From: Arthritis Rheum. 2012 Jan 27. doi: 10.1002/art.33462. [Epub ahead of print]

This study addressed the association of overweight and obesity to the presence, extent, and severity of lumbar disc degeneration on MRI in adults. A population-based cross-sectional study of 2,599 Southern Chinese volunteers. Radiographic and clinical assessment, including weight and height, was conducted. Sagittal T2-weighted MRIs of the lumbar spine were obtained. The presence, extent, and severity of disc degeneration as well as additional radiographic and clinical findings were assessed. Asian-modified BMI (kg/m2) categories were utilized.

There were 1,040 males and 1,559 females (mean age= 41.9 years). Disc degeneration was noted in 1,890 (72.7%) subjects. BMI was significantly higher in subjects with disc degeneration compared to subjects without degeneration. A significant increase in the number of degenerated levels, global severity of disc degeneration, and end stage disc degeneration with disc space narrowing was noted with elevated BMI, in particular in overweight and obese individuals. In the adjusted multivariate logistic regression model, there was a positive linear trend between BMI categories and the overall presence of disc degeneration for overweight and obese. End stage disc degeneration with disc space narrowing was significantly more pronounced in obese individuals.

In one of the largest studies to systematically assess lumbar disc degeneration on MRI, our study noted a significant association between the presence, increased extent, and global severity of disc degeneration in overweight and obese adults.

From: Eur Spine J. 2012 Jan 17. [Epub ahead of print]

This prospective magnetic resonance imaging (MRI) study in chronic low back pain patients evaluated the natural course of degenerative lumbar spine changes in relation to Modic 1 type changes within 1 year. From 3,811 consecutive chronic low back pain patients referred to lumbar spine MRI 54 patients with a large Modic 1 type changes were selected using strict exclusion criteria to exclude specific back disorders. Follow-up MRI was obtained within 11-18 months.

At baseline Modic 1 type changes was associated with an adjacent endplate lesion in 96% of the cases. In follow-up, an unstable Modic 1 type change was associated both with an increase of endplate lesions, decrease of disc height and change in disc signal intensity, most found at L4/5 or L5/S1. In disc spaces without Modic 1 type changes, progression of degenerative changes was rare. Endplate deformation, decreasing disc height and change of disc signal intensity appear essential features of accelerated degenerative process associated with Modic 1 type changes.

From: BMC Musculoskelet Disord. 2011 Sep 13;12:202

The importance of spine stability is a central paradigm in spine care. Maintenance of spine stability, through decreasing excessive or abnormal spinal movement, is the rationale for many commonly used treatments ranging from ‘lumbar stabilization’ rehabilitation to spinal fusion surgery. The spinal degenerative cascade is an important theory related to the concept of spine stability, and was originally popularized by Kirkaldy-Willis. Kirkaldy-Willis described a ‘cascade’ of degenerative changes affecting the three joint complex comprised of the intervertebral disc anteriorly and the lumbar zygapophyseal (‘facet’) joints posteriorly. This degenerative cascade consists of three sequential clinical stages: 1) dysfunction, 2) instability, and 3) stabilization. Kirkaldy-Willis described a mutual interrelationship of the intervertebral disc and facet joints, and pointed out that precipitating events in degeneration could begin not only with the intervertebral disc, but also with the facet joints.

Over time, however, the sequence of spinal degeneration has often been viewed from a more limited standpoint, with the perspective that anterior structure changes affecting the intervertebral disc largely precede- and lead to- posterior structure changes affecting the facet joints. The notion that degeneration begins with the intervertebral disc is described in textbooks of spine care and has been supported by some research studies. Vernon-Roberts conducted a landmark study of fewer than 100 cadaveric specimens that found that degenerative disc changes were always accompanied by facet joint degenerative changes. This study concluded that disc degeneration was the primary event leading to degenerative spondylosis. In an imaging study of 68 subjects with low back pain, Butler et al. also found that facet joint degeneration did not occur in the absence of disc degeneration, but disc degeneration frequently occurred without facet joint degeneration. Butler concluded that discs degenerate before facets. These conclusions were further supported by a recent cross-sectional MRI study of individuals with low back pain. Some authors, however, have questioned the view that disc degeneration necessarily precedes facet degeneration. A prior report notes that facet arthrosis on MRI precedes disc degeneration in 20% of men. Furthermore, in a large study of skeletal specimens (n = 647), Eubanks et al. found that facet joint osteoarthritis often preceded changes of disc degeneration in younger individuals.

