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THE CLINICAL CLARITY BLOG
November 7, 2026 by DR MATTHEW D. LONG
THE CLINICAL CLARITY BLOG
Can Discs Really Slip?
November 7, 2026 by DR MATTHEW D. LONG
In 1911, Dr Joel Goldthwait, Chairman of Orthopaedic Surgery at Massachusetts General Hospital, described an intriguing case involving a patient with sciatica and a suspected intervertebral disc injury (1). When surgical exploration failed to identify the anticipated lesion, Goldthwait reportedly speculated that the disc must have somehow "slipped back into place". This may represent one of the earliest uses of the term "slipped disc", an expression that subsequently entered the medical vocabulary and, more enduringly, the public lexicon.
Of course, our understanding of intervertebral disc pathology has progressed enormously over the intervening century. Gone is the simplistic notion that disc injuries are exclusively mechanical events, with symptoms arising solely from the physical compression of adjacent neural structures. Contemporary models recognise a complex interplay between genetics, inflammatory and immunological processes, nociceptive signalling, central pain mechanisms and altered sensorimotor control. More recently, researchers have even begun exploring potential relationships between disc degeneration and the gut microbiome.
And yet, in developing this increasingly sophisticated understanding of disc pathology, perhaps we have been a little too enthusiastic in dismissing the original concept of a slipped disc.
After all, can discs really slip?
Of course, our understanding of intervertebral disc pathology has progressed enormously over the intervening century. Gone is the simplistic notion that disc injuries are exclusively mechanical events, with symptoms arising solely from the physical compression of adjacent neural structures. Contemporary models recognise a complex interplay between genetics, inflammatory and immunological processes, nociceptive signalling, central pain mechanisms and altered sensorimotor control. More recently, researchers have even begun exploring potential relationships between disc degeneration and the gut microbiome.
And yet, in developing this increasingly sophisticated understanding of disc pathology, perhaps we have been a little too enthusiastic in dismissing the original concept of a slipped disc.
After all, can discs really slip?
MORE THAN JUST A SHOCK ABSORBER
The human intervertebral disc is commonly described as a 'shock absorber', resisting compressive loads through the interaction between its hydrated nucleus pulposus and the surrounding annulus fibrosus. While this is certainly true, the disc also plays an essential role in stabilising the spinal motion segment when subjected to shear and torsional forces. To achieve this, it relies upon a remarkable combination of structural features, including the annular lamellae, their anchorage to adjacent vertebral bodies through Sharpey's fibres, the vertebral endplates and the supporting ligamentous structures. The orientation of the facet joints provides additional constraints upon movement.
However, the disc's ability to perform these functions depends upon more than the integrity of its external attachments. It also relies upon the mechanical properties of its internal nucleus pulposus, particularly its capacity to attract and retain water and generate pressure.
In this respect, the intervertebral disc has some interesting similarities to a car tyre.
A tyre is designed to operate within a particular range of inflation pressures. When appropriately inflated, its internal air pressure supports the tyre's structure, helps maintain its shape and allows the sidewalls and tread to respond predictably to the forces generated during driving. But when inflation pressure falls, the mechanical behaviour of the tyre begins to change. The sidewalls deform more readily, particularly during cornering, and the resulting distortion can produce unwanted movement, uneven loading and accelerated wear. In extreme circumstances, the tyre may even move relative to the wheel rim.
The intervertebral disc operates according to a surprisingly similar principle, although its internal pressure is generated by a very different mechanism.
The nucleus pulposus contains a high concentration of proteoglycans, particularly aggrecan, whose negatively charged glycosaminoglycan chains attract water and generate an osmotic swelling pressure. This pressure is resisted by the surrounding annulus fibrosus and vertebral endplates, creating a mechanically integrated structure capable of distributing substantial compressive loads. When the spine is loaded, pressure within the nucleus increases, generating outward forces that place the annular fibres under tension (2).
This internal pressurisation is important because it helps maintain disc height, distributes loads across the vertebral endplates and contributes to the mechanical behaviour of the surrounding annulus.
But just as a tyre becomes mechanically compromised when its inflation pressure falls, the intervertebral disc can experience significant changes when its capacity to generate and maintain internal pressure deteriorates.
Ageing, genetic influences and injury can contribute to the progressive depletion or alteration of proteoglycans within the nucleus pulposus. As its capacity to attract and retain water diminishes, the nucleus loses some of its swelling pressure and its ability to distribute compressive forces effectively. The resulting changes in load sharing can reduce the tension developed within the annular fibres and increase deformation of the disc under load (2).
