Degenerative Disc Disease & How Stiffness (Not Pain) in your Spine Leads To Mechanotransductive Diseases especially heart disease, cancer, autoimmune and diabetes!

The Science Behind How Stretching, Compression, and Shear Stress Drive Cellular Physiology and Function.

Not enough? Leads to chronic inflammation/ infection and early death…


We’re gonna look at mechanoreceptors (sensors loaded in your body that detects movement) and how they facilitate the transmission of mechanotransductive forces like that of a windmill which takes the mechanical energy from the movement of wind and transforms them into electricity. In our body this happens from the normal movement of your spine so long it’s aligned properly with good posture, not suffering from a movement dysfunction, and not suffering from unresolved DDD. It not only impacts nerve to brain and body function but even to cellular biochemical actions to the expression of your DNA!


In fact, one study out of USC Santa Barbara found that even baby forming in the womb is impacted by these forces. Turns out, doctors recommending bed rest when pregnant, unless for serious reasons, is unsafe and dangerous to your baby because it affects embryogenesis or the formation of your baby in utero!

In cells, mechanotransduction like that of a windmill is the means by which physical forces, such as stretching, compression and shear stress, are translated into biochemical impulses and signals. These biochemical changes are startling as we never knew this until very recently. They can include adjustments to intracellular concentrations of all kinds of biochemistry like enzymes and elements such as potassium and calcium, for example, as well as the activation of various signaling pathways, each of which may, in turn, result in changes to both cellular and extracellular structures. That’s huge, we never knew this! We’re starting to understand why chiropractic clinical research has numerous case studies from everything from A to Z.

It turns out, Through these various mechanotransduced pathways, the mechanical forces of the three‐dimensional environments in which cells exist contribute to the regulation of even the most fundamental of cellular processes. Meaning. We need to rewrite our basic science textbooks to include the most fundamental thing lacking in medical school. And that’s movement. Not just exercise, but all-day tiny movement.

Even when mechanotransduction‐related processes within cells are functioning normally, disturbances in the physical inputs they receive from their extracellular environments, especially from, and I’m quoting from a major mechanobiology study, “damaged joints, degenerative or stiff joints, especially your spine, can subsequently cascade to produce pathological results in a whole host of disease and premature death”. 

Stiffness in your spine is usually caused by injury or lack of movement. It mimics what happens to astronauts in space.  The loss of bone mass experienced by astronauts living for extended periods in reduced gravity is one interesting example of such a disturbance and its effects. The minimal amount of gravitational force exerted on the astronauts (relative to the gravitational force on the earth’s surface), causes disruptions to normal mechanotransductive processes in bone tissues that lead to diminished tissue production and reduced bone mass. 

A far more common but not unrelated example is the atrophying of muscle tissue that occurs in patients who become bedridden or otherwise immobilized for extended periods of time. And of course in all the devastating effects of sitting disease and what it does to the body‘s biological processes. Sitting for just seven hours a day increases your chance of risk of death by 40%.

How do we know this? Listen up, unlike most evidence-based sciences, which is rat and animals, not human. Mechanobiologist have novel ways to look at humans safely. They do use animals, but they seem more sensible as they try to study human safely using novel techniques to validate their opinion. Unlike nearly everyone else, who does a rat study and then rationalizes it calling it human. So, the rat study was good, so drink that and take this in your body. Makes no sense.

Well, I’m not alone in this thinking, turns out mechanobiologists have developed new novel ways to detect the changes of force and compression on cells and tissues and how it all interacts safely with humans. 

But I wanted to talk about what they discovered about these changes of force and stress and between tension stress and compressive stress on the intravertebral disc and how it relates both to chiropractic care and all-day movement.  They have actually developed many ways to detect this and measure this, let me cover some of those, as I believe it will help you understand why you need to move all day long with a well-mobile functioning spine, and why a chiropractor is necessary for the family.

For example, the unique functional and physical characteristics of IVDs, which link the vertebral bodies constitute the main joints of the spine, they indicate that mechanotransduction plays a particularly prominent role in their normal function and, as the discs age, their dysfunction. 

The purpose of the discs is to transmit physical forces, namely, physical forces resulting from muscle movement and the weight of the body, to the spinal column, with the discs providing the tension, flexion, and bending capacity that give the spine its flexibility 29. In effect, each disc functions much like a small shock absorber in a car, taking in the physical forces delivered to the spine and protecting the bony vertebrae above and below it by keeping them separate. Of course, the main purpose of the disc is to keep the whole opening where the major nerves exit, which then supplies every tissue, cell, and organ in the body. 

