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doi:10.5312/wjo.v4.i2.42
World J Orthop 2013 April 18; 4(2): 42-52
ISSN 2218-5836 (online)
© 2013 Baishideng. All rights reserved.
REVIEW
Pathophysiology, diagnosis, and treatment of discogenic
low back pain
Bao-Gan Peng
Bao-Gan Peng, Department of Spinal Surgery, Institute of Spinal Surgery of Armed Police Force, General Hospital of Armed
Police Force, Beijing 100039, China
Author contributions: Peng BG solely contributed to this manuscript.
Correspondence to: Bao-Gan Peng, MD, PhD, Professor,
Department of Spinal Surgery, Institute of Spinal Surgery of
Armed Police Force, General Hospital of Armed Police Force, 69
Yongding Road, Beijing 100039, China. pengbaogan@163.com
Telephone: +86-10-57976611 Fax: +86-10-57976937
Received: January 4, 2013
Revised: March 19, 2013
Accepted: April 10, 2013
Published online: April 18, 2013
procedures including spine fusion and recently spinal
arthroplasty. However, these treatments are limited to
relieving symptoms, with no attempt to restore the disc’
s structure. Recently, there has been a growing interest
in developing strategies that aim to repair or regenerate the degenerated disc biologically.
© 2013 Baishideng. All rights reserved.
Key words: Intervertebral disc; Degeneration; Diagnosis; Treatment; Discogenic low back pain; Classiication;
Internal disc disruption; Internal annular disruption;
Internal endplate disruption
Core tip: Discogenic low back pain is the most common
type of chronic low back pain. Why lumbar disc degeneration leads to pain is one of the most important topics in medical ield. Studies have revealed that pathologic features of painful discs were the formation of the
zones of vascularized granulation tissue, with extensive
innervation in annular issures. Provocation discography
now still is the only available means by which to identify a painful disc. There are a multitude of treatments
used in clinical practice to treat chronic low back pain,
with little consensus amongst clinicians as to which is
the best approach.
Abstract
Discogenic low back pain is a serious medical and social
problem, and accounts for 26%-42% of the patients
with chronic low back pain. Recent studies found that
the pathologic features of discs obtained from the patients with discogenic low back pain were the formation
of the zones of vascularized granulation tissue, with
extensive innervation in fissures extending from the
outer part of the annulus into the nucleus pulposus.
Studies suggested that the degeneration of the painful disc might originate from the injury and subsequent
repair of annulus ibrosus. Growth factors such as basic
fibroblast growth factor, transforming growth factor
β1, and connective tissue growth factor, macrophages
and mast cells might play a key role in the repair of the
injured annulus fibrosus and subsequent disc degeneration. Although there exist controversies about the
role of discography as a diagnostic test, provocation
discography still is the only available means by which to
identify a painful disc. A recent study has classiied discogenic low back pain into two types that were annular
disruption-induced low back pain and internal endplate
disruption-induced low back pain, which have been
fully supported by clinical and theoretical bases. Current treatment options for discogenic back pain range
from medicinal anti-inflammation strategy to invasive
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Peng BG. Pathophysiology, diagnosis, and treatment of discogenic low back pain. World J Orthop 2013; 4(2): 42-52 Available
from: URL: http://www.wjgnet.com/2218-5836/full/v4/i2/42.htm
DOI: http://dx.doi.org/10.5312/wjo.v4.i2.42
INTRODUCTION
Chronic low back pain is a serious medical and social
problem, and one of the common causes responsible
for disability. It is estimated that, in all populations, an
individual has an 80% probability of having low back
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April 18, 2013|Volume 4|Issue 2|
Peng BG. Discogenic low back pain
pain at some period during their life time, and about
18% of the population experiences low back pain at any
given moment[1,2]. According to US National Center for
Health Statistics reports, 14% of new patients that went
to a hospital for treatment were patients with low back
pain, which represents 13 million people. About 3% of
all patients discharged from hospitals have symptomatic
low back pain. The expense of treating low back pain is
higher than $100 billion each year[3].
