At Dynamic Disc Designs, we believe research to be the foundation of our spine models so practitioners in musculoskeletal health feel confident in the use of an accurate model while they educate patients about their findings.  Historically, models have been inaccurate and most critically, static, making it very difficult for the doctor to be convincing to the patient in the accuracy of diagnosis.

Research is at the roots of any practice. It fuels practice guidelines and directs both the patient and practitioner down the best path of care. Our models help support that voyage. We have worked hard to bring the best to practitioners of musculoskeletal science by scouring databases of spine science, to arrive at the most accurate model for teaching possible.

With over 1000 papers read in full text, Dr. Jerome Fryer leads the way by making sure our models are keeping up to the standards of best evidence. Weekly literature searches on keywords that surround musculoskeletal health are at the core roots of Dynamic Disc Designs.

lumbar spinal canal, dural sac volume

A position-dependent MRI study 1 of 32 volunteer subjects found that the increased pressure from cerebrospinal fluid in the spines of the subjects who moved from supine to standing position while being imaged caused a significant expansion in their dural sac cross-sectional area.

The Study

A positional magnetic resonance imaging (MRI) study was conducted to evaluate how postural changes affected the lumbar dural sac. Each of the 32 male subjects was examined while in the supine, standing, and sitting positions. The L3/L4, L4/L5, and L5/S1 discs cross-sectional dural sac area and anteroposterior (AP) dural sac diameters were measured. The AP dural sac diameter and upper-endplate L1 and S1 angles were measured on midsagittal images, as well.

facet, lumbar spinal stenosis model, dural sac

Lumbar Spinal Stenosis Model

The Results

Forty-one percent of the subjects showed evidence of disc degeneration or protrusion, but no evident dural sac compression was found in any of the subjects. There were fluctuations in the mean dural sac cross-sectional area measurements and AP dural sac diameter that was posture-dependent. All subjects showed smaller mean dural sac cross-sectional areas when in a supine position. When changing the position from standing to supine, the dural area decreased more in the L5/S1 level, and the extended sitting position produced the largest increase at L5/S1. This held true for the AP dural sac diameter measurements as viewed on axial and midsagittal images.


Researchers examining the cross-sectional IVDs of asymptomatic subjects noted that there was a clinically-significant difference between the dural sac areas at the L5/S1 level that was posture-dependent, with the smallest area being noted in the images of those who were supine at the time of their MRI. The lumbar cerebrospinal fluid (S-CSF) pressures were higher in those sitting and maintaining upright positions. Gravity caused an increase in the hydrostatic CSF pressure and an expansion of the dural sac in the subjects imaged when standing or sitting, which is why those in the supine position had smaller dural sac cross-sectional area measurements.

No significant dural sac cross-sectional area differences were found at the L3/4 and L4/5 IVD levels between the sitting or standing positions, though the AP dural sac diameter was much shorter in the sitting extended position than in the sitting flexed position.

There was a decrease in the dural sac volume space and craniocaudal diameter when the subjects changed their posture from the sitting flexion to the sitting extended. On bending forward, the AP dural sac diameter increased, and it decreased when the subject bent backwards. However, the dural cross-sectional area had no significant changes at this level.

Different dural sac cross-sectional changes were noted for the L5/S1 level, which showed the highest increase after the subject moved from a supine, to standing, position. The researchers posited that this was caused by expansion of the dural sac creating a gravity related hydrostatic CSF. Subjects in the sitting and extended position showed the largest dural sac cross-sectional area at L5/S1. Researchers believe the shortened dural sac may have expanded into the smaller spinal canal space in this scenario.

Overall, there were greater differences in the dural sac cross-sectional area between supine-to-standing, and supine-to-sitting images than in flexion to extension positions. This indicates the gravity related hydrostatic CSF pressure is greater in these posture changes than in flexion/extension changes.