So, the disc in the spine is more than just spacers, as they compress and change in stress from daily movement, those forces from movement propagate nerve signals to the brain and from the brain to the body for the functioning of tissues, cells, and organs of your body; like that of a windmill or a power generator.

So, you’re healthy spinal joints which are supposed to have a normal range of motion act like a power generator to your central nervous system. Faulty spinal mechanics and or Degenerative Disc Disease have massive consequences beyond arthritic pain, it’s not just a bad back, it has negative consequences on how well your brain works, your cells function, protein synthesis, right down to gene expression in your DNA. Let me explain.

Your central nervous system which is your brain, spinal cord, and the 33 pairs of nerve roots exiting out between the IVD is the master controller to every system in your body, and its largely controlled by mechanotransductive forces through the normal motion of your spine, meaning the proper movement, spinal alignment, posture and frequency of spinal movement and it’s related structures is vital to the pathogenesis of numerous diseases and the ability to heal and regenerate. This is no longer a theoretical conjecture. It’s all worked out in science. 

We don’t want stiff spinal joints, and we want our backbones moving around 8-10 miles a day, the way our genetic constitution was written, like our ancestors who moved that way for a millennium. That’s what you need to take from this video. But I like to geek out on that science, time to prove what I said earlier. It’s all worked out in science…. so here we go…

Structurally speaking, IVDs consist of two main parts: the annulus fibrosus and the nucleus pulposus. The annular fibrous is a thick outer ring consisting of several layers of fibrocartilage, over 60 layers; feels like plexiglass, it surrounds the nucleus pulposus which forms an inner core and has a softer, more gelatinous texture. A relatively minor but nonetheless distinct third part of IVDs are the cartilage endplates on the top and bottom of each disc that provides an interface between the given disc and the vertebrae above and below it, effectively sandwiching both the inner nucleus pulposus region and outer annular fibrosus ring.

The primary proteoglycan of the disc is aggrecan, which is the main means by which the disc maintains tissue hydration. The nucleus has a much higher concentration of these proteoglycans than the annulus—this means that the nucleus has a much higher degree of hydration, which is itself the basis for the more gel‐like texture of the nucleus. It’s this increased water binding capacity provided by the proteoglycans in the nucleus and expressed through the normal motion of the spine that is critical to the compressive strength of the spine 30. At the same time, the actual amount of loading placed on the spine while you engage in all-day movement likely plays a role in proteoglycan production and activity within the disc, and muscle tissue growth or atrophy, strength, or weakness. 

The relationship between the body and its physical environment is mediated, in large part, by the process of the normal movement of the spine and the resulting nerve signaling stimulation of mechanotransduction.

What this means is the growth and maintenance of IVDs, as well as their healthy function and pathological degeneration, involve a complex interplay between mechanical, electrochemical and biochemical forces, which mechanotransduction from the normal all-day movement of the spine provides the means by which external mechanical forces are translated into biochemical activity and processes within cells, tissues, organs, even your DNA.

In fact, various studies have already shown that mechanical stress affects gene expression and metabolism in IVD cells both in vivo (meaning whole organisms/humans) and in vitro (meaning in glass, microorganisms, cells, biological molecules outside normal biological context impacting basic biological function, healing and/or pathology in virtually every level of disease anywhere in the body. 
And as I said at the beginning of this video, it impacts your baby forming in the womb. Another reason chiropractic and pregnancy go together like peanut butter and jelly.

But this is what’s startling. They discovered that mechanical forces are critical, not only for the nerve to tissue signaling but for all cell types, even protein synthesis in the DNA. Again, it also impacts disc formation during embryogenesis. Recent in utero research concerning the IVD found that notochord cells are required for normal disc formation in humans and are likely pushed into the IVDs during embryogenesis by a mechanical force spurred by the formation of the vertebral bodies. 

In contrast, in a study examining the effects of in vivo mechanical forces on human lumbar discs, scientists used discs from patients with idiopathic adolescent scoliosis as a biological model to determine how tensile stress and compression affect disc health. Their results indicated that such stress can lead to decreased water content and cell density, matrix degeneration and calcification, and site‐specific breaks in discs.

