From: Spine. 2003 Jun 1;28(11):1113-21

Low back pain is acute or chronic pain involving the lumbosacral, buttock, and/or thigh. Discogenic low back pain is aggravated by the sitting position, which is necessary in many occupations and daily activities. About 100 million workdays are lost annually in the United States due to low back pain. Despite improved knowledge and health care resources for spinal pathology, chronic disability resulting from nonspecific low back pain is rising exponentially. Although the causes of discogenic low back pain are multifactorial and complex, sitting postures could increase stresses within the disc and contribute to disc degeneration and pain. Two major occupational risk factors are static muscle load and flexed curvature of the lumbar spine; both are involved in seated work tasks.

During sitting, the head, arm and trunk weight is carried mainly by the ischial tuberosities and surrounding tissues. High pressure at the tuberosities is closely associated with high load to the spine. A significant mechanical spine loading is associated with low back pain resulting from trunk muscle coactivation. Ischial and lower back interface pressure vary with different sitting postures and body positioning. Repositioning of the lumbar support to redistribute the interface pressure and load is essential in preventing low back pain associated with inappropriate sitting in a working environment. Therefore, a device that decreases the sitting pressure and load carried by the ischial tuberosity may decrease forces within the disc and associated degeneration and pain.

Physiologic lumbar lordosis in the standing position ranges from 40° to 60°, with the lordosis occurring mainly at S1-L5 and L4-L5, and with the sacral inclination ranging from 30° to 40°. Compared to standing or lying supine, sitting could cause the pelvis to rotate posteriorly, resulting in decreased sacral inclination and lumbar lordosis and increased forces at the discs. A number of investigators have reported interaction between low back pain and biomechanical changes such as decreased lumbar lordosis, malalignment of lumbar curvature, and narrowing of disc spaces. Williams et al reported that use of a lumbar roll that increased lumbar lordosis reduced low back pain, and the chair backrest also helps increase the lumbar lordosis and decrease intradiscal pressure.

Numerous chairs or cushions have been developed to reduce or redistribute the sitting pressure on the ischial tuberosities using custom-fit seat pans. Others chairs are designed to maintain lumbar lordosis by adjusting back support or using a forward tilted seat. However, few chairs use adjustable mechanisms for both ischial release and lumbar support.

The purpose of this study was to investigate the biomechanical effects of tilting down the back part of seat and adjusting the backrest. The hypotheses were the following: 1) when the back part of seat is tilted down, load on the ischial tubercles will be reduced and shifted to the thighs, and low back muscle activity will be reduced; and 2) an increase in lumbar lordosis, forward rotation of the sacrum, and larger disc height will be observed when the back part of seat is tilted downward in combination with a properly adjusted back support.

This study investigated quantitatively the biomechanical effects induced by adjusting ischial and back supports, including the contact pressure distributions, reactive forces between the buttock-thighs and seat and between the back and backrest, muscular activity in back muscles, sacral inclination, lumbar lordosis, and intervertebral space of the lumbar spine. It was found that sitting with this lowered back part of seat and adjusted backrest distributed contact pressure more evenly, significantly reduced peak pressure under ischia, reduced muscular activity, rotated the sacrum forward, increased total and segmental lumbar lordosis, and increased lumbar intervertebral disc height.

When the back part of seat was tilted downward by θ = 18° and the backrest was utilized, Ftot exerted on the backrest was significantly increased. The peak contact pressure on the backrest was significantly increased, and it was significantly decreased on the seat; the largest change was found for the upright with backrest condition. The center of pressure and center of force were significantly shifted anteriorly to the thighs for all sitting conditions. All of these measurements for load and pressure redistribution on the seat and backrest indicated that load on the ischial tubercles was significantly decreased and shifted to the thighs, while load on the back support was increased, mainly with the load component in the posteroanterior direction to maintain lumbar lordosis. Using this new sitting concept made the thighs take up more load over a larger surface area, with less load on the ischial tubercles.

Measurement of load and contact pressure redistribution are important in assessing tissue viability, as prolonged sitting can lead to pressure sore development, increased disc degeneration, and low back pain. Repositioning of the lumbar support to redistribute the interface pressure and load is essential to prevent low back pain. Furthermore, for patients who have limited mobility, body repositioning remains the only way to change their pressure distribution at the body-seat interface.

Muscle activity was decreased in most of the sitting conditions when the back part of seat was tilted down, especially in the lumbar region. Relieving the ischial support may have made the pelvis rotate forward and relaxed muscles in the lumbar region more than in the thoracic regions. Another reason may be different amounts of pressure on the lumbar and thoracic regions during EMG recording for sitting conditions using backrest, especially for the relaxed condition. Under the relaxed sitting condition, the body did not show any significant change in muscle activity at the thoracic regions.

