Sensory Disc Model

Goal of the study?


In this review 1, the authors have two goals:


  1. To determine how changes that occur to the sensory nervous system in intervertebral disc degeneration (IVDD) impact lower back pain.
  2. To look at potential therapeutic approaches for lower back pain (LBP).


Why are they doing this research?


Lower back pain (LBP) is a prevalent problem that causes serious discomfort and disability for individuals and can also place a significant economic and medical burden on society. While the development of LBP can be seen in individuals with many different conditions such as arthritis, trauma and infection, it is widely thought that intervertebral disc degeneration (IVDD) is the leading cause of LBP. However, there is still a lack of knowledge about the development of IVD-related LBP, particularly how changes to the sensory nervous system play a role in developing and maintaining back pain. Understanding how LBP occurs may help to enable the development of new treatment approaches for patients with LBP.


What did they find?

Role of the sensory nervous system in IVD-related lower back pain


Existing research suggests that changes to the sensory nervous system (particularly pain-transmitting pathways) play a significant role in the relationship between IVDD and LBP. Changes to these pain transmitting pathways are the result of mechanical, inflammatory and other potentially damaging triggers. 


As IVDD progresses, inflammatory and sensory neuropeptides are overproduced in the IVD and further deteriorate the intervertebral disc. New nerve fibres, supported by nerve growth factor (NGF) receptors, grow into the increasingly degenerated intervertebral disc resulting in increased sensitivity and inflammation, enabling LBP development.


Disc herniation is commonly associated with IVDD. Studies show that mechanical compression on nerves from a herniated disc causes nerve swelling and can increase activation of inflammatory cells (such as glial cells) and hypersensitivity and lead to LBP. Research has shown that degenerated discs contain higher inflammatory cytokines and chemokines such as TNF (tumour necrosis factor), IL-1 (interleukin 1) that serve to inflame.



Potential therapeutic targets for LBP


Understanding how changes to the sensory nervous system plays a role in IVD-related lower back pain provides a pathway to potential treatments. To date, there are both pre-clinical (animal) and clinical studies looking at potential treatments across a range of targets. For example, some studies have looked at how to stop new nerves’ growth in the deteriorated IVD by using anti-NGF antibodies or anti-inflammatory therapies that target cytokines such as TNF or IL-1. Other studies have used animal models to look at ion channels (that help regulate nerve sensitization) as potential targets for reduced pain.


(there are two good tables that you may want to include on the studies they looked at)


Why do these findings matter?


As back pain is a prevalent problem for many people, there is a need to find non-surgical approaches to treatment. Research has demonstrated the role of the sensory nervous system in IVD related LBP. This review highlights how targeting the pathological changes of the sensory nervous system (specifically the pain pathways) has the potential for numerous treatment targets for patients and their healthcare providers. 

At ddd, we create models that include disc innervation so professionals can have intelligent conversations with the low back patients they care for.



properties of the annulus, disc model

Researchers examined the effects of endplate fractures  1 on the mechanical properties of the annulus fibrosis (AF) in porcine spinal segments and found that laminate adhesion strength was significantly compromised in the fractured spines. The findings suggest that microdamage may occur beyond the vertebra, into the interlamellar matrix of the AF—information that could be helpful in the diagnosis and treatment of adolescent spinal growth-plate fractures.

The Study

The authors of this study wished to examine the effects of high-intensity pressurization on the intervertebral discs (IVD) to see how it effected the mechanical and physiological properties of the posterior AF. They used 28 fresh, recently-thawed functional porcine spinal units from 14 porcine specimens that were approximately six months old.  Control units were also used as a comparative measure against the units subjected to pressure.

A hydraulic pump and high-pressure inflation needle were used to pump hydraulic fluid into the IVD of specimens. The researchers were careful not to pierce the AF in the samples. Pressure in the needle was measured by a pressure transducer and converted from analogue to digital at 2048 Hz. The needle was subsequently removed, and the vertebral bodies were assessed for damage. Although fractured endplates created an audible ‘pop,’ the condition was only confirmed after dissection of the IVD. The control-group segments were not tested for fractures. Measurements were taken following the dissection, and the end-plate area was quantified. Bilayer AF samples were then dissected and tested for tensile endurance in the circumferential direction. A second multi-layered sample was then dissected and subjected to delamination and a peel test. Mathematical ratios were then plotted to mark the variable results for each sample.