So, how do we know this is true? That it’s truly worked out in science, and not some philosophy or theory…

Using glass pipettes and pressure jets, scientists can now measure the activation of nerve terminals subjected to pressure. Using compression hypo-osmotic stretching we can illicit dorsal root ganglion on sensory neurons and measure them. But these tests failed to fully amount for the structural interaction, like focal adhesions in tissues. So, scientists have developed new methods to address this, something called elastomeric matrices that actually stimulate the actual physiological conditions of living tissues. 

Let me geek out a moment and go through some of this because guess what…your doctor has never heard this before…get over it. They have enough to know, that’s why he has a doctor of chiropractic!

We actually have ways to measure the following forces on cells and tissues. Which eventually in the future may be applied in chiropractic research facilities as well. Sheer loads can be measured. Compressive loads can be measured. And twisting loads can be measured using the following scientific test.

  1. Using an elastic substrate we can measure pressure changes similar to a rubber band or holding outstretched saran wrap and placing something on it deforming it, well they can determine how pressure changes from tiny movement and mechanical forces to this 3-dimensional network in your cells consisting of extracellular macromolecules and minerals, such as collagen, enzymes, glycoprotein and others that provide structural and biochemical support to surrounding cells, they can measure how sensory neurons or your nerve signaling following movement stimulation like walking, but especially the movement of the spine- actually affects all these chemical changes within the cell.
  2. Using nanotechnology we can also measure traction forces which occur naturally to the body when we move from squatting positions to standing, or sitting to standing, or getting out of bed, and just bending over; small traction forces between spinal joints occur and it impacts cellular responses within the IVD and all the surrounding tissues in your joints like ligaments, muscles, and tendons on a cellular level.
  3. Using traction force microscopy. We can look at mechanical interactions of fibroblast migration and collagen deposition which promote regeneration of tissue like that of a wound and even regeneration of collagen within the IVD.
  4. Using Magnetic twisting cytometry to induce sheer loads and forces on the cell which influence the spine morphology on IVD disc loads and healthy stresses during the normal movement of the spine due to proper postural load balance and spinal alignment of the spine. A study in The Spine Journal proved how chiropractic adjustments and postural corrections influence spinal coupling and mechanical loads on spinal tissues and that by correcting spinal alignment, posture and spinal mobility following chiropractic care normalized the postural and shear loads of the spine. And you guys know, that when those motion segments are restored and your posture is improved with chiropractic care, that means your windmills, that power generator, due to these sensors loaded in your spinal joints, act like a windmill transforming these healthy mechanical signals into stronger nerve signaling to the brain and every tissue, cell, organ, down to your biochemistry in your cells to the expression of your DNA.

IVDs are affected by a wide variety of mechanical stimuli including shear stress, hydrostatic pressure, torsion, flexion, and electrokinetic changes. Chiropractic care along with tiny all-day movement of the spine and postural exercise and spinal hygiene exercise impacts a wide variety of these mechanical stimuli.

For example, one study recently introduced a device based on elastomeric substrates that allowed researchers to test the effects of shear fluid flow and uniaxial strip stretching on actin cytoskeleton (a key structural component of IVDs) and they also measured the cell orientation. They found that the cytoskeleton and cells began to align themselves in the direction of the applied force after only 3 hrs of application.

There is no direct correlated study yet, but I can only imagine that this means within 3 hours following a chiropractic adjustment in which the bone is mobilized and tissues are stretched it causes shear fluid flow and stretching on the cytoskeleton within cells during the chiropractic adjustment with the correct applied force from the chiropractor; meaning cells within the matrix of tissues align themselves in response to promote healing of the tissue and regeneration of the tissues like ligaments, tendons, muscle, nerve and especially the IVD.

In fact, a similar study also demonstrated how shear fluid flow and equibiaxial stretching influence the regenerative functions during fibroblast recruitment of fibronectin (another structural element of IVDs), with mechanically perturbed cells exhibiting increased fibronectin fibril formation and fibronectin localization at their peripheries (Fig. 5) 41. Meaning in real time scientists can witness and describe how mechanical forces from normalized and proper movement of our bodies, race in biochemistry similar to how our bodies heal ourselves after a wound, like a cut and regenerate our cells and tissues, even repair broken DNA.


In the future using these new nanotechnologies from mechanobiology, chiropractic research may be able to measure this. But no worries…. We know this is true, because this is the basic science research, it’s just we chiropractors like to have that direct correlated research that proves 1+2=3; though we already know it does. Understand… In other words, you and I as patients, don’t need to wait for Harvard to come out and say, “finally. Breakthru research in chiropractic…..”