The upright with backrest sitting condition was found to be more efficient to change the pelvis and lumbar structures when the back part of seat was tilted down. The results from load and contact pressure redistribution on the seat and backrest indicated that this sitting condition gave the best results to reduce load on the ischial tubercles and lower spine. Thus, this sitting condition upright with backrest was used to evaluate changes in the lumbar spine and pelvis structures with the backrest fitted partially or fully to the lower spine using radiographs.

Tilting down the back part of seat maintained sacral inclination approaching that of the standing posture. The total and segmental lumbar lordosis were also increased and resulted in an appearance in which the abdomen was particularly prominent and resembled closely that of the standing position. The sacral inclination and lumbar lordosis results from other studies for sitting and standing are given. A comparison between these results and the results from the present study confirmed the similarity.

The benefit of lumbar lordosis was suggested in a postmortem study with an association between decreased lumbar lordosis and increased disc degeneration at L5-S1, suggesting a protective effect for increased lumbar lordosis on the lumbosacral junction. Andersson et al found lordosis to be inversely proportional to intradiscal pressure. Lumbar curvature affects disc pressure by changing the distribution of load between disc and apophyseal joints and also by changing tension in the intervertebral ligaments. The increased intradiscal pressure may also be the underlying factor for the association of decreased lordosis and low back pain. In a study of osteoporotic patients by Itoi, decreased lordosis was associated with increased low back pain. Keegan, in a study of the relation between lordosis and sitting, found the most important factor in low back pain with prolonged sitting to be a decreased trunk-thigh angle with consequent flattening of the lumbar curve. Using a lumbar roll that increases lordosis has been found to decrease low back pain. With decreased lordosis, sitting pressure increases over the ischium and coccyx with resultant pain. Others have also found distinct differences in lumbar lordosis when comparing low back pain patients with healthy patients.

All disc heights were significantly increased by lowering the back part of seat. Extensive and consequent segmental lordosis may decrease intradiscal pressure. The effect of disc height on mechanical properties caused by compressive forces was investigated and found that biomechanical axial stress for the intervertebral disc increased most at L4-L5 due to the decreased disc height in upright posture. The highest incidence of lumbar disc diseases was generally found at L4-L5. 52 The reason for the relatively high frequency of lumbar disc disease was connected to a relatively wide range of motion and high loads at L4-L5 and L5-S1 with lumbar flexion and extension.

It has been reported that a backrest with a protruded part to support the lumbar spine would result in an increase of the lumbar lordosis and the load on the back. The present study supports such an observation. Furthermore, a much greater load reduction was observed in this study for proper lumbar support combined with the ischial tubercles load relief. However, the benefits of unloading the ischia were investigated during a short sitting time. The outcome needs to be evaluated for longer period of sitting with unsupported ischia with the concern that load shifted to the thighs may cause hip pain. Tilting the back part of seat down and up alternately is needed during prolonged sitting. Future study is needed to find the optimal tilting angle of the back part of seat and optimal period for tilting the back part of seat down and up during long periods of sitting.

From: Ergonomics. 2008 May;51(5):637-48

The objective of this prospective cohort study was to evaluate if peak or cumulative musculoskeletal discomfort may predict future low back, neck or shoulder pain among symptom free workers. At baseline, discomfort per body region was rated on a 10 point scale six times during a working day. Questionnaires on pain were sent out three times during follow-up. Peak discomfort was defined as a discomfort level of 2 at least once during a day; cumulative discomfort was defined as the sum of discomfort during the day. Reference workers reported a rating of zero at each measurement.

Peak discomfort was a predictor of low back pain (relative risk (RR) 1.79), neck pain (RR 2.56), right or left shoulder pain (RR 1.91 and 1.90). Cumulative discomfort predicted neck pain (RR 2.35), right or left shoulder pain (RR 2.45 and 1.64). These results suggest that both peak and cumulative discomfort could predict future musculoskeletal pain.

From: Phys Ther. 2008 Aug 8; [Epub ahead of print]

Pain is currently evaluated with “subjective” methods (eg, patient self-report). This study aimed to test whether fatigue indexes are able to accurately discriminate between subjects with and subjects without low back pain. Sixty subjects separated into 2 groups-a group with low back pain (n=30) and a group without low back pain (n=0)-participated in this study. Electromyographic (EMG) and force data were obtained during a muscle fatigue test. The same test was repeated to monitor recovery. Linear regression analysis was used to obtain fatigue indexes. Subjects with pain produced significantly lower force values than those without pain. The use of fatigue indexes and force values permitted accurate classification in 89.5% of cases. The results confirm that subjects with pain show early myoelectrical manifestations of muscle fatigue and that EMG can be a useful tool in the evaluation of low back pain.