The prerequisite for successfully treating low back
pain is to make an accurate pathological diagnosis. Despite the inherent challenge in elucidating the specific
etiology of chronic low back pain, diagnostic procedures
can reveal its source in 90% of patients. DePalma et al[4]
found that the prevalence of zygapophysial joints, sacroiliac joints, and lumbar discs was 31%, 18%, and 42%, respectively. They conirmed the disc as the most common
etiology of chronic low back pain in adults. Crock[5] irst
proposed the concept of internal disc disruption (IDD),
which indicated the discogenic pain syndrome caused by
disc degeneration and non-nerve root referred pain. IDD
causing discogenic low back pain accounts for 26%-42%
of chronic low back pain patients[4,6,7]. IDD had been assigned as a separate clinical entity to differentiate it from
other types of disc degenerative low back pain, such as
lumbar disc herniation, degenerative disc disease (DDD)
and lumbar segment instability[8]. Lumbar X-ray images
of IDD patients show no characteristic changes in degenerative disc diseases such as intervertebral space narrowing, osteophyte formation, endplate sclerosis, and gas
formation within disc space[8].
This paper reviews the pathophysiology, diagnosis,
and treatment of discogenic low back pain according to
the existing literature.
chain to form aggrecan. Aggrecans are held together by
type Ⅱ collagen, which is cross-linked by type Ⅸ collagen. Aggrecan is the most common proteoglycan in the
disc, and comprises approximately 70% of the nucleus
pulposus and 25% of the annulus fibrosus. Aggrecan
provides a high level charge density, which creates a high
osmotic pressure for retaining water within the nucleus
pulposus[10]. A young healthy disc behaves like a water
bed, with the high water content of the nucleus and inner
annulus enabling the tissue to act like a fluid. Only the
outermost annulus acts as a tensile “skin” to restrain the
nucleus.
Disc cells synthesize their matrix and break down existing matrix by producing and activating degradative enzymes, including matrix metalloproteinases (MMPs) and
“a disintegrin and metalloproteinase” (ADAMS). Degradation of the matrix allows it to be refreshed by newlysynthesized components. Several growth factors, such as
bone morphogenetic protein-2 (BMP-2), BMP-7 (also
known as osteogenic protein-1; OP-1), growth differentiation factor-5 (GDF-5), transforming growth factor-β
(TGF-β), insulin-like growth factor-1 (IGF-1), and others
have been found to stimulate matrix production, while
interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α)
inhibit the synthesis of matrix by enhancing its catabolism[9,10].
Disc degeneration will occur if the matrix is not normal. At a molecular level, degeneration will be expressed
by the production of abnormal components of the
matrix or by an increase in the mediators of matrix degradation, such as IL-1 and TNF-α, and of MMPs and a
reduction in the levels of tissue inhibitors of metalloproteinases (TIMPs). Several factors have been considered
to cause disc degeneration. Genetic predisposition, mechanical load, and nutritional factors are widely regarded
as important contributors to the degenerative process[11].
However; detailed characterization of this complex interplay remains elusive. With the disc degeneration, there is
a net loss of proteoglycans and water from the nucleus,
leading to poor hydrodynamic transfer of axial stresses
to the outer anulus ibrosus. The disc degeneration may
result from an imbalance between the anabolic and catabolic processes or the loss of steady state metabolism
that is maintained in the normal disc. Alterations in both
anabolic and catabolic processes are thought to play key
roles in the onset and progression of disc degeneration.