We already know! Got it! But , yes. It’s nice, that were getting closer, I can see that happening very soon.

Such studies are of great interest in terms of understanding mechanotransduction in general. However, considering mechanotransduction in IVDs—its better to focus more closely on two of the most important forces affecting the spine: tensile stress and compression.
Cyclic tensile stress versus compressive stress.

Tensile stress is the form of stress caused by pulling forces (resulting in the lengthening of the stressed material in the direction of the applied force) and is one of the main types of stress that is regularly applied to IVDs and the spine in general.
Cyclic tensile stress refers simply to tensile stress that changes over time in a repetitive fashion. It might explain why repetitive chiropractic care is so helpful and important in changing the structures of the spine.

Compression, on the other hand, consists of inwardly directed (or ‘pushing’) forces that decrease the length of an object in the same direction as the force applied; gravity is one major example of a compressive force applied to the spine.
Like cyclic tensile stress, dynamic compression refers to any compressive force that changes over time in a repetitive fashion (as opposed to static compression).

In the spine, the annulus fibrosus provides the primary resistance to tensile stress and the nucleus pulposus provides most of the resistance to compressive forces 42. In fact, when a compressive force is applied to the nucleus pulposus, the nucleus is deformed, resulting in the application of tensile force to the surrounding annulus fibrosus and endplates. So, even though the two types of forces effectively occur in conjunction, the nucleus pulposus absorbs the compressive force, while the annulus fibrosus dissipates the secondary tensile force. This might explain why nonsurgical decompression actually targets a herniated disc and heals the annular fibers.
The two types of cells also respond differently to the application of cyclic tensile strain. For example, when the cyclic tensile strain was applied in vitro to bovine nucleus pulposus and annulus fibrosus cells, the majority of observable responses—including, for example, inhibition of MMP expression and increased type I collagen transcription—occurred only in the annulus pulposus cells, a fact that likely reflects the different forces encountered by the two different cell phenotypes in vivo.

Don’t freak out here, I’m just saying, The positive or negative effects of tensile strain on IVDs are highly dependent on the circumstances and the specific cell types to which they are applied. For example, in a study I noted earlier, they found a variety of negative effects because of tensile stress applied to scoliotic discs, whereas another study by different authors demonstrated that tensile stress applied to fibrochondrocytes isolated from the annulus fibrosus of rats actually has a protective effect under conditions of inflammation.

Specifically, they showed that exposing cells to tensile stress at the same time as they were exposed to an inflammatory stimulus moderated the inflammatory response by decreasing cellular expression of the catabolic mediators of inflammation. You see in bodybuilding, that tensile stress on the muscle has an anabolic effect and the resulting stress builds and strengthens the muscle. The same effect happens when you restore normal motion to the spine, the disc also receives anabolic effects and it regenerates.

Scoliosis or curvature of the spine has negative effects, too many to discuss here. But after we restore motion through chiropractic care, it decreases cellular expression of the catabolic mediators of inflammation, and using these methodologies, we now have the backing in science as well as the clinical evidence on before and after x-ray evidence following chiropractic care. Again, this is why chiropractic care decreases inflammation naturally and halts or stops the catabolic mediators of inflammation and even stimulating new cartilage cells, especially if you move a restored joint for three minutes every half an hour. I’ll talk later about that.

Another study by one scientist meanwhile, demonstrated further how different cell types and different stimuli can lead to a highly divergent outcome. Specifically, they found that the responses of annulus fibrosus cells to cyclic tensile strain depend both on the frequency of the strain applied and whether or not the annulus fibrosus cells are derived from degenerated or non‐degenerated tissue.

For example, cyclic tensile strain at a frequency of 1.0 Hz caused annulus fibrosus cells from non-degenerated tissue to decrease the expression of catabolic genes, whereas cyclic tensile strain at a frequency of 0.33 Hz caused the same type of annulus fibrosus cells to increase matrix catabolism. This is another reason we need to move our spine for three minutes every half an hour, to make sure we stimulate the anabolic in our biology and not the catabolic mechanisms.

So maintaining your spinal hygiene by making sure your spine has its all day normal range of motion and all day tiny movement hygiene along with regular chiropractic checkups is essential in today’s sedentary world.

I’m Dr. Matt Hammett, reminding you to: ‘Lighten Up, Move Better and Live Fuller’.


