Patient engagement is at the core of a patient-centered approach to spine care. Spine professionals engage with their patients with different tools. We all use language but to enhance it, very often a physical model can support the words chosen to educate.

In the past, models have been static, so it made it very difficult to connect patient’s back and neck pain to the specific movements that cause the pain. At Dynamic Disc Designs, we have developed models to help the practitioner engage in a mechanical way through a better rendering of a motion segment. We have created a dynamic disc with the ability of the models to bulge or herniate. We have integrated a dynamic nucleus pulposus and a stiffer annulus fibrosus as well as added features of the ligamentum flavum to show how the facets are inter-related to one another.

Explore how a dynamic model can enhance the language one uses in a clinical setting of a musculoskeletal practice.

facet osteoarthritis, facet joint pain

Goal of the Study?

The objective of this study 1 evaluates the feasibility of sensory mapping of lumbar facet joint pain in patients scheduled to undergo radiofrequency (RF) denervation. 


Why are they doing this study?

Lower back pain (LBP) is a widespread condition that can result in chronic pain.  While there are many treatment approaches, one of the most established interventions uses diagnostic blocks to identify the source of nociception. Though many parts of the back can be involved in LBP, facet joints are among the most common sources contributing to back pain. Most often, for treatment in clinical practice, the medial branches are anesthetized to establish the diagnosis of facet joint pain. RF denervation of these nerves, which is a process to stop nerves from transmitting pain, is used as pain management. 

The authors argue that while this approach has been well established, the use in a clinical setting has been questioned due to the high rates of false-positive (30%), cost-effectiveness and lack of standardization and anatomical variation. For this reason, the authors hope to develop a strategy for a more precise identification of the nerves involved in LBP.

facet capsule nerves, facet joint pain


What was done?

In total, they had 15 participants for this study. After written consent, participants completed a pre-procedure pain diagram and rated their pain on a scale of 1-10. The researchers used a standard procedure for RF denervation, including a single diagnostic block and imaging in determining cannula placement. To reproduce the pain in patients with chronic back pain, medial branches were stimulated using 50Hz electrical stimulation to determine the threshold. This was then increased threefold to achieve the suprathreshold stimulation, after which participants were asked to map their pain and compare this against the initial pre-procedure pain diagram.


What did they find?

A total of 71 nerves were scheduled for RF denervation. Sensory stimulation was successful in 68 out of 71 nerves using 50Hz electrical stimuli. All 15 participants reported either pain or paraesthesia (tingling or prickling) during suprathreshold stimulation, and 14 (93%) reported complete coverage of their usual painful area. In one participant, the upper lumbar pain was not covered by suprathreshold stimulation. For 60% of the participants, they reported pain/paraesthesia outside of their normal pain area during suprathreshold. Overall, in their population, 7.5% of the denervated nerves did not contribute to pain transmission. The average sensory detection threshold was 0.3V, with the suprathreshold was 0.6V.


Why do these findings matter?

Using suprathreshold stimulation, lumbar facet joint pain can be mapped and offers objectivity by reproducing patients’ back pain. This approach can also improve patient safety and experience by limiting RF denervation to nerves involved in pain transmission. This can improve patient safety and experience. 


Goal of the article?


Back pain is very common in people who practice sport at the elite and non-elite levels. In this article 1, the authors look at the existing research to understand how physical exercise can impact biologic and structural changes to the intervertebral disc (IVD) and spine. 


What is the IVD?


The IVD is the hydraulic cushion between vertebrae, making up almost one quarter of the spinal column. IVD provides stability by absorbing and distributing the stress and shock of the body during movement and preventing the vertebrae from approximating one another. Each IVD is made up of two parts: 


  1. Annulus fibrosis – this is the outside of the disc, made up of water and elastic collagen fibers
  2. Nucleus pulpous – this is the inside of the disc, made up of a gel like elastic substance


What did they find?


Research shows that different types of exercises have different outcomes for the IVD and spine. Low-impact and moderate physical exercise are beneficial to IVD as they can promote regeneration and muscle function. For example, regular walking or low demand running can help to improve IVD structure and support by providing nutrition to the IVD in the form of oxygen and lactate. 