Disc degeneration usually appears in magnetic resonance imaging (MRI) T2-weighted images as a decline
in signal intensity, i.e., the so-called “black” disc. MRI
may identify a degenerative disc and an annular tear,
but it will not help differentiate between a disc which is
pathologically painful and one which is physiologically
aging[12]. Disc degeneration is a very complicated biological process. Previous views on disc degeneration and the
mechanism underlying it were mainly based on histological and biochemical studies using human disc herniation
specimens from surgery and animal models of aging and
degenerative discs[13,14]. However, the main histological
PATHOPHYSIOLOGY
The intervertebral disc is the main joint between two
consecutive vertebrae in the vertebral column. Each disc
consists of three different structures: an inner gelatinous
nucleus pulposus, an outer annulus fibrosus that surrounds the nucleus pulposus, and two cartilage endplates
that cover the upper and lower surfaces of vertebral bodies. The cells that form the annulus ibrosus, particularly
in the outer region, are ibroblast-like and arranged parallel to the collagen ibers, whereas those in the inner annulus ibrosus are chondrocyte-like. The nucleus pulposus
contains collagen ibers that are randomly distributed and
elastin fibers that are radially organized embedded in a
highly hydrated aggrecan-containing gel. Chondrocytelike cells synthesize type Ⅱ collagen, proteoglycans, and
non-collagenous proteins that form the matrix of the
nucleus pulposus and the cartilage endplate. Fibroblastlike cells synthesize type I and type Ⅱ collagen for the
annulus ibrosus[9]. Proteoglycans consist of a core protein from which radiate chains of glycosaminoglycans
containing keratin sulphate and chondroitin sulphate.
Multiple proteoglycans are joined to a hyaluronic acid
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April 18, 2013|Volume 4|Issue 2|
Peng BG. Discogenic low back pain
changes and the exact molecular mechanisms underlying
the painful pathological disc remain unknown.
With the development and popularization of lumbar
fusion, a greater number of painful pathological disc
specimens can be obtained, which are beneicial for studies regarding the pathogenesis of painful disc degeneration. Based on our previous histological studies[15-17], we
found that the composition and structure of painful disc
differed from those of non-painful degenerative disc.
Specifically, normal fibroblasts in the annulus fibrosus
were replaced by cartilage-like cells. The annulus ibrosus
lamellar structure was disordered and fractured. The normal highly hydrated gelatin-like nucleus pulposus, whose
matrices showed obvious ibrosis, and cartilage-like cells,
were completely replaced with ibroblasts, was substituted
by ibrous tissues. The histological changes in the nucleus
pulposus were divided into 3 major types: obvious ibrosis, vascular invasion, and inlammatory granulation tissue
formation. In addition, we found that the characteristic
change in painful pathological discs was the formation of
inlammatory vascular granulation tissues with extensive
innervation along the tears in the posterior annulus ibrosus, along with mass expression of some growth factors
such as basic ibroblast growth factor (bFGF), TGF-β1,
and connective tissue growth factor (CTGF). Vascular granulation tissue was not formed in asymptomatic
degenerative discs, and only a few growth factors were
expressed. Asymptomatic degenerative discs with tears
are not painful, because these discs have not been innervated[15].
Blood vessels only exist in the longitudinal ligaments
and the outermost layers of the annulus fibrosus in a
normal disc. The ingrowth of vascularized granulation
tissue along the tear deep into the inner annulus and
nucleus pulposus in the painful disc probably begins soon
after the injury when repair of the tear starts from the
margin of the annulus ibrosus[15]. Owing to the absence
of blood vessels in the inner annulus ibrosus and nucleus pulposus, it is unlikely that vascularized granulation
tissue which is induced by the tear should originate from
there. Different animal models of outer annular injury
have proved that the healing of the annulus might initiate
a progressive degeneration of the disc[18-24]. In addition,
the whole process of healing of annulus ibrosus injury,
including inflammatory reaction, formation of granulation tissue, and tissue reconstruction had been observed,
implying that the disc has actually been torn and there
has been a process of healing in progress[16].
According to recent researches on injury and repair,
growth factors have been considered to be essential to
regulate and control the whole process of repair of an
injury. Some growth factors, such as bFGF, TGF-β, and
CTGF, may be important as promoters in tissue repair.
Growth factors that control cellular proliferation and
differentiation in vitro have been identified. These factors mediate cellular interactions in vivo, which not only
contribute to development and growth, regeneration, and
wound healing, but also may incite abnormal changes[16].