Though there was no dural sac cross-sectional area influence on the L3/4 and L4/5 segments when the subjects were seated in flexion or extension, their lumbar spinal canal space at all levels decreased when they changed their posture from sitting in flexion to sitting in extension. The researchers postulate dynamic variations of the cross-sectional dural area during flexion and extension are created not only by the degree of IVD bulging or buckling and thickness of the ligamentum flavum, but by a variance in total lumbar spinal canal space. The difference could be more pronounced in lumbar spinal stenosis patients with no additional epidural space to moderate the dural tube.


The study showed that posture affected the size of the dural sac cross-sectional area in a group of asymptomatic volunteer subjects. Specifically, when the subjects changed from the supine to standing position, increased pressure of the CSF expanded their lumbar Dura sac volume. The smallest changes were noted when the subjects were in the supine position.

Total lumbar spinal canal space plays a factor in the dural sac cross-sectional area in flexion and extension. Gravity-related hydrostatic CSF pressure appears to be the most important factor in increasing the dural sac cross-sectional area in otherwise asymptomatic subjects.

no pain, congenital insensitivity

A topical review 1 of the literature on congenital pain insensitivity highlights the complexity of pain perception as it relates to anatomical and physiological defects—congenital, or acquired—and concludes the deficits may preferentially affect carious components of the medial pain system, including the anterior cingulate cortex. Because the studies reviewed failed to locate the origin of the deficits observed, the authors of this review emphasize the need for careful assessment of all pain sensory components in patients to better understand the pathways involved in pain perception. They also propose that gene mapping afflicted patients may help provide understanding about the molecular mechanisms at work in pain perception. This could lead to more effective and selective therapies in the future.

What’s at Stake?

There is overwhelming evidence about the necessity of pain perception to human survival. Studies of patients with congenital disorders that inhibit their abilities to experience or respond to pain show that many people afflicted with pain insensitivity die during childhood due to their inability to notice discomfort from illness or injuries. A recent lack of scholarly interest in the United States about pain insensitivity necessitated an updated review of the clinical literature of the phenomenon to help better understand its mechanisms and origins. The authors of the review stress the importance of a better and more complete assessment of the components of pain perception and insensitivity—possibly through gene mapping of patients—in order to provide more comprehensive and effective therapeutic measures in the future.

About Pain Insensitivity

Medical literature about pain insensitivity has existed since the 1930’s. The condition—in which patients are either unable to experience, have a reduced sensitivity to, or can feel, but have little-to-no-reaction to pain, has been termed “congenital general pure analgesia,” “congenital universal indifference to pain,” and “congenital absence of pain” over the years. More recently, the predominate terms used to describe the affliction have been “congenital insensitivity to pain” or “congenital indifference to pain.” The terms, which have been used interchangeably, have now been distinguished to reference two separate groups of patients, depending upon the specific origins and symptoms of their condition.

Insensitivity to Pain

Patients who are insensitive to pain have a reduced or inability to experience pain sensations. They may be unable to distinguish between different types, intensities, or qualities of painful stimuli.

Indifference to Pain

Patients with a congenital indifference to pain can feel pain but have no affective response to it. They will not react to painful stimuli by withdrawing from the source of pain.

In the past, individuals with pain insensitivity were diagnosed and treated based upon a set of observational criteria that included unaccounted for wounds or lesions and excluded from the diagnosis when their pain impairment that could have been caused by other underlying conditions or injuries. As technological medical diagnostic advancements allowed for better assessment methods of nerve pathologies, patients with irregular sensory nerves who in the past might have been classified as “congenital indifference to pain,” are now classified under a subheading of “congenital pain insensitivity arising from peripheral neuropathies of various types”.

Components of Pain Perception

There are three recognized components to pain perception—sensory-discriminative, affective-motivational, and cognitive-evaluative. Those suffering from pain insensitivity may demonstrate their sensorial deficits across a broad range of responses to stimuli.

Pain Discrimination Loss

When a patient loses the ability to discriminate between types of painful or uncomfortable stimuli, they may not be able to distinguish between sharp and dull sensations or hot and cold temperatures. They may, however, experience a negative emotional reaction to these stimuli, even though they cannot name the source of their discomfort.

