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 vertebra

A study of Modic changes in 228 middle-aged male workers found a strong association between LBP frequency and intensity and Modic changes observed on magnetic resonance imagery (MRI) scans. These Modic chances were most likely to be at the L5-S1 spinal level and were more strongly correlated with LBP symptoms when Type 1 lesions were present.

What’s at Stake?

Bone marrow lesions—also known as vertebral endplate changes— that are visible on MRIs are considered evidence of disc degeneration. There are three types of lesions recognized by Modic: Type 1, where fissuring and an increase in the subchondral marrow vascularity is apparent; Type 2, where there is fatty degeneration of the bone marrow; and Type 3, where subchondral bone sclerosis is suspected.

Previous studies seeking to establish a positive correlation between Modic changes and clinical LBP symptoms have been inconclusive due to flawed designs and/or limited subject pools. This cross-sectional study used middle-aged male workers to investigate how or if Modic changes affected the intensity and frequency of sciatica and LBP in its subjects.

The Study

The subjects involved in this study were all male—128 Finnish train engineers, and 69 Finnish paper mill and chemical factory workers—with a mean age of 47 years. The train engineers had worked at their jobs, which involved long hours of standing and approximately five hours per day of subjection to intense, whole-body vibrations, an average of 21 years. The control group of chemical and paper workers claimed a mostly sedentary experience during their working hours and were not exposed to intense vibrations while on the job.

Both groups were assessed prior to the MRI study about the number of prior LBP and leg pain episodes, particularly those with a duration of 14 days or more. They were asked to comment on the pain’s intensity over the past week and over a three-month period before the study. They were also questioned about any history of LBP and whether they were experiencing LBP on the day of the assessment. MRI scans were taken and analyzed by two radiologists with no knowledge of the names or histories of the scanned subjects. Modic changes were identified and sorted into groups based upon the three types, with mixed types (I and I/II, and II and II/III) combined, representing more active and less active degeneration types. Other disc irregularities were noted independently and blinded to the clinical data analysts when observed. Disc herniation was either normal, bulging, protrusion, or extrusion in the notation. Neural compromise was identified as no compromise, nerve root contact, or compression. Stenosis was defined and noted according to Willen et al criteria.

modic changes, vertebra model

Modic changes with basivertebral nerve vertebra.


Though the engineers reported the highest sciatica and 1 week and 3-month pain scores, Modic changes at one or more levels were like those observed in the control group—roughly 56%. In the combined groups, 15 % of the subjects showed Modic Type I changes only, and 32% had Modic II changes at one or more-disc levels. Ten percent showed Type 1 or II changes at the same, or separate levels. The combined subject groups had 178 Modic changes across various lumbar levels, with 30 % experiencing Type I and 66 % Type II. None of the scans showed Type III Modic changes. Eighty percent of all Modic changes were located at L4-5, or L5/S1 levels, and 61% of these changes were described as “extensive,” while 39% were minimal.

There was a positive correlation between the reports of LBP episodes—especially those experienced within the past week and three-month period prior to the study— and observed Modic changes at any level. Modic changes at the L5-S1 levels were positively correlated with previous LBP and/or sciatica, especially where high levels of pain were reported within the past week prior to the study. There was little-to-no correlation between reported pain and Modic changes at higher disc levels or at L4/5.

Type II changes at any level was positively correlated with a higher number of previous LBP, especially episodes occurring during the past week or three-month period prior to the study.

Extensive changes were positively associated with more LBP episodes in the past and higher levels of LBP or sciatica within the past week or three months prior to the study. This was especially true when extensive Modic changes were found at the L5-S1 levels or when minimal changes were noted, but the subject had an extensive history of LBP episodes. The LBP had little correlation with the extent of the Modic changes at upper spinal disc levels or at L4/5.


The results of the study—the first to analyze Modic changes as they relate to specific IVD levels— suggest that there is a positive correlation between Modic changes occurring at the L5-S1 IVD level and that LBP is more likely to be associated with Modic Type 1 lesions at this level than at other levels or with other lesion types. The authors of the study suggest more research—particularly of how Modic changes correlate with pain in a younger subject set—is necessary to verify these findings.



biomedical cause, LBP

An Australian study 1 into what male and female lower back pain (LBP) patients believe about the cause of their LBP flair-ups found that the subjects were most likely to attribute the source of their recent pain to biomedical causes, including active movements and static postures, rather than psycho-social factors. Though current evidence points to a positive correlation between mental health issues, including stress, anxiety, and depression, and LBP, few of the patients in this study attributed the onset of LBP flair-ups to psycho-social causes.