End-plate size measurements remained consistent across the control and fracture group samples. Bilayer stiffness, toe-region stretch ratio and stress, and stress at 30% stretch were consistent in the control and fracture group samples. However, there was a clinically-significant variance in peel strength—but not peel strength variability— between the two groups. In the fracture group, the peel strength was 31 percent lower than in the control group. Dissection and manual delamination were significantly easier in the fracture group of samples, as well.


The results of this study indicate that growth-plate fracture damage may not be limited to the vertebra and may cause microdamage in the nearby AF. This was indicated by the reduction of laminate adhesion strength in the posterior AF of the fracture IVD samples subjected to pressure in the tests. This information should be taken into account when practitioners are examining and treating adolescent or childhood vertebral fractures involving the endplates.


KEYWORDS: damage during spinal growth-plate fractures, effects of endplate fractures on the mechanical properties of the annulus fibrosis, effects of high-intensity pressurization on the intervertebral discs, mechanical and physiological properties of the posterior AF, delamination and a peel test, Bilayer stiffness, toe-region stretch ratio and stress


intradiscal pressure, model

A study of in vivo intradiscal pressure in subjects with and without lower back pain (LBP) sought to find out how disc degeneration affects intradiscal pressure, measure the loading capacity of the L4/L5 IVD segment, and determine any relationship between movement in that disc segment and the spinal loading capacity. The researchers found that there was a significant relationship between spinal loading and the angle of the motion segment in healthy discs in vivo. In degenerated discs, the intradiscal pressure was much lower than that measured in healthy discs. Further study with wider parameters is suggested to fully understand the phenomenon and the problems associated with it.

Study Motivation and Design

The only way to directly measure spinal loading in humans is via the measurement of intradiscal pressure—a complex in vivo task. Most current knowledge about loading capacities were derived from pioneering studies in the 1960’s and 1970’s by Nachemson, but little corroborating evidence has been published on the topic since. These early studies utilized an inefficient means of evaluating intradiscal pressure—the polyethylene coated disc pressure needle until 1965, and after that, another needle designed specifically for intradiscal pressure measurements. This new needle was not without its deficits and required special handling and was prone to destroying structural defects on insertion. The current study’s authors utilized a newly designed silicone-based needle to measure the pressure and spinal load in 28 patients suffering from LBP, sciatica, or both at the L4/L5 segment, and in eight healthy volunteers with an average age of 25 years-old.

Magnetic resonance imaging (MRI) was performed on the healthy subjects prior to the beginning of the study to ensure no disc degeneration in the volunteers. The 28 LBP patients (10 women and 18 men with a mean age 45 years) were also imaged prior to pressure measurements being taken to visualize the amount of water content in their discs. These patients were diagnosed with disc herniation (16 patients) or spondylosis (12 patients).

The subjects were measured while in the prone position, without sedation but with a “local” dose of anesthesia. A guiding needle was used to position the pressure sensor needle into the nucleus pulposus of the L4/L5 IVD discs. Fluoroscopy was used to confirm correct placement of the needle had been achieved. The subjects were measured in eight positions: prone, upright standing, lateral decubitus, flexion and extension standing, and upright, flexion, and extension sitting positions. Radiograms of the lateral view were also taken of each of the subjects during their testing.


Pressure measurements in this study indicate that respiration creates a fluctuation in intradiscal pressure even when subjects are in the prone position and utilizing no other muscle activities. An IVD that is healthy is also elastic, with an intradiscal pressure that fluctuates in correspondence to muscle activities and respiration. It is possible that the normal pressure changes involved with respiration could be associated with the maintenance of the nutritional content inside the nucleus pulposus. There was a slight difference between horizontal and vertical pressures in healthy and degenerated discs and in the silicon gel, which may indicate that the nucleus pulposus has a similar pressure tropism to silicon gel. Normal discs had high water content, which explains the small difference between the horizontal and vertical pressure measurements. There was, however, a significant difference between the pressures of the total value (horizontal and vertical and whole posture) of healthy and degenerated discs. These values may not have been significant enough to measure in previous studies utilizing the less efficient needle-types. The information obtained in this study through the use of the sensitive silicone pressure needle will help in developing a better understanding of degenerative disc disease.