Affective-Motivational Response Deficit

Patients with affective-motivational response loss experience painful and uncomfortable stimuli but have no reaction to it. When a patient has this condition, also known as “Pain Indifference,” they do not withdraw from painful stimuli. This makes them vulnerable to burns and other injuries. Some patients with affective-motivational deficits may have a negative reaction to pain but will not withdraw from it and will allow repeated painful stimulus to be applied without objection.

Pathways to Pain

Pain perception is modulated in large part by two ascending pathways—the lateral pain system projecting through lateral thalamic nuclei to the somatosensory cortex, and the medial pain system, which projects to the anterior cingulate cortex and insula through the medial thalamic nuclei. The sensory-discriminative pain component is modulated by the lateral system, and the affective response to pain is modulated through the medial system.

Pain perception impairments may be caused by lesions in specific regions of the brain or loss of peripheral afferents, which may create deficits in sensory and affective pain responses. Depending on the size and location of a lesion, the impairment may be localized and subtle or severe.

Congenital and Hereditary Pain Insensitivity Syndromes

Many children with peripheral neuropathies experience sensory-discriminative and affective-motivational impairments and may be diagnosed with hereditary sensory and autonomic abnormalities (HSAN). There are five sub-categories of HSAN currently recognized, and all of the types are known to exhibit small-diameter C and A-delta fiber involvement. These fibers are responsible for the transmission of pain sensation.

There is a wide spectrum of HSAN features, including an inability to experience the sensation of burns, digit mutilation, and injuries to the joints. Many of the patients are unable to distinguish between the type and intensity of painful stimuli and do not take precautionary measures to prevent the recurrence of pain or remove themselves from painful situations. Genetic causes have been investigated, and specific genes have been identified for many forms of HSAN, but the condition is at present uncurable.


Congenital Pain Indifference

Patients with congenital indifference to pain may have normal sensory reactions when examined but experience painless injuries as early as infancy. On past examination of peripheral nerve samples, clinicians found no abnormalities and thus characterized the disorder as a deficit in pain response. Because no analysis of nerve fiber density was performed on these patients, it is unclear if their disorder might have been caused by a selective loss of nerve fibers.

It has been suggested that these patients might have been experiencing a neurotransmitter disturbance that affected their central sensory processing pathways. Other reports indicate that this type of disorder may have peripheral and central nerve origins.



Deficits in pain perception can also occur as a result of brain lesions in areas that modulate the processing of painful stimuli. This can create congenital pain insensitivity-type disorders. When these lesions occur in the anterior cingulate cortex or insular cortex, they may affect the function of the medial pain system and cause a loss of affective-motivational function. Sensory-discriminative components of pain may be affected by lesions in the primary and secondary somatosensory cortex affecting the lateral pain system.

Patients with affective-motivational deficits who retain a sense of sensory discrimination are suffering from ‘asymbolia for pain.’ They may experience pain but have no—or an unusual—response to it, such as laughter. It is possible an impairment of the sensory-discriminative pain components, without affective-motivational components, could be caused by central lesions.


The variations of pain insensitivity syndromes and the deficits they cause make clear the complexity of pain perception physiological and anatomical processes. Though it remains unclear exactly how the disorder originates, current research suggests the need for a more complete assessment of how the different components of pain perception affect sensory intensity and response in HSAN patients. Genetic mapping may assist clinicians in developing better, more selective therapies for patients in the future.



facet, lumbar spinal stenosis model

A retrospective CT scan and medical record review [ 1. The Prevalence of Asymptomatic Cervical and Lumbar Facet Arthropathy: A Computed Tomography Study] of 50 patients with no history of spinal pathology used a four-point scale to grade the severity of evident arthritis and found that arthritic spinal changes were frequently evident—even in asymptomatic patients. The incidence of these changes corresponded positively with aging and was more prevalent in scans of the lower lumbar spine.

What’s at Stake?