  1. Tsung-Ting Tsai, Chao-Min Cheng, Chien-Fu Chen, Po-Liang Lai. Mechanotransduction in intervertebral discs. Jour Cell Mol Med. 2014; Vol. 18 Issue 12: 2351-2360. Open Access
  2. Butcher DT, Alliston T, Weaver VM. A tense situation: forcing tumour progression. Nat Rev Cancer. 2009; 9: 108–22.
  3. Wozniak M, Chen CS. Mechanotransduction in development: a growing role for contractility. Nat Rev Mol Cell Biol. 2009; 10: 34–43.
  4. Hahn C, Schwarz MA. Mechanotransduction in vascular physiology and atherogenesis. Nat Rev Mol Cell Biol. 2009; 10: 53–62.
  5. Lansman JB, Franco-Obregon A. Mechanosensitive ion channels in skeletal muscle: a link in the membrane pathology of muscular dystrophy. Clin Exp Pharmacol Physiol. 2006; 33: 649–56.
  6. Holaska JM. Emerin and the nuclear lamina in muscle and cardiac disease. Circ Res. 2008; 103: 16–23.
  7. Marian AJ. Genetic determinants of cardiac hypertrophy. Curr Opin Cardiol. 2008; 23: 199–205.
  8. Burger EH, Klein-Nulend J. Mechanotransduction in bone – role of the lacuno-canalicular network. FASEB J. 1999; 13: S101–12.
  9. Uhlig S. Ventilation-induced lung injury and mechanotransduction: stretching it too far? Am J Physiol Lung Cell Mol Physiol. 2002; 282: L892–6.
  10. Affonce DA, Lutchen KR. New perspectives on the mechanical basis for airway hyperreactivity and airway hypersensitivity in asthma. J Appl Physiol. 2006; 101: 1710–9.
  11. Ichimura H, Parthasarathi K, Quadri S, et al. Mechano-oxidative coupling by mitochondria induces proinflammatory responses in lung venular capillaries. J Clin Invest. 2003; 111: 691–9.
  12. Ostrow LW, Sachs F. Mechanosensation and endothelin in astrocytes—hypothetical roles in CNS pathophysiology. Brain Res Rev. 2005; 48: 488–508.
  13. Jacques-Fricke BT, Seow Y, Gottlieb PA, et al. Ca2+ influx through mechanosensitive channels inhibits neurite outgrowth in opposition to other influx pathways and release from intracellular stores. J Neurosci. 2006; 26: 5656–64.
  14. Klein-Nulend J, Bacabac RG, Veldhuijzen JP, et al. Microgravity and bone cell mechanosensitivity. Adv Space Res. 2003; 32: 1551–9.
  15. Lammerding J, Kamm RD, Lee RT. Mechanotransduction in cardiac myocytes. Ann NY Acad Sci. 2004; 1015: 53–70.
  16. Yokoyama K, Hiyama A, Arai F, et al. C-Fos regulation by the MAPK and PKC pathways in intervertebral disc cells. PLoS ONE. 2013; 8: e73210.
  17. Cho H, Shin J, Shin CY, et al. Mechanosensitive ion channels in cultured sensory neurons of neonatal rats. J Neurosci. 2002; 22: 1238–47.
  18. Drew LJ, Wood JN, Cesare P. Distinct mechanosensitive properties of capsaicin-sensitive and -insensitive sensory neurons. J Neurosci. 2002; 22: RC228.
  19. Hu J, Lewin GR. Mechanosensitive currents in the neurites of cultured mouse sensory neurones. J Physiol. 2006; 577: 815–28.
  20. Sanchez D, Anand U, Gorelik J, et al. Localized and non-contact mechanical stimulation of dorsal root ganglion sensory neurons using scanning ion conductance microscopy. J Neurosci Methods. 2007; 159: 26–34.
  21. Geiger B, Bershadsky A, Pankov R, et al. Transmembrane crosstalk between the extracellular matrix–cytoskeleton crosstalk. Nat Rev Mol Cell Biol. 2001; 2: 793–805.
  22. Cheng CM, Lin YW, Bellin RM, et al. Probing localized neural mechanotransduction through surface-modified elastomeric matrices and electrophysiology. Nat Protoc. 2010; 5: 714–24.
  23. Lin YW, Cheng CM, LeDuc PR. Understanding sensory nerve mechanotransduction through localized elastomeric matrix control. PLoS ONE. 2009; 4: e4293.
  24. Cheng CM, LeDuc PR, Lin YW. Localized bimodal response of neurite extensions and structural proteins in dorsal-root ganglion neurons with controlled polydimethylsiloxane substrate stiffness. J Biomech. 2011; 44: 856–62.