Professional LxH Model

Our Professional LxH Model


KEYWORDS: Link Between Lower Back Pain, Disc Degeneration and Intradiscal Pressure, relationship between spinal loading and the angle of the motion segment in healthy discs, respiration creates a fluctuation in intradiscal pressure, degenerative disc disease

inflammatory mediators

A review investigating the role of inflammatory mediators in the degeneration of intervertebral discs (IVD) found that in-vitro disc cells exposed to inflammatory conditions can release cytokines and other neurogenic and angiogenic factors and that these, along with the development of nerve and vessel roots within the fissured annular fibrosis (AF), can contribute to the development of discogenic lower back pain (LBP) in patients suffering from disc degeneration (DD).

The Role of the AF and Nucleus Pulposus (NP)

The collagen-rich AF of an adult intervertebral disc has roughly 25 lamellae with parallel fibers that help to support the spine during bending and twisting. Randomly aligned collagen fibers in the NP help to capture anionic proteoglycan fluids and allows for swelling that will resist forces of compression in the disc during loading. The pressure created by the high fluid content in the NP inhibits the ingrowth of nerves and blood vessels in the AF. A healthy disc should not contain nerves or vessels, but degeneration creates fissures that allow for the escape of fluids and infiltration of nerves and blood vessels into the AF and decrease disc height and weight bearing potential. In extreme cases of degeneration, the NP may extrude through the lamellar walls and create pain when the in-grown nerves become compressed. Better understanding of how inflammatory mediators assist in the development of DD and LBP may help practitioners better target therapies and preventative interventions.

While it appears that greater degeneration is associated with the presence of greater IVD inflammatory mediators, other factors also may contribute to inflammation. These factors include heredity, mechanical loading, extant inflammation, oxygenation, and other types of cells infiltrating the AF of the disc. The introduction of cytokines into IVD cells, for example, create an upregulation of several types of inflammatory mediators, and certain loading configurations can increase or decrease inflammation within the disc, depending upon the loading conditions and location of the IVD being stressed when mechanical loads are applied. The health of the surrounding IVD tissues may also play a role in determining the effect of potential inflammatory mediators, as well as levels of oxygenation within the IVD. The exposure of a DD to macrophage or notochordal cells may also affect levels of prostaglandin and other cerebrospinal fluids, and studies have shown higher levels of these fluids exuded from dissected herniated lumbar and cervical discs in cultured biopsies from LBP patients.


Disc degeneration is a common malady that is associated with pain and social and economic costs worldwide. Despite the prevalence of DD, there are still few ways to diagnose and effectively treat the early stages of DD. A review of the available medical studies data suggests that a biochemical matrix within the degenerating disc may cause a release of fluids that serve to pressurize the IVD environment and prevent the in-growth of nerves and vessels that can activate pain. Further study of this biochemical matrix may lead to more effective therapies in treating the underlying cause and symptoms of DD and LBP.

KEYWORDS: the role of inflammatory mediators in the degeneration of intervertebral discs, in-vitro disc cells exposed to inflammatory conditions can release cytokines and other neurogenic and angiogenic factors, development of discogenic lower back pain, disc degeneration, heredity, mechanical loading, extant inflammation, oxygenation, exposure of a DD to macrophage or notochordal cells may also affect levels of prostaglandin and other cerebrospinal fluids

High Intensity Zone

A high intensity zone should not be overlooked-especially with a symptomatic patient. This is a bright white finding on MRI, most notable on the posterior annulus.

High Intensity Zone

In a recent study in The Journal of Medical Investigation, researchers looked at the pathogenesis of low back pain (with and without leg pain) and described it being caused by annular fissures and disc degeneration. 1 2.