Chronic neck and lower back pain affect between 66 and 84 percent of the U.S. population and is responsible for approximately 87 billion dollars of lost income and medical expenses annually—a figure that is only surpassed by the yearly wage loss and expenditures on diabetes and heart disease.

Diagnosing CNP and LBP is problematic due to the number of possible factors—including dysfunction of the intervertebral discs (IVD’s), facet joints, spinal nerve roots, ligaments, and muscles surrounding the spine— that can contribute to these disorders.

Some studies have indicated that facet arthropathy, rather than nerve root irritation, cause axial neck and back pain. The increase of CNP and chronic LBP in aging populations may be associated with a progressive degeneration of the IVDs that subsequently increases facet joint loading and creates favorable conditions for the development of facet arthritis. Facet joint blocks by injection have been shown to be ineffective in providing symptomatic relief in up to 90 percent of patients diagnosed via CT scan in previous studies. This suggests that scan observations alone may provide prevalent false positive results and therefore cannot be a reliable diagnostic tool.

Disc replacement may alleviate pain and restore spinal fluidity of motion, but the presence of facet joint arthritis is considered a contraindication to this surgical procedure. Understanding more about facet joint arthritis can assist practitioners in developing effective treatment plans for LBP and CBP patients—including the determination of which patients may be ill-suited for IVD replacement. This study of asymptomatic patients was conducted with the aim of understanding the prevalence of facet joint arthritis to help quantify the percentage of patients for whom facet injections are ineffective.

The Study

An approved review of archived CT scans of 100 total non-spinal patients was conducted using scans of 500 cervical facet joints from 50 subjects and 500 lumbar facet joints from an additional 50 subjects. All of the patient subjects’ medical records and scans were previously analyzed and evaluated as spinally asymptomatic for the purpose of this study.

The images were each graded and evaluated by an orthopedic spinal surgeon, neuroradiologist, and trained medical student on an independent basis. An additional three observers with separate clinical backgrounds also conducted a review of the facet joints to ensure no bias existed due to training backgrounds of the first group. The severity of facet joint arthritis symptoms were graded and statistical analysis was applied across different subject age groups. An average of all groups was then calculated using a coefficient.

The Results

Cervical Data

Of the 500 cervical facet joints from 50 patient subjects studied, asymptomatic cervical facet joint arthritis was evident in more than 33 percent of the scans. Nearly 60 percent of these patients showed only mild narrowing of the joint space and irregularities. About half of the subjects over the age of 40 demonstrated signs of arthritic changes. There were fewer “normal” or non-degenerated facet joints in patients in the aging (over 45) subject population. The prevalence of degenerative changes increased at all cervical levels in the aging subjects.

In all age groups, greater changes occurred more prevalently in the caudal spine area. At the C6-C7 spinal level, 78 percent of patients over-40 demonstrated facet joint arthritis. At the C2-C3 level, however, only 29 percent of the patients of the over-40 age group showed arthritic changes.

Lumbar Data

Thirty-seven percent of the patient subjects in the lumbar data group demonstrated asymptomatic lumbar facet joint arthritis, and up to 2/3 of these subjects showed grade 1 changes. As with the cervical data set, the lumbar set demonstrated a positive correlation with aging (over 45) and arthritic changes and degeneration of the facet joints. Caudal levels (L5-S1, for example) were more likely to show increased arthritic degeneration compared to cephalad levels. Only 12 percent of the patients over 50 years old showed changes at the L1-L2 levels, while 54 percent demonstrated these changes at the L5-S1 level.

Lumbar Spinal Stenosis Model


This study found a statistically significant positive correlation between aging and asymptomatic arthritic changes and degeneration of the facet joints of patients over the age of 45. These changes were evident at all spinal levels but were most prevalent in the lumbar facet joints and the C2-C3 and C6-C7 levels of the caudal spine. Approximately one third of the patient population in this study were found to have evident facet joint arthritic changes that were asymptomatic and associated with aging. When considering motion-preserving spinal implants, the age of the patient should be considered, as the treatment may not be as effective in patients over the age of 45, who are more likely to have or develop asymptomatic facet joint arthritis—a contraindication of the implant procedure.