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Growth factors through their each receptor signal transduction pathway, promote cellular proliferation and
collagen synthesis of matrix cells such as ibroblast and
vascular endothelial cells, which exert a strong effect on
adjustment and control of wound and repair[16]. Previous studies have indicated that bFGF as an important
mitogen accelerator may directly act on the mitotic cycle
of tissue repair cells (for example fibroblast), resulting
in shortening of G1 phase, prolongation of G2 and M
phases, thus mitotic cycle is shortened, and cell division
and proliferation accelerates. TGF-β, as a multi-functional growth factor, not only can attract inlammatory cells
and tissue repair cells to aggregate in the wound region,
but also directly act on ibroblasts to stimulate synthesis
of type Ⅰ procollagen, formation of granulation tissue,
and tissue reconstruction in the later stage of repair[25-27].
Nagano et al[28] in an animal model of disc degeneration
found that bFGF was a proliferation stimulating factor promoting proliferation of chondrocytes to replace
normal annular cells in degenerated discs in an autocrine
or paracrine manner. Tolonen et al[29] studied expression
of bFGF and TGF-β in painful degenerative discs, and
found that growth factors strongly express in both the
annulus fibrosus and the nucleus pulposus. Their study
suggests that these growth factors promote cellular remodeling, and create a cascade in the process of disc
degenerateion.
Disc tissues are different from other tissues because
they comprise the largest avascular tissue. In other tissues,
injury healing proceeds from the inside to the outside.
On the contrary, healing in disc tissues proceeds from the
outside to inside[16]. When the annulus ibrosus is lacerated or injured, vascular tissues can only gradually develop
from the outer to the inner annulus ibrosus. Endothelial
cells migrating into discs form the principal parts of a
new capillary vessel. With the help of various growth
factors, endothelial cells migrating into the avascular disc
tissues differentiate, proliferate, and gradually form complicated capillary networks. Our studies[15-17] suggested
that as annulus ibrosus injuries stimulated local vascular
inflammatory reactions, cells including macrophages
and mast cells in inflammatory regions produce a large
number of growth factors such as bFGF, TGF-β1, and
CTGF. The cells in normal disc are separated from the
circulatory system. These increased growth factors acted
on the intervertebral disc cells, and promoted disc cell
dedifferentiation and proliferation, as well as large-scale
extracellular matrix synthesis via signal transduction.
This may be the main cause of painful disc ibrosis and
degeneration. The strong expression of proliferating cell
nuclear antigen (PCNA) in painful discs seemed to be
an evidence of this hypothesis. PCNA, a nucleoprotein
of nonhistone, is an essential auxiliary protein of DNA
polymerase-δ [16]. It can markedly increase activity of
DNA polymerase-δ, and its expression level is believed to
be an important measure of cell proliferation activity[30].
The normal disc is believed to be an organ that is
poorly innervated supplied only by sensory and sym-
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April 18, 2013|Volume 4|Issue 2|
Peng BG. Discogenic low back pain
pathetic perivascular nerve fibers. In the early 1980s,
Bogduk[31] clariied the innervation of the outer layers of
the annulus. The posterior part of the human disc was
supplied not only from the sinuvertebral nerve but also
received direct branches in its posterolateral aspect from
the ramus communicans or the ventral ramus. Branches
from the grey ramus communicans also supplied the
lateral aspect of the disc. Anterior discal nerves were
observed to arise solely from the sympathetic plexus surrounding the anterior longitudinal ligament. The sensory
ibers that innervated the disc are mainly nociceptive and,
to a lesser extent, proprioceptive. The sympathetic ibers
are considered vasomotor efferents, and also sympathetic
afferents conveying pain impulses[32]. The close association of the postganglionic efferent and sympathetic afferent ibers relected a similar pattern to that seen in certain
enteric organs, leading them to suggest that low back
pain is a kind of visceral pain[33-35]. In human degenerated
disc, as well as in animal models of disc degeneration,
the number of nerve fibers in the disc increases[15,36,37].