In contrast, high impact activities that over rotate the spine or force it to overly compress can break down the IVD early and result in back pain. This pain can result in a reduction in muscle strength and muscle activation. It can also result in a worsening of coordination and proprioception (the sense of self-movement and body position). This means that individuals with lower back pain can have a reduced ability to sense how the body is moving and its’ actions. 


However, not only does pain have an impact on how a person can move, but it can also result in changes to the brain or what is called cortical neuroplasticity. These brain changes can alter the body’s motor and behaviour control. They can also limit the effectiveness of learning a new skill by reducing the ability of an individual to make necessary adaptions to movements that further deteriorate the spinal tissues. 


Why does this review matter?


Back pain is a very common finding in exercise and sport. Therefore, it is important to understand what types of exercise are beneficial to IVD and what types can deteriorate the spine and spinal tissues. Understanding how prolonged back pain can change the way human bodies experience and adapt to pain, and the long-term impacts that can have on learning a new skill, are important to addressing treatments for patients living with back pain. 


At Dynamic Disc Designs, we work to model the biology of the spine in a flexible and interactive way so professionals can make the best clinical decisions for their patients.


In a recent podcast hosted by Shireesh Bhalerao of Tulip Seminars, Jerome Fryer reveals the backstory behind the origins of Dynamic Disc Designs among many other topics.

Spotify click here to listen

Apple click here to listen

Topics include:

  1. Practice (down time between patient visits)
  2. Pain is dynamic should be modeled for patient education
  3. Connecting patients and their anatomy with self awareness
  4. The connection between Dynamic Disc Designs and Degenerative Disc Disease
  5. Explaining and revealing the progressive changes of the disc
  6. The patient encounter and optimizing outcomes
  7. Jerome’s research in joint cavitation
  8. Jerome’s inspiring background
  9. How do you find a receptive audience to partner with?
  10. Cavitation research from the observations of research and development of a Dynamic Disc Model
  11. Collapsing Bubble vs. Bubble Formation does that make any sense?
  12. Early discoveries of sound origin of joint cracking, it may not be either — formation nor collapse
  13. Vacuum phenomenon – vacuum sign. (unpacking of joint cracking research)
  14. Tulip seminars and teaching moments from dynamic disc models. Students are blown away.
  15. How one should connect with patients.
  16. Pathoanatomic diagnosis vs. movement based diagnosis – Jerome does not think they should be separated.
  17. Empowering patients with their understanding
  18. Chiropractic and Physiotherapists tension – why? There is no need.
  19. Surgical world – NASS meetings
  20. Making Jerome work with advancing modeling of different pathoanatomical models
  21. Bridging medical and chiropractic
  22. Optimize patients with Dynamic Disc Designs
  23. The Pain Meter – new venture.
lordosis. degenrative joint disease

Flat Back (Lack of Lumbar Lordosis) and Disc Herniation

Lordosis, or the lack of it, has been thought to be a biomechanical precursor to disc herniation in the lumbar spine. To investigate this possible correlation, a group of researchers from Gothenburg University looked at sixteen young active young patients with a median age of 18yrs old who experienced a disc herniation and underwent discectomy surgery. 1

Lordosis is the curve in the lower back—which they measured before and after the surgery.


Researchers used the Roussouly 4-type classification system to measure the degree of lordosis in the lumbar spine.

The researchers found less lordosis in the subjects that had surgery for their disc herniation. In other words, disc herniation was twice as likely to be present in the group with a flatter back. All the disc herniations were found to be in the lowest two levels of the lumbar spine (L4-5 and L5-S1), consistent with other epidemiological studies. 2

Dynamic Disc Designs Models

At Dynamic Disc Designs Corp. we have worked to represent the anatomy accurately. Our Professional LxH  Dynamic Disc Model is created with 12mm of disc height anteriorly and 10mm posteriorly providing a slight lordotic curve. Further, the model has been created with a higher percentage of nucleus pulposus which is often found in younger lumbar spines. To demonstrate that disc herniation occurs more likely with less lordosis all one has to do is dynamically move the single-level model into a less lordosis position and manually create compression. With more lordosis, the nucleus has a more difficult time penetrating through the outer annulus fissure. This can be an important posture teaching point in the prevention of disc herniation.