A study 1 compared different treatment efficacies in two groups of patients with degenerative spinal disease-related buttock pain and found that the group receiving a selective nerve root block had clinically-significant improvement outcomes at post-procedure through 6-weeks, compared to the group that were treated with a facet joint block. This suggests that the cause of spinal-related buttocks pain is most likely radiculopathy, rather than facet joint degeneration.

What’s at Stake?

Many patients with spinal stenosis complain of back pain, buttock pain, or pain radiating from the buttock to the lower legs. As it is assumed that nerve root inflammation can contribute to lumbar and lower leg pain radiating from the spine, a common and frequently effective treatment may involve steroid or procaine injections. Selective nerve root block is used effectively in the treatment of degenerative scoliosis and has been demonstrated to be a successful form of short-and-long-term treatment for the pain. Similarly, a facet joint block has been used as an effective treatment for buttock pain, post-procedural lumbar pain, and morning stiffness associated with spinal degeneration.

Though various treatments have proven effective in alleviating or reducing pain in a percentage of the spinal patients receiving injections and blocks, the exact etiology of spinal-related buttock pain and radiating pain remains unclear. Because of this, uniform diagnostic and treatment guidelines for buttock pain—especially without concurrent radiating lower leg involvement—have been difficult to establish. This study links positive treatment outcomes with a more definitive diagnostic cause of buttock pain and seeks to contribute to the diagnostic and treatment criteria of buttock pain discussion.

The Study

Researchers treated 146 male and female patients presenting with spinal-related buttock pain without lower leg radiation by one of two methods—a) selective nerve root block (76 patients), or b) facet joint block (70 patients). The mean age of patients in both groups was 65 years. Both groups shared similar demographics when it came to age, sex, and health. Each of the patients was evaluated prior to their procedure and on day one, week 2, week 6, and at 12 weeks post-procedure. Their evaluation results were compared by their group injection method, and the results were then analyzed.


On the DAY 1 post-procedure analysis, 7 percent of the patients in the nerve block group (GROUP A) were shown to have experienced an “excellent” response, and 6 percent of those in the facet joint block group (GROUP B) had an “excellent” response. In GROUP A, 46 percent of the patients treated showed a “good” response to the treatment, while only 13 percent of the patients in GROUP B had a “good” response.

At the two-week post-procedure follow up, 11 percent of the GROUP A patients demonstrated an “excellent” response, with only 4 percent of the patients from GROUP B had an “excellent” response. Similarly, 41 percent of the GROUP A patients were classified as having experienced a “good” response, compared with only 20 percent of those in GROUP B.

At the six-week post-procedural follow up, 11 percent of the GROUP A patients were classified in the “excellent” response group, while only 7 percent from GROUP B had this distinction. Forty-one percent of the patients from GROUP A demonstrated a “good” response, and only 20 percent of the GROUP B patients had a “good” response.

At 12-weeks, 47 percent of the GROUP A patients were classified in the “good” response category, and 46 percent of those in GROUP B experienced a “good” response to the treatment.


Researchers in this study sought to identify the cause of buttock pain associated with spinal stenosis. Specifically, they used a retrograde methodology to discover if the buttock pain was radiating pain or caused by facet joint degeneration. They treated two groups of patients using either selective nerve root block or facet joint block, and the data collected and analyzed indicates that the selected nerve root block was more effective through post-treatment follow ups through 6 weeks. The implication of this data suggests that spinal-related buttock pain is most likely caused by radiculopathy, rather than facet joint degeneration.

IVD Problems, Disc Degeneration

A study 1 of how dietary advanced glycation end-products (AGEs) effect the structure and function of intervertebral discs (IVDs) in male and female mice concluded that high dietary AGEs impaired IVD collagen quality, altered annulus fibrosus (AF) organization and changed the biomechanical properties of female IVDs, while having no clinically-significant effect on male mice subjects. The results of the study suggest the importance of targeting AGEs in spinal health assessments and treatments of female patients—particularly those at risk for, or suffering from, Diabetes Mellitus (DM).