This is not merely a theoretical proposition. In 1999, Sato and colleagues measured intradiscal pressure in healthy volunteers and patients with low back pain or sciatica, demonstrating that pressure was significantly reduced with increasing MRI-assessed disc degeneration (3).
More recently, a 2025 investigation by Liebsch and Wilke examined intradiscal pressure in 107 human lumbar motion segments obtained from 68 donors. They found that discs exhibiting mild or moderate degeneration demonstrated significantly reduced intradiscal pressure compared with non-degenerative specimens. Pressure also declined significantly with increasing age, with the researchers observing these differences across multiple loading directions, including flexion, extension, lateral bending and axial rotation (4).
These findings lend considerable support to the concept that degeneration compromises the internal pressurisation of the disc, potentially altering the distribution of mechanical loads between the nucleus and annulus.
And this is where the tyre analogy becomes particularly interesting.
An underinflated tyre may still be securely attached to its wheel, but its ability to resist deformation during cornering is compromised. Similarly, a degenerative disc may remain firmly anchored between adjacent vertebrae while becoming less effective at resisting the forces that attempt to deform or translate the spinal segment.
The consequences may include greater annular bulging, altered load distribution, increased shear stresses between annular lamellae and progressive disruption of their structural organisation. Over time, these changes may contribute to further mechanical deterioration, creating a potentially self-perpetuating cycle in which degeneration alters mechanical loading, and abnormal loading contributes to further degeneration (2).
Of course, unlike a car tyre, the disc is a living, viscoelastic structure whose internal pressure varies continuously with posture, activity and loading. Furthermore, degeneration does not invariably produce excessive spinal movement; advanced degenerative changes may ultimately make a motion segment less mobile rather than more unstable.
Nevertheless, the underlying principle remains remarkably similar: when a pressurised structure loses its capacity to maintain internal support, the mechanical demands placed upon its surrounding walls change, potentially compromising their ability to resist deformation.
And this brings us to an interesting question. If degeneration reduces the disc's internal pressurisation and alters the mechanical behaviour of its annular wall, just how much of its ability to resist shear might be lost?
A recent investigation provides some fascinating answers.
However, the disc's ability to perform these functions depends upon more than the integrity of its external attachments. It also relies upon the mechanical properties of its internal nucleus pulposus, particularly its capacity to attract and retain water and generate pressure.
In this respect, the intervertebral disc has some interesting similarities to a car tyre.
A tyre is designed to operate within a particular range of inflation pressures. When appropriately inflated, its internal air pressure supports the tyre's structure, helps maintain its shape and allows the sidewalls and tread to respond predictably to the forces generated during driving. But when inflation pressure falls, the mechanical behaviour of the tyre begins to change. The sidewalls deform more readily, particularly during cornering, and the resulting distortion can produce unwanted movement, uneven loading and accelerated wear. In extreme circumstances, the tyre may even move relative to the wheel rim.
The intervertebral disc operates according to a surprisingly similar principle, although its internal pressure is generated by a very different mechanism.
The nucleus pulposus contains a high concentration of proteoglycans, particularly aggrecan, whose negatively charged glycosaminoglycan chains attract water and generate an osmotic swelling pressure. This pressure is resisted by the surrounding annulus fibrosus and vertebral endplates, creating a mechanically integrated structure capable of distributing substantial compressive loads. When the spine is loaded, pressure within the nucleus increases, generating outward forces that place the annular fibres under tension (2).
This internal pressurisation is important because it helps maintain disc height, distributes loads across the vertebral endplates and contributes to the mechanical behaviour of the surrounding annulus.
But just as a tyre becomes mechanically compromised when its inflation pressure falls, the intervertebral disc can experience significant changes when its capacity to generate and maintain internal pressure deteriorates.
Ageing, genetic influences and injury can contribute to the progressive depletion or alteration of proteoglycans within the nucleus pulposus. As its capacity to attract and retain water diminishes, the nucleus loses some of its swelling pressure and its ability to distribute compressive forces effectively. The resulting changes in load sharing can reduce the tension developed within the annular fibres and increase deformation of the disc under load (2).
This is not merely a theoretical proposition. In 1999, Sato and colleagues measured intradiscal pressure in healthy volunteers and patients with low back pain or sciatica, demonstrating that pressure was significantly reduced with increasing MRI-assessed disc degeneration (3).