Many prior studies of the degenerative cascade that have concluded that disc degeneration uniformly precedes facet degeneration have been based on convenience samples of individuals with low back pain. Given the prevailing notion among clinicians that much low back pain originates from the disc, recruitment from spine clinics therefore presents a probable selection bias in prior samples. No studies have examined a large, community-based sample that is unselected for low back pain. Furthermore, no studies examining the interrelationships between anterior and posterior structure degeneration have used multivariate analyses to adjust for important demographic and anthropometric factors thought to be related to spinal degeneration.

The authors conducted an epidemiologic study of patterns of degeneration in the community-based population of the Framingham Heart Study. The aims of the present study were: 1) to determine the prevalence of different patterns of anterior and posterior spinal structure degeneration in the community-based population, and 2) to examine whether the observed epidemiology is consistent with the view that degeneration always begins with the intervertebral discs, and 3) to determine the independent relationship between anterior structure and posterior structure degeneration, while adjusting for important demographic and anthropometric factors.

The current study is consistent with the view that, for a majority of individuals, degeneration begins with the anterior spinal structures. However, a minority of individuals (10-20%, depending on the definition of anterior degeneration used) across the age spectrum exhibits a pattern of isolated posterior degeneration without substantial loss of disc height, occurring most frequently at the L5-S1 and L4-L5 spinal levels. For these individuals, the factors of age, gender, and BMI may explain, at least in part, the development of posterior structure degeneration without concurrent changes in the disc

Kirkaldy-Willis described spinal degeneration as the result of a complex interaction between the intervertebral discs and facet joints, which begins with precipitating events that could take place in any component of the three-joint complex. He stated clearly, ‘In some patients the changes seen during the course of the progressive degenerative process affect mainly the facet joints’. These findings that some individuals have changes of facet degeneration without any changes of disc height loss is therefore consistent with the Kirkaldy-Willis view, and furthermore is supported by some earlier studies. The seminal cadaveric study by Lewin reported that facet joint osteoarthritis sometimes occurred in the absence of disc degeneration or vertebral osteophytosis. Eubanks’ study of skeletal lumbar spines found that lumbar facet joint osteoarthritis appeared early in the course of aging, often preceding anterior vertebral changes. On the other hand, some cadaveric and imaging studies described above have concluded that disc degeneration always precedes facet degeneration. Taken together, the existing literature suggests that many exceptions exist to the generalization that anterior changes precede posterior changes. These exceptions may be explained by the contributions of increased age, female gender, and higher BMI.

Longitudinal studies in humans are needed to verify whether any of the previously proposed biomechanical, demographic, or anthropometric risk factors for posterior structure degeneration are truly causal. A compelling alternative explanation exists: the predominant influence of heredity in disc degenerative changes has already been shown, and heredity may well explain much of the variation seen in facet degenerative changes as well.

Future longitudinal studies should ideally allow for examination of genetic factors, and should account for other covariates not considered in this study, including occupational loading, prior physical trauma, lumbosacral alignment, and facet joint orientation and tropism. In particular, these findings that isolated posterior degeneration occurred predominantly at the L5-S1 and L4-L5 levels may warrant more detailed consideration of lumbosacral biomechanical factors. Furthermore, since disc height narrowing is a relatively nonspecific finding with poorly understood determinants, future studies should take into account other parameters of disc degeneration, including quantitative assessments of desiccation, herniation, and annular pathology.

The observed epidemiology of lumbar spinal degeneration in the community-based population is consistent with an ordered sequence beginning in the anterior structures, for a majority of individuals. However, some individuals demonstrate atypical patterns of degeneration, beginning in the posterior joints. Increased age and BMI, and female gender, may be related to posterior degeneration in these individuals. Longitudinal studies are needed to better understand the importance of segmental level biomechanics in degeneration, and ideally should include not only these important covariates, but also examination of genetic factors.

Disc desiccation, herniation, annular pathology and genetics are additional variables that affect degeneration and were not factored into the study results.

Source: The source also goes into details regarding the grading methods of anterior and posterior degeneration -Does lumbar spinal degeneration begin with the anterior structures? A study of the observed epidemiology in a community-based population

From: Ann Rheum Dis. 2011 Oct;70(10):1740-5

Low back pain is a common musculoskeletal condition in all ages worldwide and in Europe in particular. The lifetime prevalence of non-specific low back pain may reach 80%, with the annual prevalence ranging between 25% and 60% in different ethnic groups. Radiological features of lumbar disc degeneration are almost universal in adults, and have been proposed repeatedly as one of the main causes of low back pain. Although an association has been demonstrated, the individual risk factors for low back pain remain unclear and universal consensus regarding the extent of lumbar disc degeneration–low back pain association is lacking. The lack of standardised clinical criteria and radiological definitions has further hampered the undertaking of well-executed epidemiological studies. More sensitive imaging modalities, such as MRI, have fallen in cost and become more widely available and are paving the way for new, large-scale epidemiological studies of lumbar disc degeneration.

