Adapting? Or failing?
How tissue copes with stress is still remarkably mysterious.
“What doesn’t kill you makes you stronger.” Except, it doesn’t always! We can only adapt to so much stress so quickly — but it’s almost miraculous when we do adapt. How does tissue adaptation work? How good at it are we really? And can it be exploited for a treatment effect? Some popular therapies like Graston Technique and Prolotherapy are based on this idea.
There are two “laws” of tissue adaptation, one each for hard and soft tissue. Wolff’s law is that bone will adapt to loading. This was first noticed by Julius Wolff in the 19th Century, who got the naming rights. It was greatly refined in the mid 20th century by Dr. Harold Frost, an American surgeon who studied bone biology (and published scientific papers more often than I change my socks). The full details of how bone responds to stress are described in his Mechanostat model.1 A great example of Wolff’s law at work is found in pro tennis players: the humerus in their dominant arm is bigger by 16–21%.2
Bones serve as the Federal Reserve for the body’s calcium, constantly giving and collecting loans of calcium to and from other organs. And part is for the sake of bone itself, allowing it to gradually rebuild and change its shape in response to need. How else do cowboys’ bow-legged legs get bowed from too much time on a horse?3
Robert M Sapolsky, Why Zebras Don’t Get Ulcers, 2004, p. 115.
But bone cells are trapped deep in rigid bone. As biologist Dr. Sheldon Weinbaum put it, they “live in caves.” How do they know what’s going on? How can bone adapt to anything? There are several mechanisms. It’s worth going over a couple of them.
- Bone uses microscopic fluid-filled tubes to detect bone stress. The moving fluid tugs on incredibly fine cellular feelers in the tube, and the signals tell bone cells how much bone to make or dissolve. This system fails in zero gravity … which is how we figured it out. The system fails in astronauts.4
- Equally cool is the way bone uses piezoelectric effect as a signalling mechanism. This was discovered by an orthopedic surgeon, Robert Becker, way back in the 70s, and described in his fascinating book, The Body Electric (this website has a salamander logo because of that book). Piezoelectric effect is a tiny electrical current produced by deformation of a crystal. Bone, as it happens, has a crystalline structure. As the structure is ever-so-slightly flexed by stresses, it lights up with tiny electrical signals to the cells, telling them exactly where the stress is being felt. Clever!
Cross-sections of a former pro tennis player’s dominant upper arm (top row) compared to his other arm (bottom row). The bone in the dominant arm is about 18% bigger. That’s Wolff’s law at work. Source: Haapasalo 2000
Going soft: Davis’ law
The corollary of Wolff’s law for soft tissue is the obscure and much less developed Davis’ law.5 Although there’s no question soft tissue does adapt to stress, the responses of muscles, tendons, ligaments, and intervertebral discs are much more complex and less well understood. Bone is one tissue, but “soft tissue” is a whole spectrum of tissues, with diverse functions and properties, as varied as the inhabitants of a zoo.
In its mildest form, Davis’ law is simply the “use it or lose it” principle: the growth of muscles in response to exercise, say. At the other extreme of stress — trauma — scarring is a fairly obvious soft tissue “adaptation.” An intermediate example would be the way we can “seize up” — everything from minor transient sticky adhesions between layers of tissue, to significant shortening of structures. Heavily used tendons go through a complex progression of responses to stress that leads to repetitive strain injury if pushed too far.
Flexibility is a wonderfully complex example. On the one hand, it’s obvious that the soft tissues of extremely flexible athletes like dancers, gymnasts and martial artists have been changed by years of stretching regimens — often brutal and injurious. For most of the rest of us, however, there’s good evidence that flexibility changes are all in the mind: a neurological adaptation, and not a change in the tissue.6 Does a difference in the behaviour of physical unchanged soft tissue count as an example of Davis’ law? Your guess is as good as mine — it’s an almost philosophical question.
The Twa people of Africa provide another great example. A lifetime of climbing trees leads to amazing ankle mobility:7
These guys have a huge range of motion into dorsiflexion. They can get their foot almost forty five degrees to the shin. (The normal range of motion for a westerner is about ten to twenty degrees.) This allows them to get their body weight closer to the tree which makes climbing much easier.
Barefoot Running, Squatting Like a Baby, and Pygmy Feet, Hargrove (BetterMovement.org)
Finally, the best example of all: we now know, thanks to first evidence of its kind published in 2017, that intervertebral discs do adapt to exercise.8 These structures have always been considered one of the least adaptable soft tissues. For decades, almost everyone has assumed that the jarring impact of running constitutes a source of relentless wear and tear on the spine, and that the discs in particular probably cannot keep up with the onslaught, and aren’t able to adapt and recover — a slow losing battle. Specifically, data on “turnover rates” — how quickly tissue is replaced — have “lead to the assumption that positive adaptation in the mature intervertebral disc is unlikely to occur during the normal human lifespan.”