If you want to take your patient education to a dynamic level, explore what Dynamic Disc Designs models can do for you, your practice and ultimately, your patients.

facet osteoarthritis, facet joint pain

Facet osteoarthritis pain is common and thought to be a significant contributor to back pain in the US. Within the United States, it costs 100 Billion dollars annually to combat this endemic problem. However, back pain can originate from many anatomical structures, and the facet joint is only one of them but thought by many as significant. Other common pain structures are the intervertebral discs in the case of disc bulges, disc extrusions, disc protrusions and frank nuclear sequestration. There are also more severe causes of back pain like aneurysm and other organ pathology, so it is crucial to have a professional look carefully at the diagnostics of each case.

In the case of mechanical lower back pain (others use the term non-specific lower back pain), the facet joint garners good attention. The word ‘facet’ comes from the French facette (12c., Old French facete), diminutive of face “face, appearance” and are two anatomical structures that reside behind the intervertebral disc.

Facet osteoarthritis

Modeling facet osteoarthritis is tricky because of the complexity of motion at the spinal level. The intervertebral disc height plays a role with respective facet compression because it resides on the front of the spinal motion segment. It is this compression thought to be contributing to back pain.

Clincally, facet osteoarthritis pain is often unilateral in nature

In a study conducted recently 1, researchers worked to induce facet joint arthritis by creating compression with a spring. Over time the researchers found the increased expression of interleukin‑1β and tumour necrosis factor‑α expression. In other words, with more compression elapsing over time, the more the expression of the molecules related to many low back pain patients.

This is an important study linking the mechanics of compression and the associated physiology of molecules, which are thought to be markers of back pain patients.

At Dynamic Disc Designs, we have developed models to help explain the associated compression of facet joints as it relates to disc height loss and gains. We are committed to bringing the best in modelling. Explore our website for more.

Crack Propagation Osteoarthritis

Osteoarthritis is common and causes much disability in the world to many. It is a joint condition that causes pain, which often leads people to seek therapy. Despite the efforts to learn the underlying causes, researchers have been confused as to the source and propagation of degenerative osteoarthritic changes. We know that surface injury to cartilage can occur from high-risk competitive sports and result in the development of osteoarthritis; the precise reasons as to this has eluded researchers in the field. Understanding the mechanobiology of the early stages of OA when micro-cracks start will be an important piece of the puzzle in the prevention of osteoarthritis.

Just this month, a group of researchers out of the University of Calgary, looked at the finer micro-structure of the cartilage. 1 They looked at crack propagation (micro-fracturing) of the cartilage to get a better understanding of the load and respective magnitude as it relates to the damage. Their objective included looking carefully at the local strain distribution of the cartilage nearby to the microcracks.

What did they do?

Cylindrical osteochondral punch plugs were harvested from pig knees and fixed to a custom design compression testing device. The cartilage thickness was measured at three different locations of the surface. To prevent dehydration, which can often occur in these testing environments and affect the results, they fully immersed the sample in a phosphate-buffered solution. The thickness of the cartilage was measured using light microscopy. Measures of strain were applied. To simulate the crack in the cartilage found in-vivo, vertical cuts were made in the cartilage at the most superficial part of the surface cartilage along with the middle zone.

What did they find out?

Axial strains were significantly more abundant at the damage zone compared to the non-damaged cartilage. This indicates that the ability of the cartilage to resist compression is less in the damaged or micro fractured cartilage, disrupting the biomechanics.

Crack Propagation Osteoarthritis


What can we take away from this study?

The drive to learn about osteoarthritis is essential. Billions of dollars are spent annually for a multitude of therapeutics, including joint replacement, injections, pharmaceuticals and manual therapy. By learning about how cracks propagate in the cartilage and, ultimately, how we prevent the development of osteoarthritis will be a great asset to the planet.

At Dynamic Disc Designs, we work to follow the research and work to bring that to the doctor-patient engagement process. Our latest modelling now includes a crack in the cartilage of the facet joint.




A very recent systematic review 1, in the Journal of Pain, went over the neurotransmitter systems associated with the placebo and nocebo effects in healthy humans as well as those with chronic pain. It did offer a fascinating insight.

What Was the Context?