More recently, a 2025 investigation by Liebsch and Wilke examined intradiscal pressure in 107 human lumbar motion segments obtained from 68 donors. They found that discs exhibiting mild or moderate degeneration demonstrated significantly reduced intradiscal pressure compared with non-degenerative specimens. Pressure also declined significantly with increasing age, with the researchers observing these differences across multiple loading directions, including flexion, extension, lateral bending and axial rotation (4).
These findings lend considerable support to the concept that degeneration compromises the internal pressurisation of the disc, potentially altering the distribution of mechanical loads between the nucleus and annulus.
And this is where the tyre analogy becomes particularly interesting.
An underinflated tyre may still be securely attached to its wheel, but its ability to resist deformation during cornering is compromised. Similarly, a degenerative disc may remain firmly anchored between adjacent vertebrae while becoming less effective at resisting the forces that attempt to deform or translate the spinal segment.
The consequences may include greater annular bulging, altered load distribution, increased shear stresses between annular lamellae and progressive disruption of their structural organisation. Over time, these changes may contribute to further mechanical deterioration, creating a potentially self-perpetuating cycle in which degeneration alters mechanical loading, and abnormal loading contributes to further degeneration (2).
Of course, unlike a car tyre, the disc is a living, viscoelastic structure whose internal pressure varies continuously with posture, activity and loading. Furthermore, degeneration does not invariably produce excessive spinal movement; advanced degenerative changes may ultimately make a motion segment less mobile rather than more unstable.
Nevertheless, the underlying principle remains remarkably similar: when a pressurised structure loses its capacity to maintain internal support, the mechanical demands placed upon its surrounding walls change, potentially compromising their ability to resist deformation.
And this brings us to an interesting question. If degeneration reduces the disc's internal pressurisation and alters the mechanical behaviour of its annular wall, just how much of its ability to resist shear might be lost?
A recent investigation provides some fascinating answers.
A FASCINATING STUDY
A 2025 investigation published in JOR Spine by Bader and colleagues (5) examined the mechanical behaviour and structural organisation of the outer annulus fibrosus in symptomatic degenerative human discs, comparing these findings with tissue obtained from non-degenerative donors.
The investigation involved 13 non-degenerative donor discs and 30 symptomatic degenerative discs obtained during surgery. Small tissue specimens were prepared from the outer annulus and subjected to controlled mechanical testing, allowing the researchers to evaluate their resistance to shear deformation in both radial and circumferential orientations.
These distinctions are important because the annulus is not mechanically uniform. Its layered architecture provides different degrees of resistance depending upon the direction in which forces are applied. By testing the tissue in different orientations, the investigators were able to examine how degeneration affected these properties.
The results were remarkable.
The degenerative annular tissue demonstrated approximately a 71% reduction in radial shear stiffness and a 76% reduction in circumferential shear stiffness.
These were not insignificant changes. They represented a profound deterioration in the ability of the outer annulus to resist deformation when subjected to shearing forces.
But perhaps even more interesting was the relationship between these mechanical changes and the underlying tissue architecture.
Using optical coherence tomography, the researchers examined the organisation and thickness of the annular lamellae. Degenerative specimens exhibited thicker lamellar structures, with increasing lamellar thickness strongly associated with reductions in shear stiffness. The investigators also identified alterations in the tissue's viscoelastic behaviour, including changes in hysteresis and phase shift, suggesting that degeneration affects not only the magnitude of deformation but also the way in which the tissue responds to changing mechanical loads.
Taken together, these observations provide compelling evidence that degeneration fundamentally compromises the shear-resisting properties of the outer annulus fibrosus.
And that raises an intriguing question.
If the annulus is substantially less capable of resisting shear, what happens to the movement of the vertebrae that it helps to stabilise?
The investigation involved 13 non-degenerative donor discs and 30 symptomatic degenerative discs obtained during surgery. Small tissue specimens were prepared from the outer annulus and subjected to controlled mechanical testing, allowing the researchers to evaluate their resistance to shear deformation in both radial and circumferential orientations.
These distinctions are important because the annulus is not mechanically uniform. Its layered architecture provides different degrees of resistance depending upon the direction in which forces are applied. By testing the tissue in different orientations, the investigators were able to examine how degeneration affected these properties.
The results were remarkable.