  25. Engler AJ, Sen S, Sweeney HL, et al. Matrix elasticity directs stem cell lineage specification. Cell. 2006; 126: 677–89.
  26. Sniadecki NJ, Lamb CM, Liu Y, et al. Magnetic microposts for mechanical stimulation of biological cells: fabrication, characterization, and analysis. Rev Sci Instrum. 2008; 79: 044302.
  27. Munevar S, Wang YL, Dembo M. Distinct roles of frontal and rear cell-substrate adhesions in fibroblast migration. Mol Biol Cell. 2001; 12: 3947–54.
  28. Bellin RM, Kubicek JD, Frigaulta MJ, et al. Defining the role of syndecan-4 in mechanotransduction using surface modification approaches. PNAS. 2009; 106: 22102–7.
  29. Puig-De-Morales M, Grabulosa M, Alcaraz J, et al. Measurement of cell microrheology by magnetic twisting cytometry with frequency domain demodulation. J Appl Physiol. 2001; 91: 1152–9.
  30. Raj PP. Intervertebral disc: anatomy-physiology-pathophysiology-treatment. Pain Pract. 2008; 8: 18–44.
  31. Adams MA, Roughley PJ. What is intervertebral disc degeneration, and what causes it? Spine. 2006; 31: 2151–61.
  32. MacLean JJ, Lee CR, Grad S, et al. Effects of immobilization and dynamic compression on intervertebral disc cell gene expression in vivo. Spine. 2003; 28: 973–81.
  33. MacLean JJ, Lee CR, Alini M, et al. The effects of short term load duration on anabolic and catabolic gene expression in the rat tail intervertebral disc. J Orthop Res. 2005; 23: 1120–7.
  34. Wuertz K, Urban JP, Klasen J, et al. Influence of extracellular osmolarity and mechanical stimulation on gene expression of intervertebral disc cells. J Orthop Res. 2007; 25: 1513–22.
  35. Kasra M, Goel V, Martin J, et al. Effect of dynamic hydrostatic pressure on rabbit intervertebral disc cells. J Orthop Res. 2003; 21: 597–603.
  36. Choi KS, Harfe BD. Hedgehog signaling is required for formation of the notochord sheath and patterning of nuclei pulposi within the intervertebral discs. PNAS. 2011; 108: 9484–9.
  37. Rajasekaran S, Vidyadhara S, Subbiah M, et al. ISSLS prize winner: a study of effects of in vivo mechanical forces on human lumbar discs with scoliotic disc as a biological model: results from serial postcontrast diffusion studies, histopathology and biochemical analysis of twenty-one human lumbar scoliotic discs. Spine. 2010; 35: 1930–43.
  38. Li H, Wang Z. Intervertebral disc biomechanical analysis using the finite element modeling based on medical images. Comput Med Imaging Graph. 2006; 30: 363–70.
  39. Wilke HJ, Neef P, Caimi M, et al. New in vivo measurements of pressures in the intervertebral disc in daily life. Spine. 1999; 24: 755–62.
  40. Sato K, Kikuchi S, Yonezawa T. In vivo intradiscal pressure measurement in healthy individuals and in patients with ongoing back problems. Spine. 1999; 24: 2468–74.
  41. Steward RL, Cheng CM, Wang DL, et al. Probing cell structure responses through a shear and stretching mechanical stimulation technique. Cell Biochem Biophys. 2010; 56: 115–24.
  42. Steward RL, Cheng CM, Ye JD, et al. Mechanical stretch and shear flow induced reorganization and recruitment of fibronectin in fibroblasts. Sci Rep. 2011; 1: 147.
  43. Klein JA, Hickey DS, Hukins DW. Radial bulging of the annulus fibrosus during compression of the intervertebral disc. J Biomech. 1983; 16: 211–7.
  44. Li S, Jia X, Duance VC, et al. The effects of cyclic tensile strain on the organisation and expression of cytoskeletal elements in bovine intervertebral disc cells: an in vitro study. Eur Cell Mater. 2011; 21: 508–22.
  45. Sowa G, Agarwal S. Cyclic tensile stress exerts a protective effect on intervertebral disc cells. Am J Phys Med Rehabil. 2008; 87: 537–44.