Furthermore, the nociceptive nerve ibers grow into what
are usually aneural inner parts of the annulus and even
into the nucleus. In addition to the sensory nerve ibers,
there is growing evidence that sympathetic afferents are
also increased in degenerated disc and that they play a
significant role in low back pain[38-40]. In human normal
disc, protein gene product 9.5-positive nerve fibers, either associated with blood vessels or distant from them,
innervate the outer layers of the annulus. These nerve
fibers are also positive for acetylcholinesterasem NFP,
SP, CGRP, VIP, neuropeptide Y, C-lanking peptide and
synaptophysin. The nerves entering the rat disc have an
identical expression pattern[32]. Mechanical stimuli which
are normally innocuous to disc nociceptors can, in certain
circumstances, generate an ampliied response which has
been termed ‘peripheral sensitization’. This may explain
why some degenerative discs are painful and others not.
There is growing evidence that these pain receptors in
painful disc are peripherally sensitized by the activity of
sympathetic efferents which may initiate a pain impulse in
response to ischaemia, pressure changes or inlammatory
irritation[32].
It is accepted that the lumbar disc, which are the main
source of discogenic back pain in humans, are innervated
segmentally. However, the ventral portions of the rat
lower lumbar discs are innervated by upper (L1-L2) dorsal root ganglion neurons and the nerve ibers innervating the posterolateral portion of the disc come from the
upper and lower dorsal root ganglion (L3-L6)[38,39]. Nerve
fibers reach the lumbar disc through the sinuvertebral
nerves or from branches of the paravertebral sympathetic trunks[40]. Clinical studies have indicated those local
anaesthetic blocks of L2 nerve root can relief discogenic
low back pain[41].
ternational Association for the Study of Pain (IASP) are
emergence of a concordant pain response during discography, internal annular disruption shown by CT after
discography (CTD) and at least one adjacent disc without
concordant pain[42]. The term IDD was first coined by
Crock[5] on the basis of a large group of patients whose
disabling back and leg pain became worse after operation
for suspected disc prolapse. He reported this condition,
characterizing it by disruption of the internal architecture
of the disc, discogenic back pain in the absence of peripheral disc shape abnormality, and the absence of nerve
root compression. At present, IDD has been described
as a distinct clinical entity to be distinguished from other
painful processes such as degenerative disc disease and
segmental instability[8]. In our a previous study, according
to discography, we classified discogenic low back pain
into two types that were annular disruption-induced low
back pain (IAD) and internal endplate disruption-induced
low back pain (IED), which have been fully supported by
clinical and theoretical bases[43]. The term IAD should be
more reasonable than the term IDD clinically and pathologically. Clinically, these two types of low back pain
should be confirmed by lumbar discography. The diagnostic processes, radial tear and pain responses are identical. During the process of contrast medium injection, the
contrast medium was either lowing to the outside of disc
through a radial annular tear, or lowing to the vertebral
body through the radial endplate tear. The concordant
pain responses would be induced in either way.
According to the “Modified Dallas Discogram Description” method[44,45], the degrees of annular disruption
could be classiied into four grades. The deinitions are
Grade 0: the contrast medium is confined within the
normal nucleus pulposus; Grade 1: the contrast medium
flows into the inner third of the annulus through annular fissure; Grade 2: the contrast medium flows into
the middle third of the annulus; Grade 3: the contrast
medium flows into the outer third of the annulus, and
extends circumferentially less than 30° arc at the disk
center; Grade 4: the contrast medium lows into the outer
third of the annulus, and extends circumferentially more
than 30° arc at the disk center; and Grade 5: the contrast
medium leakage into the outer space. Grades 0, 1 and 2
are normal, while Grades 3 and above are indicative of
annular disruption. We combined the discogram and CT
scan after discography to evaluate the degree of endplate
disruption in IED patients. The disruptive degrees were
classiied into four grades (Figure 1): Grade 0 (no disruption), Grade 1 (contrast medium lows into the cartilage
endplate through tear), Grade 2 (contrast medium lows
into the bony endplate), Grade 3 (contrast medium lows
into the cancellous bone of vertebra under endplate,
showing local dispersion) and Grade 4 (contrast medium
disperses extensively in the cancellous bone)[43]. In this
group of patients with IED, all intervertebral discs that
showed concordant pain responses had endplate disruptions more severe than Grade 3, which was consistent
with the distributions of blood vessels and nerves in the
DIAGNOSIS
The diagnostic criteria for IDD established by the In-
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April 18, 2013|Volume 4|Issue 2|
Peng BG. Discogenic low back pain
Grade 0
Grade 1
Grade 2
Grade 3
Grade 4
Figure 1 Endplate disruption grading method schematic diagram.