From: Semin Spine Surg. 2007 June; 19(2): 65–71

The intervertebral disc is characterized by a tension-resisting annulus fibrosus, and a compression-resisting nucleus pulposus composed largely of proteoglycan. Both the annulus and the nucleus function in concert to provide the disc with mechanical stability. Early disc degeneration begins in the nucleus with proteoglycan depletion. Quantitative MRI techniques have been developed to non-invasively quantify the earliest degenerative changes that occur within the disc. Our ability to identify and quantify these early biochemical changes will provide a better understanding of the pathophysiology of disc degeneration and facilitate the study of interventions that aim to halt or reverse the degenerative process.

Degenerative disc disease of the intervertebral disc is the most common cause of back-related disability among North American adults. This sometimes debilitating condition affects nearly 12 million people in the United States, and may generate direct and indirect costs exceeding 50 billion dollars annually in health-related expenditures. The radiographic evaluation of patients with degenerative disc disease often begins with plain film radiography and a standard T1- and T2-weighted MRI to assess for structural changes within the nucleus and annulus indicative of disc degeneration including a loss of T2-weighted MRI signal, loss of disc height, disc bulge or herniation, posterior element arthrosis, stenosis, and potential vertebral body compromise. While standard MRI is able to detect these later stage developments, it is not able to provide a quantitative measure of the early changes that characterize early degenerative disc disease. This limitation has led to the search for quantitative, non-invasive measures to evaluate the earliest changes involved in the initiation of the degenerative cascade. Such an imaging tool will be important for the evaluation of the patients with early degenerative disc disease, and also in the assessment of disc regenerative or restorative technologies that aim to halt or reverse the degenerative process.

The intervertebral disc has 3 sub-structures: the annulus fibrosus, which envelops the gel-like nucleus pulposus, and the endplates. The proteoglycan rich nucleus pulposus is comprised of a network of randomly distributed collagen fibrils in a hydrated extra-fibrillar matrix. In contrast, the annulus fibrosus is highly organized. It has 15–40 lamellae (layers) enveloping the nucleus pulposus. In each lamella, collagen fibers are positioned at a 30° angle to the axial axis of the spine. 70–80% of the nucleus pulposus and about 65% of the annulus fibrosus consist of water. After water is removed, an intervertebral disc is composed of collagens (50–70%), proteoglycans (10–50%), and other non-collagenous proteins (up to 25%). Collagen in the annulus fibrosus gives the intervertebral disc its tensile strength. The glycosaminoglycan branches of the proteoglycan are negatively charged, and they bind water. This water-binding property of glycosaminoglycan gives an intervertebral disc its hydrostatic pressure, which resists loading.

The initial stage of degenerative disc disease is marked by proteoglycan degradation and subsequently a reduced capacity of the nucleus pulposus to bind water. In later stages of the disease, morphological changes such as a loss of disc height, annular tears and rim lesions, and osteophyte formation materialize. Previous studies have implicated degenerative disc disease with low back pain. During the intial proteoglycan degradation, the proteoglycans of nucleus pulposus breakdown to clusters of short aggregated and non-aggregated molecules, the glycosaminoglycan content decreases, and the nucleus pulposus’s capacity to bind water reduces. The increased modulus and decreased hydrostatic pressure triggers the nucleus pulposus to undergo a phase change, from a fluid-like material to a more solid-like material. Mechanical function of degenerated motion segments is compromised in all loading conditions. The current standard surgical treatment for lower back pain with advanced intervertebral disc degeneration is lumbar spinal fusion. However, if degenerative disc disease can be detected at an earlier stage, the condition may benefit from emerging alternative treatments (e.g., nucleus replacement, total disc arthroplasty, cell therapy, growth factor therapy). Evaluation of the viability of potential degenerative disc disease therapies and longitudinal monitoring of degenerative disc disease progression demands an objective and quantitative imaging strategy, one that is sensitive to the biochemical changes in the early stages of degenerative disc disease. In this section, we will begin with a brief overview of conventional diagnostic quantitative MRI strategies (T1 and T2 relaxation mapping, dGEMRIC), followed by emerging novel quantitative MRI techniques (sodium, magic echo, and T 1?) that show promise as noninvasive, accurate diagnostic imaging tools for the quantitative assessment of early stage degenerative disc disease.