Here are some key point of the research:

  1. They identified that more than two-thirds of the high intensity zones were found in the lower lumbar motion segments with the most at L4-5 followed by L5-1.
  2. They commented that they were unable to determine whether the intensity of the MRI magnet played a role in distinguishing HIZs.
  3. It is important to identify reliable measures to find HIZs.
  4. New treatment strategies are developing for the treatment of HIZ including laser.
  5. HIZs are not only a measure of degeneration but an active inflammatory tissue.

Dynamic Disc Designs develope models to help identify the movements that can stress the posterior annulus. Visit the Professional LxH Model to see an example of a high intensity zone.

High Intensity Zone, HIZ, Lumbar Disc


  1. Rozen D. Discogenic Low Back Pain. Pain Prac. 1: 278-86, 2007
  2. Peng B, Zhang Y, Hou S, Wu W, Fou X : Intradiscal Methylene blue injection for the treatment of chronic discogenic low back pain. Pain. 149 : 124-9 2010
Degenerated Disc Model - Dynamic Disc Designs

Coming this fall, a Dynamic Degenerative Disc Model with the ability to show innervation of the nucleus pulposus dynamically.

Dynamic Disc Designs strives to showcase important research in a dynamic platform so spine doctors can effectively educate their patients. This new design includes many new features including:

  1. dynamic two-part disc that is easier to squeeze
  2. neoinnervation into the dynamically mobile and fully visible nucleus pulposus
  3. facetogenic arthropathy narrowing the lateral recess
  4. dynamic disc bulge vs. herniation
  5. degenerative specimen chosen to copy
  6. much much more…

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With these features, spine professionals can quickly demonstrate pain generators and the solutions related to mechanical back pain. Help patients understand how to centralize the nucleus during movements in the teaching of lumbar lordosis with load, for example.

Centralization of pain is an important goal in the treatment/management of back and leg pain as well as neck and arm pain. Patients often think in terms of muscles but the core of the issue is often more central. With this new model, a greater understanding of how the nucleus moves can be a huge benefit as patients can work to minimize annular stress and disruption. If patients understand the mechanical forces responsible for their pain, they are better equipped to work as a team player in the management of back pain. Teaching containment of the nucleus will now be an asset with this new model design.

Degenerated Centralizer

This new Degenerative Centralizer Lumbar Model will change the way doctors and physiotherapists talk to their patients. We expect those that use this model for education will have better outcomes. Pre-orders being accepted now with discount offered to those early on the list.

Discogenic pain is controversial–or is it?

Low back pain is common, really common, and responsible for the second most common reason why people visit their doctors. And yet, it still continues to elude scientists of its specific origin.

One convincing theme in low back pain are findings associated with the intervertebral discs. Often it is first recognized with reduced disc height on x-ray and then if persistent, followed up with MRI demonstrating the same but with evidence of hypointesity in a T2 weighted MRI. Most researchers agree that this finding indicates a reduction in water and proteoglycan content.

Discogenic Pain Model - Dynamic Disc Designs

Professional LxH Model demonstrating discogenic pain

Since the development of upright MRI, we are now able to see the spine under load and motion. This has provided us a window into the dynamic movement of the vertebrae and the discs in between them–showing spondylolisthesis in flexion and retrolisthesis in extension.

Some believe the only way to discern whether the disc itself is the painful anatomical structure, is to do a discogram. This is a procedure that punctures the disc with a needle and over pressurizes it to see if it is painful to the patient. This is kind of like over inflating a bicycle tire. The problem with this procedure is we know when a disc is punctured, it facilitates the degeneration process.

Discogenic pain is often a deep kind of pain because it is an anterior structure and heavily innervated. It is often relieved by lying down and worse with sitting.  It is also known to get sore after a long period of recumbency–like after a nights rest.

Engaging and educating patients about these symptoms can curtail their worries and helps when 3d models are used to explain the avoidance of activities that increase intradiscal pressures.

Dynamic Disc Designs enables the practiotioner to explain the inner workings of the disc. When patients understand flexion load stresses the posterior annulus, they quickly get motivated to maintain their lordosis with bending and lifting. This modification behaviour improves outcomes with spine.

Discogenic pain is for real. We are learning more and more about how the discs are at the core of low back pain.