A
B
Figure 2 Discography and computed tomography. A: Discography showing a radial disruption on the lower endplate of L4 vertebra and that the contrast medium
lows into the cancellous bone of the lower endplate of L4 vertebra through the issure; B: Computed tomography scan showing the contrast medium dispersed in the
lower endplate of L4 vertebra, with Grade 4 endplate disruption.
endplate (Figure 2)[43].
Theoretically, any innervated vertebra and its peripheral structures might be the source of low back pain. An
intervertebral disc has such a structure that, except for
the peripheral parts around annulus fibrosus, the endplate also has nerve supplies. Normally, one vertebral
endplate has two nerve supplies: one enters the endplate
along with perivertebral blood vessels, while the other
that belongs to the sinuvertebral nerve branch that enters
the endplate through the intervertebral foramen. The
nerve density within the endplate is similar to that of the
annulus, indicating that the endplate is also an important
source of discogenic low back pain[46]. Recently, we published a clinical study article[47], 21 patients with chronic
back pain originating from the endplate injuries were
selected to explore the methods of diagnosis and surgical
treatment. Pain level of disc was determined through discography in each patient. All 21 patients with a diagnosis
of back pain originating from endplate injuries according
to discography were treated with anterior or posterior
fusion surgery. After operation, through a mean followup of three years and ive months, we found that in all
the 21 patients, 20 (20/21) reported a disappearance or
marked alleviation of low back pain and experienced a
definite improvement in physical function. The study
suggests that discography and fusion surgery may be very
effective methods for the diagnosis and treatment, respectively, of chronic back pain originating from the endplate injuries. In fact, endplate damage-induced low back
pain occurs quite often clinically. In clinical research, we
found that endplate damage-induced low back pain accounted for 16.7% of chronic discogenic low back pain.
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Epidemiological investigation showed that the incidence
of endplate damage among populations without low back
pain was 30%[48].
Theoretically, the pathogenesis of endplate disruption-induced discogenic low back pain is presumed to
be consistent with that of annular disruption. A large
number of animal experiments have indicated that damage to the outer layer of the annulus could induce a
progressive degeneration of the entire disc[19-23]. Similarly,
animal models have indicated that needle punctures from
the vertebral side all the way through the endplate into
the disc could induce a progressive degeneration of the
entire disc[49]. It was found that the apoptosis of nucleus
pulposus cells increased and the proteoglycan content
decreased after endplate injury in the endplate damage
animal model[50]. The ingrowth of nerves and blood vessels is a characteristic of tear discs, and is also directly
correlated with discogenic low back pain. Freemont et
al[51] found that blood capillaries grew in companion with
nerve endings into the painful discs through endplates.