Standard T1 and T2 relaxation mapping are capable of detecting biochemical changes in the nucleus pulposus but have limitations, including increased scan time, limited dynamic range, and a lack of consistency between in vivo and in vitro values. Recent advancements in MRI, such as sodium MRI, magic echo, and T1? MRI, have been shown to be even more sensitive to PG degradation in the nucleus pulposus. As these quantitative MRI methods are still in the research phase, their efficacy still needs to be more fully evaluated in a clinical setting. However, preliminary clinical data on sodium, magic echo, and T1? MRI have demonstrated great potential to become noninvasive quantitative diagnostic tools for early degenerative disc disease.

From: Spine J. 2008 May-Jun;8(3):510-21. Epub 2007 May 25

By using a unique, prospective study of occupational back pain claims, they examined health care satisfaction by provider type and its effect on return to work. They estimated satisfaction differentials by provider type, decomposing overall satisfaction into two components: bedside manner and effectiveness of care. They also examined how health care satisfaction affects the duration of jobless claims. The Arizona State University Healthy Back Study is a prospective study of work related back pain; 1,831 workers completed a baseline interview, with follow-up interviews at 1 month, 6 months, and 1 year. The Arizona State University Healthy Back Study merged demographic and claim characteristics from the workers’ compensation claim files with self-reported severity measures, measures of satisfaction, and postonset employment from worker interviews.

Overall and detailed satisfaction with treatment and workers’ compensation claim duration. They performed a nonparametric descriptive analysis of satisfaction by provider type and used multivariate regressions to decompose overall satisfaction into component parts. The duration analysis links differentials in health care satisfaction to differences in claim durations. Workers treated by surgeons, chiropractors (DCs), or physical therapists are more satisfied with their health care than those treated by MDs. Workers are more concerned with the effectiveness of care than with the bedside manner of their provider. A one standard deviation improvement in satisfaction with the health care provider reduces claim duration by about 25%.

From: Zhonghua Wai Ke Za Zhi. 2008 Feb 1;46(3):213-6 Article in Chinese

To build subendplate microcirculation disturbance animal model and to investigate the potential pathogenesis of intervertebral disc degeneration. Twenty four New Zealand white rabbits were divided into treatment group (Group A) and control group (Group B). In Group A, animals received endotoxin and corticosteroid application to build subendplate microcirculation disturbance animal model, validated by microthrombus staining. In Group B, animals were given no drug, but standard feeding. After 3 month, the extent of intervertebral disc degeneration was evaluated by the water content, biochemistry analysis, and morphology. Subendplate microthrombus staining confirmed the exist of microcirculation disturbance.

The water content and biochemistry components content of disc in Group A were lower than those of disc in Group B, and intervertebral disc degeneration was observed in morphology. Subendplate microcirculation disturbance can directly contribute to intervertebral disc degeneration, the nutrients diffusion barrier is the potential pathogenesis of intervertebral disc degeneration.

From: Arthritis Res Ther. 2008 Aug 5;10(4):R87 [Epub ahead of print]

Chronic and debilitating low back pain is a common condition and a huge economic burden. Many cases are attributed to age related degeneration of the intervertebral disc, however, age related degeneration appears to occur at an accelerated rate in some individuals. We have previously demonstrated biomarkers of cellular senescence within the human intervertebral disc and suggested a role for senescence in intervertebral disc degeneration. Senescence occurs with ageing, but can also occur prematurely in response to stress. We hypothesised that stress induced premature senescence occurs within the intervertebral disc and here we have investigated the expression and production of caveolin-1, a protein that has been shown previously to be upregulated in stress induced premature senescence.

Caveolin-1 gene expression in human nucleus pulposus cells was assessed by conventional and quantitative real-time PCR and caveolin-1 protein expression examined within human intervertebral discs using immunohistochemistry. Correlation between caveolin-1 and p16INK4a biomarker of cellular senescence gene expression was investigated using quantitative real-time PCR.

Caveolin-1 gene and protein expression were demonstrated within the human intervertebral disc for the first time. Nucleus pulposus cells from degenerate discs exhibited elevated levels of caveolin-1 that did not relate to increasing chronological age. A negative correlation was observed between gene expression for caveolin-1 and donor age and no correlation was found between caveolin-1 protein expression and age. A positive correlation was identified between gene expression of caveolin-1 and biomarker of cellular senescence.