The degenerative annular tissue demonstrated approximately a 71% reduction in radial shear stiffness and a 76% reduction in circumferential shear stiffness.
These were not insignificant changes. They represented a profound deterioration in the ability of the outer annulus to resist deformation when subjected to shearing forces.
But perhaps even more interesting was the relationship between these mechanical changes and the underlying tissue architecture.
Using optical coherence tomography, the researchers examined the organisation and thickness of the annular lamellae. Degenerative specimens exhibited thicker lamellar structures, with increasing lamellar thickness strongly associated with reductions in shear stiffness. The investigators also identified alterations in the tissue's viscoelastic behaviour, including changes in hysteresis and phase shift, suggesting that degeneration affects not only the magnitude of deformation but also the way in which the tissue responds to changing mechanical loads.
Taken together, these observations provide compelling evidence that degeneration fundamentally compromises the shear-resisting properties of the outer annulus fibrosus.
And that raises an intriguing question.
If the annulus is substantially less capable of resisting shear, what happens to the movement of the vertebrae that it helps to stabilise?
REVISITING THE CONCEPT OF 'SLIPPAGE'
Before answering that question, an important distinction needs to be made. Bader and colleagues investigated the mechanical properties of isolated annular tissue, rather than measuring movement between intact vertebrae. Their findings therefore do not directly demonstrate that degenerative discs produce excessive vertebral translation, nor do they establish that reduced shear stiffness is necessarily responsible for pain.
Nevertheless, the biomechanical implications are interesting.
The intervertebral disc forms an integral component of the spinal motion segment, working alongside the facet joints, ligaments and surrounding musculature to control movement. A substantial reduction in annular shear stiffness would reasonably be expected to influence the mechanical behaviour of this system, although the extent of any resulting instability would depend upon the contribution of these other structures.
Furthermore, degeneration does not necessarily produce a uniform increase in movement. Depending upon its severity and the accompanying changes in the facet joints and surrounding tissues, a degenerative spinal segment may exhibit increased motion, altered patterns of movement or, eventually, progressive stiffness.
This complexity is precisely why the findings deserve careful interpretation.
However, they also challenge the familiar assertion that discs simply cannot slip.
When clinicians reject the expression 'slipped disc', they are generally referring to the mistaken belief that an entire disc can slide out from between two vertebrae, much like a bar of soap squeezed between wet hands. Clearly, this is not what occurs. The disc is firmly attached to the adjacent vertebral bodies, and even substantial herniations involve displacement of disc material rather than migration of the entire structure.
But slipping can also describe relative movement between two surfaces, or shearing deformation within a structure. Viewed from this perspective, the concept becomes considerably more interesting.
A damaged annulus can lose much of its ability to resist shear deformation. And because the annulus contributes to the control of vertebral translation, this loss of mechanical integrity may also influence the stability of the spinal segment.
Perhaps, then, the expression 'slipped disc' is not quite as anatomically absurd as we have been taught to believe.
Nevertheless, the biomechanical implications are interesting.
The intervertebral disc forms an integral component of the spinal motion segment, working alongside the facet joints, ligaments and surrounding musculature to control movement. A substantial reduction in annular shear stiffness would reasonably be expected to influence the mechanical behaviour of this system, although the extent of any resulting instability would depend upon the contribution of these other structures.
Furthermore, degeneration does not necessarily produce a uniform increase in movement. Depending upon its severity and the accompanying changes in the facet joints and surrounding tissues, a degenerative spinal segment may exhibit increased motion, altered patterns of movement or, eventually, progressive stiffness.
This complexity is precisely why the findings deserve careful interpretation.
However, they also challenge the familiar assertion that discs simply cannot slip.
When clinicians reject the expression 'slipped disc', they are generally referring to the mistaken belief that an entire disc can slide out from between two vertebrae, much like a bar of soap squeezed between wet hands. Clearly, this is not what occurs. The disc is firmly attached to the adjacent vertebral bodies, and even substantial herniations involve displacement of disc material rather than migration of the entire structure.
But slipping can also describe relative movement between two surfaces, or shearing deformation within a structure. Viewed from this perspective, the concept becomes considerably more interesting.
A damaged annulus can lose much of its ability to resist shear deformation. And because the annulus contributes to the control of vertebral translation, this loss of mechanical integrity may also influence the stability of the spinal segment.
Perhaps, then, the expression 'slipped disc' is not quite as anatomically absurd as we have been taught to believe.
