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.

facet osteoarthritis

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.

 

 

Disc Herniation Spondylolisthesis

Spondylolisthesis is the slippage of one vertebra on another—frequently found with disc herniation. However, in this recent paper titled: “Over-reporting of the disc herniation in lumbar spine MRI scans performed for patients with spondylolisthesis” 1 they sought to find if disc herniation is over-reported and in turn, possibly over-treated.

Spondylolisthesis is best diagnosed when the spine is under load. Many MRI scans, because done in the lie-down position, miss these small (or large) slippages. To accurately assess one for a spondylolisthesis, the spine is best visualized by x-ray in the forward bending and backward bending position. Upright MRI is also another great way to assess; however, the access to these expensive machines may not be available.

The authors of the above paper discuss how it is imperative to find an accurate diagnosis for both the conservative and surgical management of back pain.

Disc herniation is often found with spondylolisthesis. However, what they found was disc herniation reporting was often over-reported and believed that the disc herniation was more of a pseudo disc herniation rather than an actual disc herniation.

 

What do the authors mean by pseudo-herniation?

 

The authors point to a nomenclature issue. In Fardon’s 2014 paper 2 he helps clarify the language professionals use when discussing disc herniation, extrusion, protrusion and bulge. However, the authors of this paper explain that Fardon’s article does not address this nomenclature in light of spondylolisthesis.

 

They point out in this retrospective study of 258 patients that disc herniation was over-reported because the disc herniation was read with the superior vertebra in mind rather than referencing the lower vertebra. In other words, if the radiological reporting used the lower vertebra as a reference point, the reporting of a disc herniation would be much less because the outer disc border remained anterior to the posterior vertebral ring apophysis. Therefore, it is essential to deferentially diagnose whether symptoms are related to a real disc herniation or due to the mechanics of a spondylolisthesis. A spondylolisthesis can throw off the reporting in this case.

 

 

Dynamic Disc Designs creates 3d models to help reveal the dynamics of disc herniation, including the up-roofing of the disc material. This mechanism is shown in our Professional LxH Model, with the added features of spondylolisthesis.

 

lower-back-pain

A recent study done during 2019 1 by several specialists was conducted to uncover the relation of immediate and increasing back pain to exposures to seated postures. It’s a systematic review of studies that include objectively measured sitting time.

What was the Context?

Low back pain (LBP) is one of the most prominent causes of disability globally. The years spent living with a disability caused by LBP has increased to more than 50% in-between 1990 to 2015. For years, prolonged periods of sitting time are reported to be associated with LBP. 

Sitting too much because of your job has been suggested as a risk factor for LBP, however, data to support these claims are slightly unclear. One reason for this lack of data can be linked to the high prevalence of sitting and LBP in the general population. This in addition to the multifactorial nature of LBP itself.

The review study was published and done to carry out a systematic review of studies. It’s aimed to find out if sitting times measured objectively is connected to the swift increase of low back pain (LBP).

It’s measured objectively through a time trial that’s laboratory-controlled, wearable sensors, and direct observation. An increase in LBP is ascertained by the pain scale rating in individuals who are 18 years old and older.

What was the Methodology?

The review protocol was registered with the International Prospective Register of Systematic Reviews on October 19, 2017. The reporting format of the review followed the recommendations and guidelines of the Preferred Reporting Items of Systematic Reviews and Meta-analyses.

The researchers looked at four electronic databases. They were EMBASE, PubMed, SPORTDiscus, and Cumulative Index to Nursing and Allied Health Literature. All four were carefully examined from the beginning up to September 1, 2018. 

Studies used were cross-sectional studies and cohort, and randomized controlled trials. Sitting time was measured objectively, and it was matched with a measure of low back pain in adults. 

figure 1.2 LBP study

However, excluded studies are those with no control session and each done during a separate day. The full-text review, screening, data extraction, and the risk of bias assessment (Quality in Prognosis Studies) of included papers were independently completed by 2 reviewers. There was also a third reviewer present to take care of the disagreements.

What were the Results?

606 articles were pinpointed through the database searches. In addition, 3 articles were identified by reviewing a list of references or relevant papers, along with a hand search. Among these articles, the researchers removed 248 duplicates. 

Titles and abstracts of the 361 remaining articles were screened. For further review of eligibility, 75 full papers were accessed. The 65 articles were excluded. The 10 articles left and the data for 330 participants were included in this study.

All in all, a total of 609 articles have been identified. However, 361 titles and abstracts were screened. Afterward, 75 full-text articles were examined for being eligible. 10 articles fit the criteria for inclusion. 

Every one of them except for 1 reported that sitting time is associated with the immediate increase in lower back pain. 6 of the articles have reported clinically relevant pain levels.