Our findings are consistent with a role for caveolin-1 in degenerative rather than age induced changes in the nucleus pulposus. Its expression in intervertebral disc tissue and its association with the senescent phenotype suggests that caveolin-1 and stress induced premature senescence may play a prominent role in the pathogenesis of intervertebral disc degeneration.

Low back pain is a condition that affects a significant proportion of the population, with a lifetime incidence rate in excess of 70% in industrialised nations. It not only impacts on quality of life, but also places a substantial financial burden on the National Health Service and the economy in general due to loss of working days. Many cases of low back pain are attributed to degeneration of the intervertebral disc and imaging studies have indicated a link between intervertebral disc degeneration and low back pain.

To date, no clear mechanism for intervertebral disc degeneration has been identified, although the involvement of both environmental and genetic factors has been proposed. The occurrence of intervertebral disc degeneration increases with age, however a subset of individuals appear to exhibit accelerated degeneration which is independent of age. This has led to speculation that additional factors could play a key role in the development of degeneration in some individuals.

There is increasing evidence that many features of intervertebral disc degeneration, including altered matrix synthesis and enhanced matrix degradation, originate at a cellular level. Cellular senescence is a strong candidate for the prolonged alteration in cellular activity observed during degeneration. Senescence and accompanying alterations in cell function have been implicated in ageing related, degenerative and pathological changes in a variety of tissues, including atherosclerotic plaque development within blood vessels and osteoarthritic alterations to cartilage. Two groups have shown increased staining for senescence associated β-galactosidase in cells from prolapsed and degenerate intervertebral disc cells respectively when compared to non degenerate discs. More recently presented is comprehensive evidence of senescence biomarkers in human intervertebral disc samples, demonstrating increased cellular senescence during intervertebral disc degeneration. In particular, cells from degenerate discs exhibited increased β-galactosidase activity, elevated expression of the cell cycle inhibitor p16INK4a biomarker of cellular senescence gene expression, telomere erosion and a decrease in replicative potential. Furthermore, a correlation was observed between p16INK4a biomarker of cellular senescence gene expression and the expression of matrix-degrading enzymes matrix-metalloproteinase (MMP)-13 and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), suggesting a role for cell senescence in the molecular processes observed during intervertebral disc degeneration.

Senescence occurs naturally with ageing, but can also occur prematurely in response to stresses (such as exposure to cytokines or oxidative stress) in a number of cell types. Since telomeric erosion and p16INK4a biomarker of cellular senescence gene expression protein are increased in degenerate discs compared to non degenerate age matched samples, we hypothesised that stress induced premature senescence occurs within the intervertebral disc and may be responsible for the accelerated degeneration observed in some individuals.

Caveolae are plasma membrane compartments found abundantly in terminally differentiated cells such as fibroblasts, endothelial and muscle cells. The mammalian caveolin gene family codes for three kDa caveolin proteins, which are integral membrane proteins essential for the structural integrity and function of caveolae. Expression of caveolin-3 is muscle specific, whereas caveolin-1 and caveolin-2 are co-expressed in many cell types. Proposed functions include lipid transport, membrane trafficking and a role in intracellular signalling pathways which stems from the co-localisation of caveolins with a variety of signal transduction molecules. Interestingly, caveolin-1 has been implicated in the senescent phenotype of several cell types including human fibroblasts, lung adenocarcinoma cells, endothelial cells and articular chondrocytes. Moreover, caveolin-1 has been proposed to mediate stress induced premature senescence in murine fibroblasts and human articular chondrocytes in response to oxidative stress and the inflammatory cytokine interleukin-1β, both of which are known to be increased during intervertebral disc degeneration. Here we have investigated the expression of caveolin-1 in human intervertebral discs and correlated its expression with the cell cycle inhibitor and the biomarker of senescence p16INK4a biomarker of cellular senescence gene expression, focusing on the nucleus pulposus as this area was seen to show the most evidence of cell senescence in human intervertebral disc.

This study has shown that caveolin-1 expression in human nucleus pulposis cells is linked to intervertebral degeneration and associated with the senescent phenotype as depicted by increased p16INK4a biomarker of cellular senescence gene expression. Caveolin-1 expression was not linked to increasing chronological age, suggesting a role in accelerated degeneration which could be due to stress induced premature senescence, rather than replicative senescence.