WHAT DOES THIS MEAN FOR CHIROPRACTORS?
For chiropractors, these findings provide another reason to consider disc pathology in terms of mechanical function rather than simply structural appearance.
Traditionally, much of the clinical discussion surrounding disc injury has focused on compression, herniation and nerve root compromise. While these remain important considerations, the mechanical competence of the annulus itself may deserve greater attention.
A patient with a degenerative disc may experience discomfort during bending, twisting or transitions between postures, even in the absence of a substantial herniation or obvious neural compression. Although these symptoms are not specific to disc pathology, altered shear resistance offers one plausible mechanical contributor.
The outer annulus is also innervated and contains structures capable of nociceptive signalling. Consequently, abnormal deformation of compromised annular tissue could potentially contribute to pain, particularly when combined with the inflammatory and neurobiological changes associated with degeneration (2).
However, we should resist the temptation to interpret every painful movement, catching sensation or episode of acute back pain as evidence of segmental instability. Clinical symptoms alone cannot establish excessive vertebral translation, and reduced tissue stiffness does not automatically equate to a painful or unstable spinal segment.
The rehabilitation implications are nevertheless worth considering. Improving trunk muscle coordination, developing tolerance to progressively increasing loads and restoring confidence in movement may all contribute to better functional control of the spine. In patients who demonstrate sensitivity to rotational or shearing loads, modifying these activities temporarily may also be appropriate while capacity is rebuilt.
For chiropractors, the findings provide a useful reminder that painful spinal segments are not necessarily mechanically restricted. Some may exhibit altered movement control or reduced passive restraint, and this possibility should form part of a broader clinical assessment rather than an assumption that every painful segment requires increased mobility. But as we have discussed in other Clinical Clarity articles, the signature chiropractic adjustment may actually assist in generating stability through its ability to influence proprioceptive feedback.
Traditionally, much of the clinical discussion surrounding disc injury has focused on compression, herniation and nerve root compromise. While these remain important considerations, the mechanical competence of the annulus itself may deserve greater attention.
A patient with a degenerative disc may experience discomfort during bending, twisting or transitions between postures, even in the absence of a substantial herniation or obvious neural compression. Although these symptoms are not specific to disc pathology, altered shear resistance offers one plausible mechanical contributor.
The outer annulus is also innervated and contains structures capable of nociceptive signalling. Consequently, abnormal deformation of compromised annular tissue could potentially contribute to pain, particularly when combined with the inflammatory and neurobiological changes associated with degeneration (2).
However, we should resist the temptation to interpret every painful movement, catching sensation or episode of acute back pain as evidence of segmental instability. Clinical symptoms alone cannot establish excessive vertebral translation, and reduced tissue stiffness does not automatically equate to a painful or unstable spinal segment.
The rehabilitation implications are nevertheless worth considering. Improving trunk muscle coordination, developing tolerance to progressively increasing loads and restoring confidence in movement may all contribute to better functional control of the spine. In patients who demonstrate sensitivity to rotational or shearing loads, modifying these activities temporarily may also be appropriate while capacity is rebuilt.
For chiropractors, the findings provide a useful reminder that painful spinal segments are not necessarily mechanically restricted. Some may exhibit altered movement control or reduced passive restraint, and this possibility should form part of a broader clinical assessment rather than an assumption that every painful segment requires increased mobility. But as we have discussed in other Clinical Clarity articles, the signature chiropractic adjustment may actually assist in generating stability through its ability to influence proprioceptive feedback.
PERHAPS WE WERE TOO QUICK TO DISMISS THE TERM?
There is also an interesting communication issue here.
For generations, healthcare professionals have corrected patients who describe their condition as a 'slipped disc', explaining that discs cannot actually slip. The intention is understandable, particularly when trying to replace misleading anatomical concepts with more accurate explanations.
But perhaps our correction has sometimes been a little too categorical.
We can certainly explain that a disc does not simply pop out of position and then slide back into place. We can also distinguish between disc bulging, herniation, degeneration and segmental instability. These distinctions remain important.
Yet we can simultaneously acknowledge that the mechanical properties of a damaged disc may allow abnormal shear deformation and potentially contribute to altered movement between adjacent vertebrae.
The two ideas are not mutually exclusive.