What’s at Stake?

Structural disruption and chronic inflammation of the IVD is one of the leading causes of back pain, disability, and lost work wages worldwide. The many contributors to IVD damage and degeneration include DM and obesity, conditions that are increasing rapidly across the globe. Obesity increases the risk of IVD herniation, spinal stenosis, chronic inflammation, and other complications of the spine. It is also associated with an increased risk of cardiovascular disease, stroke mortality, and heart attacks–particularly in women. Since AGE accumulation is known to cause complications in populations with DM, this study investigates the effects of a high AGE diet on the IVD and how sex-differences may play a role in sex-specific IVD changes and disruption.

The Study

The subjects of the study were 21 male and 23 female recently-weaned mice, separated by sex and assigned to two groups. One group received a low-AGE diet (chow), and another group was fed only high AGE chow, which had been subjected to high-temperature heating. Each subject represented a third-generation off-spring of maternal mice fed only the respective diet used in the study groups, to exclude any effects of maternal AGES on the newly-weaned experiment mice.

The high AGE chow was representative of the typical Western human diet, with 80 percent higher AGE values than those of the low AGE chow. An increased AGE content is typically caused by thermally processing (extreme heating) the foods prior to ingesting. Examples of this include microwaving or deep-frying foods.

The feeding study lasted for 6 months, after which time the mice were sacrificed, dissected, and prepared for biomechanical IVD testing through Western blot analysis. Fasting glucose and total serum AGE levels were measured and quantified, and proteins were extracted, buffered, and sonicated. A single freeze-thaw cycle was used prior to biomechanical testing to avoid the process influencing the IVD mechanics. Axial compression-tension and torsional tests were performed on caudal motion segments, and the IVD diameter measurements were taken using a caliper. Assessments of IVD morphology, collagen molecular properties, and fiber orientation were created, measured, compared, and analyzed.


The Western blot data showed a significant accumulation of AGEs accumulation of the IVD problems of the female mice fed the high AGE (H-AGE) diet compared to those fed the low AGE (L-AGE) diet. There were no changes in the IVD AGE levels or serum samples of the male mice in either feeding group. The results indicate that even without the presence of DM or obesity, dietary AGEs are likely to systemically accumulate in the IVDs of female mice—but not in males.

Further, the H-AGE female mice IVDs showed increase stiffness and torque-range, while the date on the L-AGE female mice showed no such correlation, and the male mice IVDs of both feeding groups were unaffected. This indicates that motion segment behaviors of female mouse IVDs—but not male mouse IVDs— are negatively affected by the H-AGE diet.

In addition, the AF organization and collagen fibers of H-AGE diet female mouse IVDs—but not male mouse IVDs— appeared compromised, particularly in the anterior AF. The H-AGE diet also appears to have contributed substantially to AGE accumulation and collagen damage in the AF of the female mice subjects but not the male mice subjects.


The results of this study, combined with previous study literature, suggests that female mice are negatively affected by a H-AGE diet, which appears to increase glycation within the AF collagen matrix and damage collagen and molecules in the IVD. High IVD crosslinking and collagen damage can contribute to biomechanical changes in the IVD and disrupt form and function in the unit. It appears that high AGE diets may increase these risks in female spinal tissues. Future research is needed to investigate ways to promote spinal health through dietary interventions to lower AGE levels, particularly in at-risk populations. This includes patients suffering from obesity and DM, especially females.






Stuart McGill, ddd spinal models

In an online interview with Bill Morgan, President of Parker University, world-renowned spine researcher and scientist, Stuart McGill, uses dynamic disc models from Dynamic Disc Designs to explain lumbar disc herniations, extrusions, and the mechanisms for lumbar disc injuries and treatments.