From: J Spinal Disord Tech 2008; 21:430–435

Internal disc disruption’’ is one of the prominent somatic sources of low back pain. MRI is the most common investigation performed to evaluate discogenic pain. Though MRI has advantages of being a sensitive investigation for identifying pathologic anatomy of disc degeneration, its value is limited by its inability to evaluate the physiologic status of the disc. Studies have questioned the specificity of MRI in diagnosing discogenic pain and have reported degenerative changes in 26% to 57% of asymptomatic volunteers. Discography is a useful tool to identify the painful disc responsible for patient’s symptoms. In evaluation of discogenic low back pain there has been a debate as to whether discography should replace MRI. Proponents of discography believe that it is an invaluable tool for identifying the pathologic disc producing pain. Critics believe that discography is an invasive investigation and has no place in modern practice.

Over the last decade there has been a vast improvement in the quality of MR images. Attempts have been made to identify features on MRI scans that would correlate with patient’s symptoms and would potentially eliminate the need for discography. Such features are the vertebral end plate changes described by Modic and the high intensity zone described by Aprill and Bogduk. The implications of these findings have been a subject of controversy.

This is a prospective study aimed at correlating the results of discography with new MRI classification in a consecutive series of patients with disabling low back pain considered for spinal surgery. In addition, we also aimed to compare vertebral end plate changes and high intensity zones seen on MRI with discography findings.

Woodend MRI Classification
Grade 1: White nuclear signal, normal height bean shape nucleus, annular margins well defined, no tears.
Grade 2: Speckled nuclear signal, height reduced less than 10%,distortion of nuclear shape, small radial tears not reaching the PLL on axial views.
Grade 3: Speckled or dark nucleus, height reduced by 10%-50%, radial tears extending upto or torn PLL on sagittal/axial views.
Grade 4: Dark nucleus, height reduced by greater than 50%, no difference between appearance of annulus and nucleus ± complex tears.

Disc Morphology Grading
Grade 1: cotton ball or lobular appearance of disc with no tears.
Grade 2: disc with fissures or clefts in the nucleus or inner annulus.
Grade 3: degenerate disc with radial fissures leading to outer edge of the annulus.
Grade 4: disc with complete radial fissure.

Internal disc disruption was described by Crock as a condition causing back pain without nerve root compression. Tears within the annulus fibrosus are a major hallmark of degenerative intervertebral disc disease. Tears within the annulus evoke an inflammatory response, which leads to degradation of disc matrix and chemical irritation of nerve fibers within the outer annulus. Discogenic pain is a mechanical, nonradicular pain with a somatic pattern. Therefore, the use of symptoms and signs to identify the symptomatic degenerative disc level has limited value. A method for investigating discogenic pain cannot be considered reliable unless there is a confirmed relationship between its findings and a patient’s symptomatology

Lindbolm first introduced discography in 1944. Holt raised the first major challenge to this technique in 1968. Holt reported false-positive findings in 37% of patients in a study on asymptomatic prison inmates. However, following a study carried out by Walsh et al in 1990 under more stringent conditions, doubts were raised regarding Holt’s findings. Walsh et al carried out discography in 10 asymptomatic volunteers and reported no false-positive result. Adams et al performed a cadaveric study and proposed a discography classification, which has been used, in a modified form, in this study. The Dallas Discogram Description described by Sachs et al is based on computed tomography scan after discography. We believe that this exposes patient to unnecessary radiation and increases cost without any additional benefit. The morphology of the disc as revealed by discography is irrelevant. In our study, we have used concordant pain on discography as a guide to the pain source. The analysis for sensitivity and specificity has been performed after excluding discs with discordant pain. As the investigation is performed under local anesthetic we believe that the patient’s response can be reliable.

In the late 1980s, when MRI became popular among spinal surgeons, a number of studies questioned the utility of discography in discogenic pain. Gibson et al reported 88% correlation between findings of MRI and discography in 50 patients. Discography was carried out under sedation and the authors believed that this was an unreliable sign. Schneiderman et al concluded that MRI was 99% accurate as compared with discography. In both these studies the correlation of MRI was with disc morphology rather than pain. Simmons et al reported that 37% of the discs reported abnormal on MRI were asymptomatic on awake discography. Linson and Crowe reported 94% correlation between MRI and discography. In their study, only 53% of the degenerative discs were found to be symptomatic. They concluded that discography remains the examination of choice for differentiating between symptomatic and asymptomatic discs. Collins et al reported morphologic correlation between discography and MRI in 89.5% cases. Only 13 of 73 discs were symptomatic and 10 had degeneration with annular bulges on MRI. Osti et al in a study on 108 intervertebral discs found that of the 39 symptomatic discs only 27 had abnormal signals on MRI. They concluded that discography is a more accurate investigation to detect symptomatic disc. Horton and Daftari correlated disc signals and annular bulges with pain reproduced at discography and concluded that MRI does not reliably predict or replace discography.