What’s at Stake?

LBP is the most common global cause of disability, lost income, and productivity decreases in the marketplace. Post-acute LBP flair-ups contribute to chronic job absenteeism and economic disruption at the individual and collective societal levels. While many studies have investigated the various causes of acute LBP episodes, few have focused on the fluctuations and triggers of LBP flair-ups.

Initial episodes of LBP are considered by health professionals to be overwhelmingly biomedical/biomechanical in origin, and most patients when queried agree with that assumption.

This study was conducted to determine what LBP patients believe about the triggers of their LBP flair-ups, in the hope that better understanding patient views will lead to more effective management of intermittent, non-acute episodes of LBP.


Professional LxH Dynamic Disc Model

Professional LxH Dynamic Disc Model

The Study

One hundred and thirty male and female volunteer subjects with episodic LBP participated in the online study by answering questions about their beliefs about the triggers for their flair-ups. Their answers were analyzed for common factors and were then clustered into various themes and codes by similarities. These common codes were further categorized into two overarching themes—biomedical, and non-biomedical triggers.

Overarching Theme: Biomedical Triggers

More than eighty-four percent of the subjects identified their LBP flair-up triggers as biomedical. Active movement and static postures were the most commonly identified biomedical causes for this group’s LBP recurrences. Patients reporting active movement as a trigger for their recurring LBP were most likely to cite bending and twisting as the most frequent instigator of their pain. Many of these patients felt that the quality of these movements played a role in initiating their LBP. In these cases, it was not the movement itself, but the way they performed the movement that caused their pain.

Roughly 5 percent of the patients reporting active movement as the cause of their LBP flair-ups believed it was repetition of the movement that was responsible for their pain. They claimed that “overdoing” a task could lead to LBP episodes.

Some of the patients reporting biomedical triggers believed their LBP was caused by biomechanical dysfunction. Roughly two percent reported motor control issues, and another 2.3 percent blamed their pain on spinal damage of some kind. Other biomedical themes included knee pain, endometriosis, and constipation. Some patients felt their LBP flair-ups were caused by lack of exercise, and others blamed work for their pain. Two percent reported their flair-ups were caused by not taking maintenance pain medications as prescribed.

Other biomechanical causes included participation in sex, wearing the wrong shoes, and medical treatments.

Overarching Theme 2: Non-biomedical Triggers

Only 15.2 percent of the subjects questioned reported non-biomedical triggers as the source of their LBP. Two participants—one male, and one female—believed the cause of their flair-ups to be related to stress or the weather. A few reported psychological factors—including anxiety, the lack of creative outlets, family problems, and depression— as potential triggers of pain.

The patients who claimed the weather was a factor in their pain were most likely to blame a drop in barometric pressure or the cold. One patient believed the pain episodes were triggered by rain, temperature changes, or warm weather.

Two percent of patients who attributed their discomfort to non-biomedical conditions blamed irregular or bad sleep qualities for their pain. Roughly 1 percent felt their diet had something to do with their LBP flair-ups, and another 1 percent blamed fatigue.


More than half of the patients with intermittent LBP flair-ups believed their pain was caused by biomedical dysfunctions, and only a few believed the source of their pain was something other than biomedical problems. Active movements and static postures were the most cited triggers for LBP.

The findings in this study are consistent with previous literature about what patients believe to be the cause of their LBP. However, the lack of patient emphasis on psychosocial causes of LBP contrast with current evidence that indicates a positive correlation between psychological or mental states and persistent LBP.

The authors of this study emphasize the importance of further research into the validity of the triggers identified by the LBP patients in order to better understand LBP flair-ups and how those experiencing them conceptualize the event. Evidence indicates the efficacy of patient-centric treatment in LBP clinical outcomes, and better understanding what patients believe about their pain will help clinicians to identify more effective treatment plans to manage recurring LBP in their patients.

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.