Basic and clinical studies have overwhelmingly illustrated the nerve supply of the disc and pathomorphologic correlates[6-9,15,18,36,37,52-58]. Based on controlled evaluations, the lumbar intervertebral discs have been shown to
be sources of chronic low back pain without disc herniation in 26% to 42%[4,6,7]. Because of the variety of anatomic and pathophysiologic causes of chronic low back
pain, it is a dificult diagnosis for clinicians to make. Clinicians primarily use advanced imaging techniques, such as
MRI to diagnosis low back pain. Studies show that MRI
indings such as disc degeneration do not correlate with
the presence or severity of low back symptoms. Lumbar
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April 18, 2013|Volume 4|Issue 2|
Peng BG. Discogenic low back pain
provocation discography is a procedure that is used to
characterize the pathoanatomy and architecture of the
disc and to determine if the disc is a source of chronic
low back pain. Recently, the American Pain Society developed and published multiple guidelines[59,60] in managing
low back pain which did not recommend discography as
a diagnostic test because of poor evidence for its sensitivity, specificity, and predictive value. However, subsequently, these guidelines were severely criticized[52]. There
were deiciencies and inappropriate evaluation in almost
all areas; inappropriate studies were included and appropriate studies were excluded. The basic deiciency of
these guidelines by Chou and Huffman[59] was their failure
to recognize the discography must not be performed in
asymptomatic volunteers or patients with mild low back
pain. They also utilized outdated guidelines from AHCPR
and European COST guidelines[52]. In the interim, questioning the validity of discography warrants questioning
the role of the disc as a discrete pain generator, or more
speciically, challenges the concept of symptomatic internal disc disruption. If one considers discography to be a
useless test, then one may have to abandon the concept
of the disc as a discrete pain generator and abandon the
pursuit of intradiscal therapies, whether surgical or nonsurgical[52]. Recent systematic reviews have concluded
that there is strong evidence that lumbar discography can
identify the subset of patients with chronic discogenic
pain[61,62].
side effects. Physical therapy, exercise, manipulation, and
back school seem to have some effects, but it is unknown
if effects are sustained for the long term[64]. Exercise therapy by the McKenzie method is a popular treatment for
low back pain among physical therapists. Clinical studies
have indicated that the McKenzie method is slightly more
effective than manipulation or is equal to strengthening
training for patients with chronic low back pain[66,67].
If conservative treatment fails, then epidural injections are commonly performed for chronic discogenic
pain. Epidural injections are administered by accessing
the lumbar epidural space by multiple routes including
interlaminar, caudal, and transforaminal[68-79]. Epidural
procedures continue to be debated regarding their effectiveness, indications, and medical necessity. Recent systematic reviews indicated that effectiveness of epidural
injections for treatment of discogenic low back pain was
fair[80]. The underlying mechanism of action of epidurally administered steroid and local anesthetic injection is
still not well understood. It is believed that the achieved
neural blockade alters or interrupts nociceptive input, the
reflex mechanism of the afferent fibers, self-sustaining
activity of the neurons, and the pattern of central neuronal activities[80]. Further, corticosteroids have been shown
to reduce inlammation by inhibiting either the synthesis
or release of a number of pro-inflammatory mediators
and by causing a reversible local anesthetic effect[81-85].
As alternative treatments, percutaneous treatments
directed at altering the internal mechanics or innervation
of the disc by heat (intradiscal electrothermal annuloplasty, IDET, and biacuplasty) have recently been advocated[7,86,87], but data supporting their use are controversial[86].
IDET was irst used to treat discogenic low back pain in
1996, using a concection technology with a 5 cm active
tip placed at the uncleoannuar junction. Two randomised
trials have shown either no effect or benefit in only a
small number of highly selected subjects[88-90]. Further, of
the 6 observational studies[91-96], 4 studies showed positive
results, one study showed negative results, and one study
showed undermined results. Recent a systematic review
evaluated these studied, and concluded that the evidence
is fair for IDET[97]. Biacuplasty is one of the minimally
invasive treatment methods. It creates heat across the
posterior annulus using a cooled bipolar radiofrequency
device[98]. The initial study results are promising[99,100], but
the effectiveness needs to be evaluated further to use randomized controlled trials.
During recent decades, surgical fusion of the lumbar spine has been performed in increasing number on
patients with chronic low back pain[4]. However, the reported results vary considerably in different studies, and
the complication rate after fusion surgery in the lumbar
spine is not negligible[101-105]. Consequently, artiicial disc
replacement has been proposed as a substitute for spinal
fusion with the aim of treating back pain while preserving vertebral motion at the operated levels and protecting
adjacent levels from undergoing degenerative changes,
but so far, only several studies have been reported on the
TREATMENT
Treatment for discogenic low back pain has traditionally
been limited to either conservative management or surgical fusion. However, to accurately assess the effect of any
therapy for treating discogenic low back pain, the natural history of such pain should be known beforehand.