Obesity, smoking and occupation have been reported to be associated with prevalent low back pain, although the quantitative effect of the majority of them has been found to be negligible—even insignificant. On the other hand, several studies have consistently suggested the presence of a major genetic component underlying variation of low back pain, although data remain scarce.

The major aim of this study, representing a continuation of the authors preliminary study, was to evaluate the association of non-specific low back pain with lumbar disc degeneration and putative genetic factors in a sample taken from the general population, using extensive data from the UK Twin Spine Study (TUTSS). The UK Twin Spine Study has one of the world’s largest samples for whom low back pain data and important risk factors, including MRI-determined lumbar disc degeneration status, are available in a subsample. Other relevant risk factors available for this study included age, anthropometrics, smoking and physical exercise. This allowed the authors to conduct rigorous association analysis of the low back pain with lumbar disc degeneration scores and genetic heritability, simultaneously controlling for the effect of other risk factors. Needless to say, the study does not consider several other potentially relevant risk factors, including inflammatory disease, fracture or the psychological component in back pain, which is an important contributor to pain and disability.

This cross-sectional study of a large sample of female twins shows that in addition to genetic predisposition, episodes of low back pain are strongly associated with the extent of lumbar disc degeneration as assessed by MRI. In addition, genetic variation of low back pain and lumbar disc degeneration is governed by some common but mostly independent genetic factors, the nature of which remain to be determined.

The main risk factors for reported episodes of severe and disabling low back pain in UK women include the degree of lumbar disc degeneration as assessed by MRI, being overweight and genetic heritability.

Source: Lumbar disc degeneration and genetic factors are the main risk factors for low back pain in women

From: Med Hypotheses. 2011 Oct 17. [Epub ahead of print]

Lumbar foraminal stenosis is a common pathological change, and lumbar nerve root compression in stenotic foramina was recently considered as one of the main causes of low back pain and leg pain. However, the exact mechanism of lumbar nerve root compression in foramina is still not clear. Previous studies indicated that loss of the intervertebral disc height could reduce the cross-sectional area of lumbar foramina, while lumbar nerve root compression by boundaries of foramina has not been observed in experimental reduction of the intervertebral disc height.

Given the close anatomic relationship between transforaminal ligaments and lumbar nerve roots, the authors hypothesize that transforaminal ligament can be the leading cause of lumbar nerve root compression in foraminal stenosis. They also propose that there are two possible mechanisms of lumbar nerve root compression by transforaminal ligaments:

1. nerve roots are compressed by the transforaminal ligament which moves downward with the loss of the intervertebral disc height
2. pathological transforaminal ligaments increase the risk of nerve root compression in foramina

From: Clin Biomech (Bristol, Avon). 2011 Oct 18. [Epub ahead of print]

Previous studies reported that, in non-degenerate discs, the nucleus pulposus migrates posteriorly during flexion and anteriorly during extension within the intervertebral disc. However, in these studies the differences between anterior and posterior distances have been regarded as an indicator of nucleus pulposus migration. This study investigated the reality of migration of the nucleus pulposus within the intervertebral disc with changing postures.

Magnetic resonance images were obtained of the lumbar spines of 25 asymptomatic volunteers in sitting, standing and supine postures. The anterior and posterior height of the intervertebral disc, the anterior-posterior length of the intervertebral disc and nucleus pulposus, and the positions of the anterior and posterior margins of the nucleus were measured from mid-line sagittal images.

Changing postures altered the anterior and posterior height of the disc and three types of morphological changes, including changes in the anterior-posterior lengths of the intervertebral disc and nucleus pulposus, together with the position of the nucleus in the disc were found. The length of the intervertebral disc and nucleus pulposus changed under the variations in spinal loading caused by posture.

The results of this study indicated that the apparent nucleus pulposus migration within intervertebral disc is actually deformation of the nucleus pulposus length which depends on posture and the magnitude of the load. In other words, adopting different postures deforms the nucleus pulposus and therefore, changes the position of the nucleus pulposus but there is no apparent nucleus pulposus migration within the intervertebral disc.