One-half of the studies included were found to have low risks of bias. What remained was determined simply as having a moderate bias risk.

What Has Been Discussed?

The researchers found that sitting down for total durations ranging from 1 hour to 6.96 h/d for 5 days is connected to the immediate increases in LBP in people. 

It happens with and without a clinical history of LBP — both in the field and laboratory settings. Similar results can be found when the studies included only had a low risk of bias.

table 1 01

table 1 02

table 1 03

table 2

The consistency of the findings was high. Participants who have a history of LBP report high levels of pain intensity compared to asymptomatic controls. This was reported after an identical exposure to sitting in a laboratory setting. 

However, pain responses (even if they’re lower) were in both parties, with or without LBP. It is typically assumed that sitting aggravates the existing cases of LBP. But then they also found that sitting also provoked pain in individuals, even if they don’t have a history of lower back pain.

The strength of this review is that a systematic and comprehensive search strategy was used to identify potential articles that are related to the research question. The researchers particularly looked for articles that involved sitting over sedentary behavior. 

The study also has no limitation of time or language. It minimizes the chance of missing potential articles to include.

The objective measures of sitting time are linked to the immediately increased ratings of perceived LBP in adults, with and without a recent history of lower back pain. 

However, it continues to be unknown whether this increase has clinical implications. There’s also an absence of a conclusion in-between sitting and clinically relevant episodes of LBP that can be made.

And based on their findings, the researchers would recommend and suggest prospective studies in the future that would match the objectively measured exposures, which were analyzed objectively with temporally related measures of pain. It is done to determine if sitting time is a trigger of a clinical episode of LBP.

facet-joint-biomechanics

A study 1 conducted by several researchers in the Department of Orthopedic Surgery in Rush University Medical Center in Chicago USA looked closely on the biomechanics of the lumbar facet joint, and its effects on the overall spine mechanical behavior.

Why Conduct Such a Study?

Facet joints, also known as zygapophyseal, are complicated biomechanical structures in the spine. It has a complex 3D anatomy, in addition to variable mechanical functions when there are different spinal movements and effects on the overall spine mechanical behavior.

The facet joint’s 3D morphology is linked to its biomechanical function. The failure of the facet joint’s biomechanical function can lead to osteoarthritic changes in it. It can also implicate other spinal disorders. This includes degenerative spondylolisthesis.

The review article summarized the anatomy of the lumbar facet joint relevant to its biomechanical function. It also examined the biomechanical behaviors of the lumbar facet joint when put under different loading conditions.

What Was the Methodology?

Facet joints and intervertebral disks are part of the entity called the spinal motion segment. It’s also called the three-joint complex.

Sometimes, it’s also referred to as the articular triad. As they function together, the structures in the spinal motion segments give physiological spinal motion. It protects the spine through preventing activities that can cause injury.

The loss of intervertebral disk height is associated with disk degeneration. This affects the mechanical behavior of facet joints.

Sufficient understanding and proper knowledge of the anatomical geometry of the facet joint surface and capsular structures is essential for understanding the biomechanical function of the lumbar facet joint.

What Were the Results?

Interaction Between the Intervertebral Disc and the Facet Joint

Intervertebral disks and facet joints are part of the spinal motion segment. As they function together, the structures in the spinal motion segments provide physiological spinal motion. It protects the spine through preventing activities that can cause injury.

Mechanisms of Axial Compressive Load Transmission Through the Facet Joint

There are complex mechanisms by which facet joints transfer the axial compressive load because the lumbar facet joints from a synovial joint with low friction and nearly vertical articulating surfaces.

There are 3 possible mechanisms:

  • Through the articular joint surfaces.
  • Through capsular ligaments.
  • Through direct connection in between the tips of the articular processes and the lamina (the pars interarticularis).

Axial compressive load transmission via direct contact in between the tips of articular processes and the neural arch is essential, especially when the lumbar spine is extended.

Facet Biomechanical Functions at Different Spinal Positions

Facet joints accomplish different biomechanical functions when faced with different spinal positions. This section reviewed the biomechanical behaviors in:

Extension

Contact between the tips of the inferior articular process and the pars interarticularis can occur in lumbar extension. Especially if the intervertebral disk loses its height. The results of finite element analysis simulations suggest that hyperextended activities can cause impaction of the inferior process.

Forward Flexion

In a lumbar forward flexion, the inferior articular processes move superiorly in allusion to the superior articular process of the lower level.

Facet joints have an essential part in keeping lumbar stability in forward flexion. Apart from the restriction of normal physiologic flexion, the one that is being forced over the superior process is the inferior articular process. Afterwards, the compressive loads borne by the facets amplify again compared to those supported in the neutral position.