Recently, our a clinical study indicated that the natural
history of discogenic low back pain was continuous and
chronic[63]. This result indicates that most patients are expected to experience low back pain after a longer time interval, and their pain severity is expected to remain nearly
the same. The elucidation of natural history of discogenic low back pain has important clinical signiicances
for decision-making of treatments.
There are a multitude of treatments used in clinical
practice to treat chronic low back pain, with little consensus amongst clinicians as to which is the best approach.
Pharmacologic treatment usually includes analgesics,
nonsteroidal anti-inlammatory drugs, and muscle relaxants, but the evidence for their eficacy is not compelling.
In randomized trials, the differences in pain after a patient has taken nonsteroidal anti-inlammatory agents as
compared with placebo have generally been in the minimally detectable range[64]. A meta-analysis revealed that
opioids seem to have a small effect in improving function
and relieving pain for the patients with chronic low back
pain[65]. Long-term treatment with narcotics is generally
discouraged, given the associated risks of tolerance and
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April 18, 2013|Volume 4|Issue 2|
Peng BG. Discogenic low back pain
A
relieve pain by reducing inflammation. A recent study
indicates that MSCs can induce the production of antiinflammatory cytokines[115]. However; additional studies
are needed to elucidate the underlying mechanisms of
pain relief.
B
REFERENCES
1
2
Figure 3 Magnetic resonance imaging and discography. A: A 35-year-old
woman had a 5-year history of low back pain. Sagittal T2 weighted magnetic
resonance imaging showed L4/5 disc degeneration with a high intensity zone in
the posterior annulus ibrosus; B: Discography showed L4/5 disc disruption with
exact pain reproduction. After discography, 10 mg methylene blue was injected
into the painful disc through discographic needle. Low back pain was almost
totally relieved. No recurrence was observed at a 12-mo follow-up interval.
3
4
results of lumbar disc prosthesis[106-108]. Recent a systematic review suggested that the spine surgery community
should be prudent to adopt this technology on a large
scale because harm and complications may occur after
some years[109]. The results with longer follow-up need to
be observed further.
Based on the recent insights into signal transduction
mechanisms that might lead to the induction of pain by
degenerative discs, it is conceivable that therapies aiming
at disrupting pro-inflammatory signaling pathways and
the pathway of nerve conduction might be successful in
the foreseeable future. Such therapies might not have the
ability to reverse the progressing tissue destruction which
occurs with aging but may transform a symptomatic
to asymptomatic disc degeneration and thereby greatly
improve life quality of the affected patients[10]. Recently,
a minimally invasive method, intradiscal methylene blue
injection for the treatment of painful disc degeneration, had been reported (Figure 3)[110,111]. This successful
outcome subsequently was demonstrated by the animal
experiments which indicated that methylene blue indeed
had destroyed the nerve endings or nociceptors and
alleviated inflammatory response in the degenerated
discs[112,113].
Recently, there has been a growing interest in developing strategies that aim to repair or regenerate the
degenerated disc biologically. Treatments for degenerated
discs have two main objectives: restoration of the disc’
s structure and elimination of pain[114]. The benefits of
biologically based treatments appear to be limited to restoring disc structure. Whether disc regeneration would
result in pain relief remains unclear. That said recent
data from animal studies have shown changes in cytokine
expression following growth factor injection, indicating
a possible mechanism for pain relief. Further, the first
human clinical trial for growth factor injection therapy
is currently underway and may shed light on the clinical
outcome. Mesenchymal stem cells (MSCs) may also help
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P- Reviewers Magalhães E, Manchikanti L, Helm S
S- Editor Gou SX L- Editor A E- Editor Zhang DN
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