From: J Biomech Eng. 2011 Sep;133(9):091006

The intervertebral disc receives important nutrients, such as glucose, from surrounding blood vessels. Poor nutritional supply is believed to play a key role in disc degeneration. Several investigators have presented finite element models of the intervertebral disc to investigate disc nutrition; however, none has predicted nutrient levels and cell viability in the disc with a realistic 3D geometry and tissue properties coupled to mechanical deformation. Understanding how degeneration and loading affect nutrition and cell viability is necessary for elucidating the mechanisms of disc degeneration and low back pain.

The objective of this study was to analyze the effects of disc degeneration and static deformation on glucose distributions and cell viability in the intervertebral disc using finite element analysis. A realistic 3D finite element model of the intervertebral disc was developed based on mechano-electrochemical mixture theory. In the model, the cellular metabolic activities and viability were related to nutrient concentrations, and transport properties of nutrients were dependent on tissue deformation. The effects of disc degeneration and mechanical compression on glucose concentrations and cell density distributions in the intervertebral disc were investigated. To examine effects of disc degeneration, tissue properties were altered to reflect those of degenerated tissue, including reduced water content, fixed charge density, height, and endplate permeability. Two mechanical loading conditions were also investigated: a reference (undeformed) case and a 10% static deformation case. In general, nutrient levels decreased moving away from the nutritional supply at the disc periphery. Minimum glucose levels were at the interface between the nucleus and annulus regions of the disc. Deformation caused a 6.2% decrease in the minimum glucose concentration in the normal intervertebral disc, while degeneration resulted in an 80% decrease. Although cell density was not affected in the undeformed normal disc, there was a decrease in cell viability in the degenerated case, in which averaged cell density fell 11% compared with the normal case. This effect was further exacerbated by deformation of the degenerated intervertebral disc.

Both deformation and disc degeneration altered the glucose distribution in the intervertebral disc. For the degenerated case, glucose levels fell below levels necessary for maintaining cell viability, and cell density decreased. This study provides important insight into nutrition-related mechanisms of disc degeneration. Moreover, this model may serve as a powerful tool in the development of new treatments for low back pain.

From: J Int Med Res. 2011;39(2):569-79

The vertebral column is a strong yet flexible shaft which provides support of body weight, a basis for locomotion, and protection of the spinal cord and its nerve roots. It consists of 7 cervical vertebrae, 12 thoracic vertebrae, 5 lumbar vertebrae, 5 fused sacral vertebrae, and 4 coccygeal vertebrae. The intervertebral discs are interposed between adjacent surfaces of the vertebral bodies and provide the strongest attachment between the vertebrae. The principal functions of the intervertebral discs are to allow movement between vertebral bodies, transmit forces evenly from one vertebral body to the next, and absorb and store energy.

Throughout the day the vertebral column is subjected to compressive as well as other types of loading by gravity, changes in position, muscle activity, external forces, and external work. The fluid pressure within the nucleus pulposus is related to the axial compression applied to the disc. When the compressive load exceeds the interstitial osmotic pressure of the tissues of the disc, water is extruded through the disc wall. The result is a loss in disc height, and thus, a loss in total body height. The gelatinous nature of the nucleus allows it to imbibe fluid and regain its original size when the axial compression is minimized. During the day, when a person is usually under the constant force of gravity and muscular activity, the intervertebral discs lose as much as an inch in height. However, at night, while a person is recumbent, that height is restored.

Disc shrinkage has been used as a measure of the effect of the load on the spine. Consequently, the observed changes in height can be considered to reflect the magnitude of vertebral column loading. It has been asserted that greater losses in height occur when dynamic rather than static loading is involved, and that dynamic loads on the spine result in a faster rate of shrinkage. Running studies using force plate gait analysis have shown a marked increase in the ground reaction force as compared to walking. During running the force generated at the point of heel strike has been shown to be three times that of walking. This means that significant compressive forces are being transmitted to the spine.

In this study, the lumbar spines of 25 long-distance runners were examined using an upright magnetic resonance imaging scanner. All volunteer runners were scanned before and after running for 1 h. Scanning was performed with the runners seated upright (neutral), leaning forwards (flexion) and leaning backwards (extension). All measured discs showed a reduction in disc height after 1 h of running. A significant reduction in disc height was observed in all three body positions (neutral, flexion and extension) after 1 h of running. The results showed that, in flexion, extension and neutral positions, intervertebral discs undergo significant strain after 1 h of running. The lowest disc-height reduction was found at the L5 – S1 space in the neutral position; the same space had the highest percentage of disc degeneration.

Related Source: Effects of Running on Intervertebral Disc Height

From: J Orthop Res. 2011 Oct;29(10):1585-91.