This phenomenon, however, is considered as a possibility that can cause degenerative spondylolisthesis.

Axial Rotation

The facet joint’s articular surfaces press together on one side, and then often open up on the other. This is what happens in a lumbar axial rotation.

We have the results of trabecular orientation and photoelastic experiments. And it suggests that the superior articular processes undergo bending stress within an axial rotation through compression in the tension and in the lateral direction.

Lateral Bending

There’s limited information present in publications on the facet joint’s biomechanical behavior under lateral bending. Here, the inferior articular process glides in the superior direction. It does so in reference to the superior articular process of the inferior vertebra. It’s on the convex side of the spinal curve, and on the opposite direction on the concave side.

What Was the Conclusion?

The lumbar facet joint has a complex 3D geometry. It has small components inside of the small joint. They are all directly linked to facet joint’s biomechanical functions and the motion segment in different spinal positions.

But if we oversimplify the facet joint as a flat joint, it may keep us from properly understanding the functions of the facet joint.

Axial load transmission and forward translation in motion segments can’t be wholly comprehended if one does not consider the special relationship among the lumbar spine’s posterior elements. Medical imaging modalities make room for 3D modeling plus the spinal model’s reslicing in the clinic.

But extracting valid information can’t be done if we do not understand the facet joint’s 3D geometry and its function.

What's the Relationship Between MRI Findings & Clinical Symptoms in Patients with Suspected Lumbar Spinal Canal Stenosis_

A recent study 1 published in the last legs of 2019 set out to find the correlation between clinical symptoms and MRI findings in patients who are suspected to be suffering from lumbar spinal canal stenosis.

What was the Context?

Lumbar spinal stenosis (LSS) is the most common sign that a patient over the age of 65 will need a spinal surgery. What is LSS? It is a condition that shows decrease in the available space for the vascular and neural components of the lumbar spinal cord.

Within clinical practice, symptomatic LSS comes with different symptoms. This includes: buttock pain, bilateral or unilateral neurological disorder, and pain in the lower extremities.

LSS manifests usually because of less space present for neural and vascular structures of the lumbar spine. The definition of LSS has two aspects: structural abnormalities and clinical manifestations. Both are a result of certain physical abnormalities.

Previous studies have shown that clinical symptoms showing mild to moderate lumbar LSS might exist in less than half of patients.

So in order to define destructive LSS, it’s important that clinical symptoms match up with the imaging results. This is the reason why using clinical findings along with radiological evaluation through magnetic resonance imaging (MRI) is seen as proper standard in diagnosing LSS.

Numerous clinical criteria and imaging are available for the diagnosis of LSS. But despite the availability, coming up for the right diagnosis is a challenging part for radiologists and clinicians.

Therefore, this study aims to assess and understand the relation between clinical symptoms and MRI findings in groups of symptomatic and asymptomatic patients having suspected LSS.

What was the Methodology?

Using a case-control study, there are two groups of 100 symptomatic and asymptomatic individuals involved. Their ages range from 20 to 84 years old.

Both the groups have suspected lumbar spinal canal stenosis. They were all referred to the imaging unit for lumbosacral MRI. Within the study, patients’ clinical symptoms and radiological parameters in MRI were recorded. Afterwards, the researchers evaluated the results of the correlation between clinical symptoms and MRI findings.

What Were the Results?

Throughout the duration of the case-control study, 100 patients in the case group with signs and symptoms of LSS were evaluated.

100 patients in the control group who underwent lumbar MRI were also evaluated throughout the study period. Age ranges of the case group were between 21 to 84 years old. While the age range for the control group was 20 to 84 years old.

Table 1 in the study showed the prevalence of clinical symptoms in patients who did or didn’t have LSS symptoms.

Table 1 Frequency of clinical symptoms in patients with and without LSS

Table 2 shows the quantitative and qualitative radiological features in case and control groups.
Table 2. Quantitative and qualitative radiological features in case and

What Does This Mean?

The most common clinical manifestations of patients in both case and control groups involved:

  • Mechanical low back pain
  • Radicular pain
  • Gluteal pain

There were also no significant relationships between most clinical symptoms with each of the radiological indices separately. The highest significant correlation was observed between radiological indices and neurogenic claudication.

What Was Concluded?

Based on the results of the quantitative criteria of MRI imaging findings, the central spinal canal cross-section and lateral recesses cross-section had the highest specificity and sensitivity for LSS diagnosis in asymptomatic and symptomatic patients with suspected LSS.

The strongest observed correlation? It was between neurogenic claudication and LSS diagnostic radiological markers.

nocebo

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.