissolved solutes into the disc (29). Further, the size and
ionic charge of the molecules were also shown to govern
the rate and extent of diffusion (29,30). As the high proteoglycan content in the nucleus confers a net negative
charge to the normal disc, small, uncharged molecules
such as glucose and oxygen and positively charged ions
such as sodium and calcium diffuse into the disc with relative ease. Conversely, it is much more difficult for neg-
atively charged molecules such as sulfate and chloride
ions to enter the nucleus. Macromolecules such as immunoglobulins and enzymes are totally excluded.
The relative contribution and importance of the end
plate and annular routes to disc nutrition were established
independently using biochemical (31), histologic (25),
and radiologic (32) methods. Each of these studies confirmed the importance of the central end plate in the
metabolic processes of the disc.
Soon after maturity the cartilage of the end plate
undergoes extensive mineralization and eventually this
tissue is resorbed and replaced by true bone (33,34). It is
likely that this remodeling, as well as the calcification of
vascular channels in the end plate region both contribute
substantially to a reduction in the normal exchange of
nutrients across the end plate with increasing age (35).
Since the end plate is capable of remodeling after
maturity it seems reasonable to expect the obliteration
and loss of vascular channels could also be rev ersed. This
does appear to be possible, and in fact has been demonstrated in an experimental ovine model of annular lesions
(36). In the context of that study it was presumed that
neovascularization was a basic survival mechanism for
discs undergoing severe pathologic deterioration, although it was in vain, since the y continued to degenerate.
Although not specifically tested in that study it is likely
that such new blood vessels are formed by activation of
normally latent enzymes of the matrix metalloproteinase
(MMP) family, which are regulated by tissue inhibitors
(37–41). Increased levels of several MMP species have
been detected in surgical and postmortem samples of
human discs (40,42), and although the end plate itself
was not analyzed in these studies, it is reasonable to
assume that they would be no different.
As well as providing an axis for the diffusion of nutrients to the avascular disc, the end plates also are important for the mechanical function of the spine. In the
course of normal physical activity, mechanical loading
(especially axial compression) can alter the shape of the
disc to the extent that the end plates and the subchondral
trabecular bone become deformed (43). This deformation
is reversible in young healthy end plates that are subjected to even moderate loading, but when the forces are
higher and applied repeatedly, the end plates sustain irreversible damage. There is evidence that the integrity of
the end plate and subchondral bone, rather than the
degree of disc degeneration, influence how much damage
occurs during axial compression (44). It was also noted
that the radiographic appearance of the end plates in this
study was similar to those of osteoporotic patients, in
whom the end plates become more concave with age and
progressive vertebral osteopenia (45,46).
Morphologic changes to the end plates occur with
advancing age but also may be seen in association with
pathology in either the nucleus or the annulus. Either wa y,
the changes are essentially microscopic and become evi-
48 /SECTION I/BASIC SCIENCE
dent macroscopically only in the advanced stages of disease (47).
In the earliest changes after maturity fissures and clefts
appear along the length of the end plate in the horizontal
plane. Occasionally there is evidence of chondrocyte
death. The cartilage may be invaded by microscopic
blood vessels and there also may be ossif ication extending from the adjacent bony end plate. With time the cartilage becomes depleted progressivel y and under goes further ossification. The nucleus fills the small voids created
as more blood vessels perforate the end plate, but these
defects do not breach the bony end plate.
The most dramatic changes occur after the fifth
decade. It is not unusual to observe nuclear material protruding into the adjacent vertebral marrow with foci of
bony sclerosis resulting from active remodeling at these
sites. Often there is total loss of the cartilage end plate. In
an experimental murine spondylosis model disc degeneration, including loss of the end plate, was accompanied
by increased apoptosis in end plate chondrocytes relative
to naturally aged mice, suggesting that programmed cell
death plays a role in age-related changes of the disc (48).
Of all the structural elements that constitute the disc,
the end plate appears to be most susceptible to mechanical failure. Theoretical modeling using finite element
analysis has shown that mechanical failure always begins
with separation of the end plate from the subchondral
bone (49), in complete agreement with the microscopic
observations of Vernon-Roberts (47). Autopsy studies
also confir m that por tions of the end plate become separated from the vertebral body and are herniated from the
disc along with attached annular fibers (50,51). A significant weak point of the motion segment appears to be
near the epiphyseal ring, where the annulus fibers insert
directly into the vertebral bone. Not only is it a common
site for fracture causing back pain and radiculopathy in
adolescents and young adults (52) but it has been shown
to be particularly susceptible to failure during experimental mechanical compression tests in the adolescent
pig (53). This is a different injury patter n to that seen in
adults, where the end plate and adjacent trabecular bone
are affected (54,55).