Tobacco smoking increases the risk of intervertebral disc degeneration and back pain, but the mechanisms underlying the adverse effects of smoking are largely unknown. Current hypotheses predict that smoking contributes to intervertebral disc degeneration indirectly through nicotine mediated vasoconstriction which limits the exchange of nutrients between the discs and their surroundings. The authors alternatively hypothesize that direct contact of disc cells, that is, cells in the outermost annulus and those present along fissures in degenerating discs, with the vascular system containing soluble tobacco smoking constituents could perturb normal metabolic activities resulting in intervertebral disc degeneration.

In this study, the authors tested a hypothesis by comparing the effects of direct exposure of human disc cells to tobacco smoke condensate and nicotine on cell viability and metabolic activity. We showed that smoke condensate, which contains all of the water-soluble compounds inhaled by smokers, exerts greater detrimental effects on human disc cell viability and metabolism than nicotine. Smoke condensate greatly induced an inflammatory response and gene expression of metalloproteinases while reduced active matrix synthesis and expression of matrix structural genes. Therefore, the authors have demonstrated that disc cell exposure to the constituents of tobacco smoke has negative consequences which have the potential to alter disc matrix homeostasis

From: Eur Cell Mater. 2011 Sep 20;22:137-46

Much evidence supports a fundamental role for mechanical forces in modulating differentiation, homeostasis, and remodelling of musculoskeletal cells. Little is known, however, regarding mechanobiology and gene expression of intervertebral disc cells from older individuals. To characterise the effect of mechanical stimulation on cells from older discs, an in vitro study of intervertebral disc cells harvested from different aged pigs was conducted to measure extracellular matrix gene expression in response to cyclic tensile stress.

Gene expression of annulus fibrosus cells from intervertebral discs of mature and older pigs was quantified for the predominant extracellular matrix genes; type I collagen, type II collagen and aggrecan, and matrix metalloproteinase 1 (MMP-1), a collagenase that degrades fibrillar collagens. annulus fibrosus cells cultured on flexible-bottom plates were stretched 10 % at 0.5 Hz frequency. After 24 h, gene expression was assayed using reverse transcriptase polymerase chain reaction (RT-PCR). Basal mRNA levels without stretching for type II collagen and aggrecan were lower in older annular cells whereas MMP-1 levels were higher compared to mature cells. Following cyclic tensile stress, an adaptive response was elicited in annular cells from both age groups. Extracellular matrix protein genes were upregulated, whereas MMP-1 was downregulated. The magnitude of response was significantly greater in older cells as compared to mature cells.

These data suggest that the cells from the annulus fibrosus of older animals manifest lower basal levels of mRNA for type II collagen and aggrecan and higher levels of MMP-1 possibly due to decreased tensile stress experienced in vivo and is not the result of reduced capacity for response.

Variations in the mechanical stresses in the annulus due to aging could result from increased cross-linking of intervertebral disc collagens, variation in the hoop stress resulting from changes in the nucleus composition, or simply decreased physical activity of the older animals. Various independent studies have been conducted to try to explain the various effects aging can have on the intervertebral disc. In vivo tensile deformability of human lumbar-lumbosacral motion segments and discs was decreased in older individuals and an increase in pentosidine crosslinks in the disc occurs with age. Age-related degenerative changes reduced the sagittal diameter of the functional nucleus by approximately 50 % and that the pressure within it falls by 30%. This impacts the stress experienced by the encapsulating annular tissues.

In this study, the authors utilised the information from these studies to explain how composition of extracellular matrix changes with age and how controlled mechanical stimulation can modulate the extracellular matrix genes. The intensity, frequency, and vacuum signalshape of cyclic tensile stress used in our experiments were not varied and therefore the mechanical stress was not maximised. Further studies are needed to investigate the optimal type and characteristic of mechanical stress, not only on the annular cells, but on the nuclear cells as well.

The original hypothesis that mechanical stress could modulate the degenerative processes observed in the annular cells from older intervertebral discs was based on studies showing that many MMP genes show reduced expression following dynamic tensile strain. Indeed, this was the case for both mature and older annular cells in the present study.

More relevant to health considerations is the fact that mechanical stress produced increased proteoglycan synthesis and type II collagen expression along with the reduced levels of collagenase in cells of the annulus fibrosus from older animals.

Clinically, enhancement of the anabolic side of annulus fibrosus metabolism by exercise therapy causing spinal stretching by flexion, extension, rotation, and lateral bending could prevent or reduce annular degeneration. Animal studies have demonstrated that motion and exercise increase disc metabolism. The current experiments confirm these findings and show mechanistic data supporting the benefits of exercise.