In this study, we have attempted to use an MRI classification system that will help predicting pain and allow comparison of various disc appearances. This classification embraces various aspects of disc morphology such as MRI signal, disc height, and annular tear in combination rather than considering them as individual entities. The classification uses the carefully aligned axial and sagittal images on MRI, unlike most of the previous studies in which only sagittal scans were used. We now use these scans routinely. The interobserver and intraobserver reliability of the classification system is good. The classification system can be used to communicate status of disc morphology and has a potential as a research tool. There is good correlation between the grades of degenerative disc on discography and the MRI classification system. In our study, we also found that grades 3 and 4 disc morphology has a 81% sensitivity and 80% specificity in predicting discogenic pain. We postulated that annular tears would predict a disc to be painful and included these as one of the criteria for pain prediction on MRI. These tears are best visualized on axial scans. The majority of the discs with annular tears were grade 3 or grade 4. Of the 25 grade 2 discs 14 had annular tears and 12 produced concordant or discordant pain. The presence of grade 3 or grade 4 disc on MRI scan or grade 2 with annular tear increased the sensitivity of MRI scan in detecting a painful disc to 94%.

There has been considerable interest in high intensity zones as predictors of painful lumbar intervertebral discs. Aprill and Bogduk who considered it to represent inflammation in the annulus secondary to trapped nuclear material and reported a sensitivity of 82% and specificity of 89%. Schellhas et al and Lam et al found high intensity zone to be a reliable predictor. Ricketson et al11 did not find significant correlation between high intensity zone and concordant disc pain. Ito et al described a sensitivity of 52% and specificity of 90% for concordant disc pain. The sensitivity and specificity of high intensity zone in our study is close to those reported by Saifuddin et al and Smith et al. Vertebral end plate has been identified as a possible source of low back pain. Braithwaite et al and Ito et al reported low sensitivity and high specificity for end plate changes which closely corresponds to that in our study.

In 25% of the patients, the findings of MRI and discography did not correlate. This is due to low specificity of MRI in detecting the painful level. There were 3 discs, which were grade 1 on MRI and produced concordant pain and 12 grade 3 or grade 4 discs, which were not painful. We agree with Simmons et al that, in current practice, discography has a place as it can complement the interpretation of MRI findings and help to determine management of chronic low back pain. There were 18 discs, which produced discordant pain in our study. A disc with discordant pain is still painful disc though not necessarily causing the patient’s major symptoms.

In our study, the group of patients who had previous surgery had similar discography and MRI correlation. We find MRI is also useful in evaluation of this group of patients with previous spinal surgery. Improvements in biomaterials and scanning techniques allow good quality MRI scans in patients with previous instrumentation and artifacts do not hamper assessment of disc morphology.

The use of discography has a limitation that pain on discography is subjective and dependent on interaction between patients and surgeons/radiologists, and has to be interpreted as such. We studied a selected group of patients considered for spinal surgery. We believe that discography is a preoperative investigation and should be performed only when the diagnosis of discogenic pain is highly probable as determined by systematic clinical examination, nonoperative treatment has failed, and a decision is made to proceed to surgery. Our study does not address the implications for management of patients. This cohort of patients is being followed prospectively and their long-term outcome will answer whether these findings have implications for patient’s quality of life outcome after surgical treatment. We also believe that in future techniques, which can stimulate disc in noninvasive manner while performing MRI, will benefit assessment of discogenic pain. This will improve the specificity of MRI. Yrjama et al have reported such techniques but these have not been reported from other centers.

From: Annals of the Rheumatic Diseases 2007;66:330-333

Peripheral joint osteoarthritis is characterised radiologically by the presence of osteophytes, subchondral sclerosis and joint space narrowing. Joint space narrowing is due to cartilage loss, whereas both subchondral sclerosis and osteophytes are hypertrophic responses of bone, thought to arise directly either to cartilage loss or to biomechanical stress. The pathophysiology and hence the inter-relationship of these features are however not well understood. Recently, strong associations between the presence of enthesophytes, osteophytes and bone sclerosis at various joint sites have been shown. Partly on the basis of these observations, it has been suggested that some individuals may be more likely to develop bone formation in response to disease occurrence. We looked at a series of lumbar spine radiographs and characterised the severity of the component radiographic features. Although the pathology of disc degeneration differs from peripheral joint osteoarthritis, we hypothesised that if there was a predisposition to develop new bone formation in the form of osteophyte or sclerosis in response to mechanical stress, there would be a strong association between increasing severity of the features of new bone formation. The aim of this study was to determine the strength of the association between increasing severity of osteophytes and end-plate sclerosis, and the association between both these features and disc space narrowing in the lumbar spine.