Researchers have been interested in pain for a long time. That’s why numerous studies have been conducted involving neurotransmitters. The placebo and nocebo effects associated with pain are a big part of better understanding underlying mechanisms.

However, most of the said studies feature healthy participants who are exposed to experimental pain or are experiencing acute postoperative pain.

With a continued focus on finding a way to optimize placebo effects while minimizing nocebo effects during clinical practice, it has been deemed crucial for the neurotransmitter systems (that are involved in nocebo and placebo effects) to be directly investigated in subjects with chronic pain.

According to studies, the endogenous opioid system has been observed to be involved in the placebo effects demonstrated by healthy participants. Also, placebo effects in such subjects have been reported to involve the endocannabinoid, oxytocinergic, dopaminergic, and vasopressinergic systems, too. The CCKergic or cholecystokininergic system has shown involvement in the nocebo effects in healthy subjects.

But, it’s important to note that short-duration experimental pain or acute pain (in healthy subjects) is different from subjects with chronic pain. An intact nociceptive system for modulating pain is typically present in healthy participants.

However, chronic pain is linked to various mechanisms and complex pathophysiology that might be causing the pain. Psychological components for processing pain are usually more apparent in people with chronic pain.

That’s why it makes sense to think that the mechanisms associated with placebo effects present in healthy subjects might not necessarily be the same for subjects dealing with chronic pain.

Why Conduct Such a Review?

The current systematic review is the first to go over existing evidence pertaining to the involvement of the neurotransmitter systems in healthy subjects experiencing acute postoperative or experimental pain as well as subjects with chronic pain.

The goal was to offer an answer to how placebo effects might differ in said healthy patients and those with chronic pain.

LxH Model

What Was the Methodology?

The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) was followed for the methodology and reporting of the current paper. The team identified placebo studies by searching several electronic databases, namely Embase, PubMed, Scopus, as well as the Cochrane Library. The nocebo studies were identified post hoc by using the same electronic databases.

The articles were all in English. Also, the range included the earliest dates available in the databases through May 23, 2019. Take note; to be added, some of the factors involved the articles featuring studies aiming to understand the placebo and nocebo mechanisms as well as displaying statistically significant effects.

What Were the Results?

The initial search presented 1133 placebo along with 147 nocebo articles. With the duplicates removed, 505 placebo and 74 nocebo articles remained. After further exclusion, the final review included 28 placebo and 2 nocebo articles.

A total of 16 studies showed the involvement of the endogenous opioid system in a healthy subject’s placebo effects. Also, 8 studies shared how naloxone can be used to fully or partially block the placebo effects. However, 2 studies revealed that such effects, in a healthy subject, can’t be blocked with naloxone.

Furthermore, 2 studies talked about the contribution of the endocannabinoid system with regards to healthy subjects and placebo effects. A total of 2 studies had mixed results when it came to the involvement of the dopaminergic system. The same held true for the oxytocinergic system. The vasopressinergic system was said to be involved by one study. Take note; no study shared the involvement of the CCKergic system.

As for the placebo effects in those with chronic pain, two studies shared how the endogenous opioid system wasn’t involved. No studies about the endocannabinoid system and patients with chronic pain were found. The same happened for the oxytocinergic, vasopressinergic, and CCKergic systems. Two studies about the dopaminergic system showed mixed results.

Furthermore, 2 studies observed how the CCKergic system might be involved in a healthy subject’s nocebo effects. However, no studies were found talking about the involvement of the other systems.

Coming to subjects with chronic pain and nocebo effects, no studies were found.

What Does It Mean?

More research is needed to collect data about the types of neurotransmitter systems involved in placebo and nocebo effects in healthy subjects and those with chronic pain. A majority of the studies have focused on healthy patients.

And according to certain findings (as an example), the endogenous opioid system might not be involved in the placebo effects in chronic pain as it is involved in the pain experienced by healthy participants.

Furthermore, the psychological mechanisms linked to placebo effects are suggested to differ in subjects with chronic pain and in those who are healthy. This might play a role in why verbal suggestions display minor results when dealing with chronic pain when compared to the pain that’s experimental or acute postoperative. Understanding such differences in varying populations and conditions could aid in creating better ways to treat and manage pain.