Schmorl nodes are relatively common features of the
end plate that have been characterized in considerable
detail. These v ertical protrusions of nucleus pulposus into
either (and occasionally both) of the adjacent vertebrae
were first described by Luschka in the late 19th century
and subsequently named by Schmorl (2). They are found
in more than 70% of autopsy spines with equal frequency
above and below the age of 50 years, suggesting that they
appear relatively early in life (56). Schmorl observed that
they were twice as common in men up to the age of 59
years and attributed this to lifestyle factors, in particular
a greater risk of occupational trauma. After the age of 60
years, however , they are twice as common in women, presumably at a stage w hen the disc is more liable to rupture
due to changes associated with advanced age, including
vertebral osteopenia. In any case there is clear evidence
that discs with Schmorl nodes are more degenerate than
other discs at an early age (57).
Schmorl nodes are encountered less frequently on clinical radiographs than by autopsy examination (2,58). In
general this is because they are small, but in other
instances they can be so immature to have not yet caused
any significant structural changes. Ultimately there is
loss of disc height from nuclear prolapse or subsequent
formation of a cartilaginous cap and eventually new bone
around the prolapsed tissue.
Despite being relatively common, it is still not known
how Schmorl nodes are formed. It seems obvious that
nuclear protrusion can only occur through openings in the
end plate, but under normal circumstances these defects
do not exist. Schmorl himself suggested that these lesions
could result from weaknesses in the end plate due to foci
of degenerate cartilage (2). In the absence of signif icant
destruction, such as direct trauma or neoplasm, it is
assumed that scar tissue in the end plates is a legacy of
the closure and repair of the nutrient vessels in the developing years (59), and this leaves congenitally weak spots
through which protrusion is possible (60). The latter
study also demonstrated a significantly higher proportion
of marrow contacts in the end plates of specimens with
Schmorl nodes, and suggested that these lesions could
contribute to further pathology such as Scheuermann disease in which they feature prominently.
With the development of implantable devices aimed at
augmenting spinal fusion, the end plate assumes a critical
role. It was previously thought that mechanical stability,
and therefore a good clinical outcome following interbody
fusion, could be achieved only if the end plates were preserved, whether bone was used alone or in conjunction
with these devices (61). The design of implants therefore
appears to be critical for successful fusion. It is claimed,
for instance, that threaded cages compromise end-plate
integrity, but while nonthreaded cages address this problem, their design generally does not conform to the normal
profile of the end plate, providing limited opportunity for
bony incorporation (62). The inherent strength of titanium
cages offers greater resistance to axial loading, which can
be achieved by preservation of the end plates in thoracolumbar column reconstruction (63). More recent work in
cadavers however, suggests that an implant with only
peripheral support provides the same axial strength as an
implant with full support, and that there is no mechanical
advantage gained by maintaining a solid implant face (64).
In fact, it has been claimed that removal of the central end
plate actually promotes graft incorporation without affecting mechanical strength. In another study that has implications for interbody cage design, both the sacral and inferior
end plates were shown to be stronger than the superior
lumbar end plates, while the central region of both the lumbar and sacral end plates was also identified as being a
CHAPTER 4/ MORPHOLOGIC CHANGES OF END PLATES / 49
structurally weak point (65). The importance of preserving
the end plate to prevent graft subsidence was further
emphasized in a report of compression testing conducted
on cervical spine segments (66). As we move from “classical” fusion methods to the realm of spinal arthroplasty,
where the aim is to maintain or even restore function as
well as relie ve pain, it is clear that these considerations will
have major implications for the design of implantable
devices in spinal surgery (67).
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CHAPTER 5
Clinical Spinal Instability Resulting from Injury and Degeneration
Manohar M. Panjabi, Vijay K. Goel, Allison M. Kaigle Holm, Malcolm H. Pope
The origin of most cases of low back pain is unkno wn (1).
Clinical spinal instability is considered as one of the most
common causes (2). It is hypothesized that mechanical
derangement by degeneration, injury, or muscle dysfunction produces spinal instability that results in pain or dysfunction. It is assumed that an underlying intervertebral
motion abnormality exists, which is magnitude and direction dependent (3).
Although the phrase spinal instability is commonly
used in a clinical setting, there is no single accepted definition (4). Thirty spine surgeons were asked to define
clinical instability and its symptoms and signs, and 30
different answers were received! Clinical instability has
two parts: mechanical derangement and clinical consequences. It has been concisely put in a definition with
which many clinicians agree. It is the loss of the ability of
the spine to maintain its physiologic patterns of displacement that cause no incapacitating pain or neurologic dysfunction (3).
Spinal stability is provided by three interrelated systems: the spinal column (passive system); spinal muscles
(active system); and control system, which coordinates
the muscles in response to the stability needs of the spine
(Fig. 5-1). Instability results when single or multiple
components of the systems fail or malfunction (5). This
conceptual framework is useful in understanding the
roles of various spinal system components in providing
spinal stability.