In this study, we found that increasing severity of all three radiographic features of lumbar disc degeneration was associated with increasing severity of the other features, although the association was strongest for osteophytes and end-plate sclerosis, and was stronger within than between vertebral levels. There are some methodological limitations that need to be considered when interpreting the findings. The response rate for participation in the study was 61%. Those who attended for screening could have differed with respect to the frequency of disc degeneration than those who did not attend. Given, however, that the analysis of the inter-relationships between radiographic features was based on an internal comparison of responders, non-participation bias is unlikely to have had a major effect on the observed findings.

The semiquantitative approach used here to characterise the individual radiographic features is subject to errors of precision. Formal assessment of intraobserver variability as determined by was good. At the time of assessment, the observer was not aware of any possible difference in pairwise associations between features and any errors in classification of the features likely to have been non-directional, and would tend to reduce the chance of finding true associations.

As with peripheral osteoarthritis, the pathogenesis of intervertebral disc degeneration remains poorly characterised. Degenerative changes within the disc may result in an alteration of its mechanical properties, increased flexibility and decreased disc height, which in turn contribute to changes in the local stress/strain state within the disc. Also, as has been considered for peripheral osteoarthritis, the bone may be the primary trigger responding to lifelong stress with hypertrophy and stiffening, and transmitting increased load to the intervertebral disc. In peripheral osteoarthritis, there is some evidence that increased bone mass is a predictor of radiographic osteoarthritis. It has also been shown that generalised osteoarthritis is associated with increased levels of insulin-like growth factors in extracts of cortical bone from the iliac crest.

If osteophytes and end-plate sclerosis are independent and separately related to narrowing of the disc, then we could hypothesise that as disc space narrowing increased, the severity of these features would increase in parallel. However, we observed that the proliferative features were more likely to be related in terms of severity than either separately with disc space narrowing.

There are few data concerning inter-relationships between component radiographic features of lumbar disc degeneration in the literature. In a Japanese study, there were significant correlations between osteophytes, end-plate sclerosis and disc space narrowing in the lumbar spine, although data relating to these features were pooled rather than considered by vertebral level. As in our study, the association between osteophytes and end-plate sclerosis was stronger than either of the other pairwise correlations. In a study of twins using magnetic resonance imaging, a strong correlation was seen between the same measurements (including disc height and osteophytes) across all vertebral levels within the cervical and lumbar spine, but a weaker correlation when the same features were compared between the cervical and lumbar spine.

In a series of paleopathological specimens, it was observed that individuals who had a tendency to form enthesophytes were more likely to have both osteophytes and sclerosis present at peripheral joint sites. These data have been considered to be consistent with a bone proliferative response to disease occurrence. Although the pathologies of disc degeneration and peripheral osteoarthritis are different, our data in relation to severity of osteophytes and sclerosis would be consistent with this. Further research is necessary to determine the factors affecting the occurrence and severity of these features.

We have previously shown in this population sample an association between radiographic features of disc degeneration and back pain although disc space narrowing was more strongly associated than the other features. All three features increased in frequency with age. We found evidence also of an association between bone mineral density at the femoral neck and the presence of vertebral osteophytes and end-plate sclerosis, although not disc space narrowing. However, further prospective data are required both to confirm our findings and to determine the temporal nature of the observed associations.

From: J Bone Joint Surg Br. 2005 Jan;87(1):62-7.

Discogenic low back pain is a common cause of disability, but its pathogenesis is poorly understood. We collected 19 specimens of lumbar intervertebral discs from 17 patients with discogenic low back pain during posterior lumbar interbody fusion, 12 from physiologically ageing discs and ten from normal control discs. We investigated the histological features and assessed the immunoreactive activity of neurofilament and neuropeptides such as substance P and vasoactive-intestinal peptide in the nerve fibres. The distinct histological characteristic of the painful disc was the formation of a zone of vascularised granulation tissue from the nucleus pulposus to the outer part of the annulus fibrosus along the edges of the fissures. Substance P, neurofilament and vasoactive-intestinal peptide immunoreactive nerve fibres in the painful discs were more extensive than in the control discs. Growth of nerves deep into the annulus fibrosus and nucleus pulposus was observed mainly along the zone of granulation tissue in the painful discs. This suggests that the zone of granulation tissue with extensive innervation along the tears in the posterior part of the painful disc may be responsible for causing the pain of discography and of discogenic low back pain.