When treating spinal injuries, McGill stresses the importance of recognizing that the cause of most disc extrusions and herniations is a combination of factors, occurring over time. The cumulative array of factors may present as an acute condition causing pain, but in most cases, the disruption has not been created by a single loading event.

McGill uses the analogy of cloth to explain how repetitive loading and movement fray the collagen fibers that cover the socket joints, eventually working a hole into the fibers by repetitive stress strains occurring in a back and forth motion.

“The disc is layer upon layer of collagen fibers held together with [a tightly woven lamination matrix]. If you keep moving the disc under load, the hydraulic pressure of the pressurized nucleus slowly starts to work its way through the delamination that forms because of the movement,” he says.

He explains that when the collagen is intact and supple, a person has full range-of-motion without danger of creating tears, but when the spine is stiff and has become adapted to bearing heavy loads, it is in danger of injury.

“The problem comes when you combine the two worlds and confuse the adaptation process,” he says.

“In a modern lifestyle, you might have a person who sits at a computer for eight or more hours in a flexion stressed position which—on its own—may not be that bad. But then they go to the gym for an hour every night and start lifting loads. They’re taking their spine through the range of motion, so cumulatively, the collagen is asked to move, but it’s also pressurized. The nucleus behind gets pressurized and slowly works its way through the delaminated collagen.”

Stuart McGill, Models

Stuart McGill and the many ddd models he uses.

McGill, Dynamic Disc Designs

Professor Stuart McGill and Dynamic Disc Designs endorsement.

Recreating Compression Loading, Disc Bulge, and Proper Thrust Line with our Dynamic Model

Using the disc model, McGill demonstrates how the gel inside the disc remains pressurized under compression, but in cases where the collagen has become delaminated, bending the spine under a load creates a disc bulge.

“This is exactly what we see on dynamic MRI,” he says, manipulating the disc model to demonstrate. “In the laboratory we would inject the nucleus with various radio-opaque markers. We would watch the migration as the bulge would come through. Touch a nerve root and now you would match where the disc bulges with the precise anatomic pathway. If you sit for 20 minutes slouched and your right toe goes on fire, we know it’s the right ring and that’s exactly where the disk bulge is.”

McGill stacks the disc model into a thrust line and squeezes the spine segment to show how proper alignment adapts the movement experience.

“The whole disc is experiencing movement, but there’s no pressure, and nothing comes out to touch the nerve root,” he says.

Empowering the Patient with Simple Posture and Stress Exercise

McGill says his insight is based upon years of experiments studying the exact mechanisms of spinal injury and pain. He recommends using improved posture and stress—lying on the stomach for five minutes with two fists under their chin—to help,” mitigate the dynamics of that very dynamic disc bulge.”

He says the immediate relief provided by this simple exercise can empower a patient with discogenic pain and help alleviate the potential psychological trauma of feeling hopeless at not understanding the source of, or how to mitigate, pain.

intradiscal, endplate

A study 1 on the efficacy of intradiscal biologic therapy, where new cells or genes are implanted into the degenerated disc matrix to reduce inflammation and increase matrix cell production, found that degenerated discs may not have the necessary nutrient transport capabilities to ensure proper disc nutrition during this form of therapy. The authors of the study emphasize the importance of research into the determining factors influencing disc cell nutrient transport in informing targeted treatments and strategies to improve disc nutrition in degenerated discs.

What’s at Stake?

Disc degeneration (DD) is a chronic condition that causes spinal pain in aging adults worldwide. The process of DD involves biomechanical modeling of the entire disc matrix and frequently leads to surgical intervention to remove the offending disc and restore functionality to the spine. For many patients, surgical procedures are unsuccessful, however. A noninvasive treatment that has demonstrated recent promise involves regenerating the DD by injecting it with genes, growth factors, small molecules, or implanted cells. These procedures are intended to reduce inflammation and catabolism and assist in the creation of a new disc matrix. But a cell-rich disc requires increased nutrients, and the cartilage endplate (CEP) of the DD may not have the capacity to deliver these nutrients to the matrix. In this study, researchers examined the effects of CEP transport properties in DD on nutrient diffusion and cell function and survival.