Clinical spinal instability may be described by its
causes, methods for its diagnosis, and treatments. Past
research concerned with these aspects of spinal instability is described. At present, the causes are thought to be
injury, degeneration, and muscle dysfunction or insufficiency, or a combination of all three. Diagnostic methods
generally include flexion-extension roentgenograms, but
other techniques such as magnetic resonance imaging
(MRI) are now available. Treatment methods include
exercises and surgery. Also presented are future directions for research.
CAUSES OF SPINAL INSTABILITY
The degenerative process of the functional spinal unit
(FSU) is usually described by dysfunction, instability,
and restabilization (6). (The FSU is the smallest unit of
the spine, consisting of two adjacent vertebrae and the
connecting ligaments, disc, and facet capsules.) The
unstable phase is characterized by reduction in disc
height, laxity of the ligaments and facet capsules, and
degeneration of the facet joint, which result in abnormal
spinal movement. A positive relationship with low back
pain was found if the disc height decreased by 40% (7).
Osteophytes ha v e been proposed as indicators of instability (8). A traction spur is said to result from increased tensile stresses at the annulus, whereas the claw spur results
from compressive loads.
Injury
Microtrauma occurring for long periods may lead to
accelerated degeneration and spinal instability (9). This
can include occupational exposures (e.g., whole-body
vibrations) (10). A major overload may fracture facets
and end plates, produce annular tears of the disc, or rupture ligaments, which also may lead to spinal instability.
Surgical procedures (e.g., total facetectomies) may cause
instability as well.
What roles do the ligaments, facets, and disc components play in providing stability? The contribution of the
facet joints in the lumbar spine was experimentally
determined to be 50% in resisting torsional loads (9).
The other 50% is provided by the intervertebral disc.
Using pure moments and measuring three-dimensional 6
degrees-of-freedom intervertebral motions, the effects of
51
52 /SECTION I/BASIC SCIENCE
FIG. 5-1. The spinal stabilizing system. A conceptual framework in which the passive spinal column, active spinal muscles, and neuromuscular control subsystems together provide the spinal stability. (From Panjabi M. The stabilizing
system of the spine.Part I. Function, dysfunction, adaptation,
and enhancement. J Spinal Disord 1992;5(4):383–389.)
posterior ligamentous injury and partial and total facetectomies were recorded (11). With physiologic loads of
8 nm, the average ranges of motion (and neutral zones)
for the intact lumbar spine were found to be as follows:
flexion, 8.2 (0.93) degrees; extension, 4 (0.93) degrees;
lateral bending, 6.2 (0.97) degrees; and axial rotation,
3.5 (1.1) degrees (Fig. 5-2). (The concept of neutral zone
is indicated in Figure 5-5.) Cutting of the supraspinous
and interspinous ligaments produced a 2-degree increase
in flexion, but no change in other motions. Unilateral
facetectomies produced increases of 4.2 degrees in flexion and 1.8 degrees in rotation, but no marked changes
in other motions. Bilateral total facetectomy, compared
with the case with the spine intact, produced increases of
63% in flexion, 78% in extension, 15% in lateral bend-
ing, and 126% in axial rotation. Thus, the facets play a
significant mechanical role, especially in rotatory stability. The conclusion was made that the partial facetectomy of one or both facets at a single level does not
cause spinal instability, whereas the loss of a complete
facet joint on one or both sides makes the spine acutely
unstable. These in vitro experimental results should be
carefully interpreted for clinical use because they do not
include the muscles and effects of healing. To understand
the role played by all spinal column components in providing stability, fresh cadaveric functional spinal units
were studied in response to either flexion or extension
loads, while the various spinal components were transected from either a posterior-to-anterior direction or
vice versa (12). Vertebral movements in response to transection of the components were monitored in the sagittal
plane. This study formed the basis of the guidelines for
determining thresholds of clinical instability in the lumbar (1).
Does an injury to the disc repair itself? The disc does
not have the healing potential of most other structures in
the body because it lacks a blood supply (13). Repair,
however, involves a process of vascular ingrowth. The
concept of a mechanical self-sealing phenomenon that
would seal of f the defect was adv ocated (14) but w as later
shown to be a fallacy, especially for multidirectional
instabilities (15,16).
The process of repair and restabilization after injury, if
it occurs, cannot be studied by in vitro biomechanical
studies. Neither can the clinical studies provide useful
information concerning the natural time course of an
injury, because all significant injuries in humans are usually surgically or otherwise stabilized. Thus, there is limited information regarding the natural history of most
spinal injuries. In a set of in vivo experiments using two
FIG. 5-2. Average multidirectional intervertebral ranges of motion of fresh cadaveric lumbar spine specimens as functions of injury. The motions were: flexion, extension, lateral bending, and axial rotation.
The injuries sequential were: posterior ligaments (supraspinous and intraspinous), left unilateral medial
facetectomy, bilateral medial facetectomy, left total facetectomy, and bilateral total facetectomy. (From
Abumi K, Panjabi MM, Kramer KM, et al. Biomechanical evaluation of lumbar spinal stability after
graded facetectomies. Spine 1990;15:1142–1147.)