Indeed, more than a century after Goldthwait suggested that a disc might have slipped back into position, modern biomechanical research is providing a rather different perspective on what slippage might actually mean. The disc is not merely a passive cushion between two vertebrae. It is a sophisticated mechanical structure whose ability to resist shear is essential to its function.
When that ability deteriorates, the consequences may extend well beyond the familiar changes in disc height, hydration and morphology.
So, can discs really slip?
Perhaps not in the way Goldthwait imagined.
But after more than a century of telling our patients that discs cannot slip, it may be time to reconsider just how confidently we make that assertion.
For generations, healthcare professionals have corrected patients who describe their condition as a 'slipped disc', explaining that discs cannot actually slip. The intention is understandable, particularly when trying to replace misleading anatomical concepts with more accurate explanations.
But perhaps our correction has sometimes been a little too categorical.
We can certainly explain that a disc does not simply pop out of position and then slide back into place. We can also distinguish between disc bulging, herniation, degeneration and segmental instability. These distinctions remain important.
Yet we can simultaneously acknowledge that the mechanical properties of a damaged disc may allow abnormal shear deformation and potentially contribute to altered movement between adjacent vertebrae.
The two ideas are not mutually exclusive.
Indeed, more than a century after Goldthwait suggested that a disc might have slipped back into position, modern biomechanical research is providing a rather different perspective on what slippage might actually mean. The disc is not merely a passive cushion between two vertebrae. It is a sophisticated mechanical structure whose ability to resist shear is essential to its function.
When that ability deteriorates, the consequences may extend well beyond the familiar changes in disc height, hydration and morphology.
So, can discs really slip?
Perhaps not in the way Goldthwait imagined.
But after more than a century of telling our patients that discs cannot slip, it may be time to reconsider just how confidently we make that assertion.
Something to think about...
Dr Matthew D. Long
BSc (Syd), M.Chiro (Macq), DIANM
Dr Matthew D. Long
BSc (Syd), M.Chiro (Macq), DIANM
References:
1. Goldthwait JE. The lumbo-sacral articulation; An explanation of many cases of lumbago sciatica and paraplegia. Boston Med Surg J. 1911;164:365–372.
2. Kirnaz S, Capadona C, Lintz M, et al. Pathomechanism and biomechanics of degenerative disc disease: Features of healthy and degenerated discs. Int J Spine Surg. 2021;15(Suppl 1):10–25. doi:10.14444/8052
3. Sato K, Kikuchi S, Yonezawa T. In vivo intradiscal pressure measurement in healthy individuals and in patients with ongoing back problems. Spine. 1999;24(23):2468–2474. doi:10.1097/00007632-199912010-00008
4. Liebsch C, Wilke HJ. The intradiscal pressure of the lumbar spine is affected by intervertebral disc degeneration, age, level, and motion direction: Evaluation of an in vitro database comprising 107 specimens. Spine J. 2025;25(6):1276–1287. doi:10.1016/j.spinee.2025.01.024
5. Bader TJ, Dhiman M, Lo Vercio L, et al. Reduced shear modulus and altered lamellar morphology of the outer annulus fibrosus in painful intervertebral disc degeneration compared with tissue from non-surgical controls. JOR Spine. 2025;8(4). doi:10.1002/jsp2.70123
1. Goldthwait JE. The lumbo-sacral articulation; An explanation of many cases of lumbago sciatica and paraplegia. Boston Med Surg J. 1911;164:365–372.
2. Kirnaz S, Capadona C, Lintz M, et al. Pathomechanism and biomechanics of degenerative disc disease: Features of healthy and degenerated discs. Int J Spine Surg. 2021;15(Suppl 1):10–25. doi:10.14444/8052
3. Sato K, Kikuchi S, Yonezawa T. In vivo intradiscal pressure measurement in healthy individuals and in patients with ongoing back problems. Spine. 1999;24(23):2468–2474. doi:10.1097/00007632-199912010-00008
4. Liebsch C, Wilke HJ. The intradiscal pressure of the lumbar spine is affected by intervertebral disc degeneration, age, level, and motion direction: Evaluation of an in vitro database comprising 107 specimens. Spine J. 2025;25(6):1276–1287. doi:10.1016/j.spinee.2025.01.024
5. Bader TJ, Dhiman M, Lo Vercio L, et al. Reduced shear modulus and altered lamellar morphology of the outer annulus fibrosus in painful intervertebral disc degeneration compared with tissue from non-surgical controls. JOR Spine. 2025;8(4). doi:10.1002/jsp2.70123