The Study

In order to isolate the variable of how nutrient supply affects the nucleus pulposus (NP) cell function, the researchers involved in this study mimicked the in vivo, diffusion-poor disc environment by creating diffusion chambers with similar parameters to isolate the NP nutrient supply mechanics. The cells of the NP receive nutrients that are diffused through the CEP matrix. Cells at the center of the lumbar discs can be up to 10mm from a capillary, while other cells can be just beside a CEP.

Researchers provided glucose and oxygen to cultured NP cells within the chambers. These nutrients were delivered through diffusion from human CEP’s from the open sides of the chamber. Metabolites were expelled into the culture medium by CEP diffusion. The functioning and survival of the cells require a balance between CEP transport properties and cell density, allowing for the request and supply of nutrients. The researchers reproduced the disc matrix environment and physiologic transport conditions in their CEP tissue cultures and diffusion chambers to monitor the effects of NP cell viability and gene expression across the different conditions of nutrient transport.

Specifically, intact human CEP’s from human cadaveric lumbar spines were used for the study. Full-thickness samples of the CEP’s and surrounding calcified cartilage were frozen and sectioned. The researchers calculated the diffusivity of each full-thickness CEP sample through fluorescence and photo-bleaching and using the Axelrod method. They measured each CEP’s biochemical composition spatially via imaging. They created special maps of the collagen, aggrecan, and mineral-to-matrix ratio of the CEP samples with the highest and lowest diffusivities. They measured CEP thickness with photomicrographs and then determined the average measurement across the five chambers.

Bovine NP cells were used in the study (similar to human NP cells). Post-incubation cell viability was determined using a cytotoxicity assay involving gel-stains and low-magnification imagery. Each L4-L5 donor CEP was analyzed for cell density and the anabolic and catabolic gene expressions were examined after chamber incubation. A regression model of fluorescence intensity was used to determine the NP cell gene expression and distance from the CEP. Spatial fluctuations of the CEP composition were described based upon regression models.


The diffusive transport of nutrients varied widely between the CEP samples, affecting the function, health, and survival potential of the NP cells. In fact, there was a four-fold variation in small solute diffusivity in our human CEP sample array. Those allowing less diffusive transport reduced the supply of nutrients to the NP and shortened the viable distance within the diffusion chambers up to 51 percent with typical cell density. Those permitting poor diffusion seemed to downregulate anabolic and catabolic NP cell gene expression. This may mean that a reduced number of disc cells are capable of being sustained through low nutrient CEP diffusion, and the cell’s ability to retain its matrix homeostatic condition is hindered.

When we increased cell density, there was a reduction in cell viability caused by the CEP transport properties, though increasing cell density should raise nutritional demands and shorten the viable distance.  The CEP’s in our study that exhibited low diffusive transport were unresponsive to doubling the cell density, perhaps because they did not provide enough nutrient diffusion to nurture the cell.

We imaged the CEP’s to identify any differences between those with low or high intradiscal diffusivity. Our data found that those with low-diffusivity (and shortened viable distance) contained more collagen and aggrecan, mineral, and lower cross-link maturity. This could explain the blockage of solute penetration and diffusion. At any rate, there appears to be a strong correlation between NP cell survival or function and the availability and mobility of the nutrient supply in the CEP. Compositional defects with the CEP matrix can inhibit nutrient diffusion and undermine biologic therapies that depend upon an increased supply of nutrients to the cell matrix to succeed.


Our findings suggest that the composition of CEP can contribute to or detract from the function and viability of NP cells. Deficits within the CEP matrix can cause poor nutrient diffusion and block solute passages. This can cause an abundance of collagen and aggrecan, as well as mineral, and lower cross-link maturity. When cell density is increased, CEP’s developed transport deficits, decreasing the cell’s viability. It appears NP function and survival are dependent on the proper CEP composition, as an imbalance in this makeup can reduce the supply of nutrients to the cells, reducing the success rates of biologic therapies.