But that’s all wrong: the lumbar intervertebral discs actually adapt well to the forces involved in running. They get fatter and juicier! Tellingly, not just any old running will do, and it’s not a straightforward more-is-better relationship. It’s quirky. There is a sweet spot, but it’s in the pacing, not the volume: regardless of distance, the discs adapt best to a moderate speed, a just-right amount of impact found in slow running and fast walking. Only careful research will elucidate exactly what it takes to coax adaptation out of tissues.
Tough love: the thinking behind provocation therapies
You gotta be
Cruel to be kind in the right measure
Cruel to be kind it’s a very good sign
Cruel to be kind means that I love you
Baby, you gotta be cruel to be kind
Nick Lowe, Cruel To Be Kind
Use It or Lose It has a mean cousin: No Pain, No Gain. Many treatments for painful problems are based on the idea of forcing adaptation or “toughening up” tissues by stressing the tissues — a fairly aggressive exploitation of Davis’ law. These are provocation therapies. They claim to cure by doing a little bit of careful damage first — breaking eggs to make an omelette. It’s an emotionally compelling treatment idea. Maybe it’s right, or half right. Or maybe it just makes it a terrific engine for placebo.9
Prolotherapy is the ultimate provocation therapy. A portmanteau of “proliferative therapy,” it was invented by a charismatic doctor decades ago to treat back pain by toughening up ligaments by injecting them with an irritant.10 These days we know that “weak ligaments” are not why people get back pain,11 and so it’s not too surprising that the direct evidence for prolotherapy has always been inconsistent and unimpressive at best. Prolotherapy’s earnest founder got great results in his own clinic … but his results couldn’t be reproduced under controlled conditions, by anyone else, ever again. It did not even begin to stand the test of time.
And yet it will not die. It continues to be tried for many conditions. There are promising-but-unconvincing shreds of evidence here and there.12 An allegedly evidence-based comeback in the 2010s was not impressive. The method is so notoriously sketchy and persistent that it’s an easy target for satire:
The patient who was randomized to the prolotherapy had a 0.4 improvement in their pain on the Wong-Baker scale after taking motrin. The Kool-Aid recipients had worse pain scores after the injections, so clearly we proved that prolotherapy works. No point doing any more research!
“Sports Med Doc Performs RCT Comparing Koolaid vs Prolotherapy,” GomerBlog.com (“The Onion for doctors”)
I have a much more detailed review of prolotherapy for back pain in my low back pain tutorial.
A more modern example of provocation therapy is eccentric loading (contracting while lengthening) for tendinitis.13 Eccentric contractions are (curiously) a more challenging stimulus than regular contractions — they consistently make people much more sore after exercise (delayed-onset muscle soreness). To the extent that eccentric loading makes us sore, it’s a provocative stimulus, causing minor damage and then adaptation in the muscle (which is a normal part of strength training). Whether eccentric loading forces useful adaptation in unhealthy tendons is another matter. The jury is out on that one — some of the evidence is promising, some of the evidence is discouraging.
Scraping massage (Graston, Astym, IASTM)
From alternative medicine, the eponymous Graston Technique (GrastonTechnique.com) — an invention of a chiropractor, and mostly practiced by chiropractors — is a form of strong massage using hard, edged tools — an extreme form of ordinary friction massage. There are a couple other “brands” of hard tool massage, like Astym® or the Chinese gua sha; they are known collectively as instrument assisted soft tissue mobilization (IASTM). All use sharp-looking steel or ceramic tools to apply scraping pressure and achieve “maximum tissue penetration.” Although not always painful, it often is — as a provocation therapy must be in principle. In particular, its goal is to “break down scar tissue and fascial restrictions,” and may target tissues that are chronically painful, like a case of tendinitis. It is generally badly over-hyped. There is no compelling positive evidence from clinical trials of this kind of massage,141516 some very damning results,17 and at least two examples of tools showing some minor benefit, but — crucially — no more than non-tool techniques.1819 There are seven notable studies in as of 2017, and they were reviewed by Cheatham et al with a predictable result (see note for more detailed analysis):20
The current research has indicated insignificant results which challenges the efficacy of IASTM as a treatment for common musculoskeletal pathology.
Even IASTM proponents have confessed the problem. Leonard Van Gelder, a self-described “huge advocate of IASTM,” but apparently also a critical thinker, writes:
There are some who have purported [IASTM] tools as being downright magical in their abilities to “heal” patients. Some major brands claim 80-100% success rates for nearly every musculoskeletal condition under the sun, but record and maintain these records privately, available on request only. From the published experimental study realm, far less data is available.
What IASTM is, is not, and might be, Gelder (Dynamicprinciples.wordpress.com)
And of course claims of high success rates are almost nonsense by definition.21
Jarod Hall, DPT, shared this exasperated rant about IASTM in the fall of 2021, racking up many hundreds of likes & dozens of shares — a gratifyingly popular post.
What could possibly go wrong?
It’s not hard to imagine! Clearly there is a risk of hurting instead of helping. The physiology of adaptation may be impressive, but it’s just as clear that too much stress is injurious. And one person’s “just right” may well be the next person’s “too much.”
We also now know, thanks to the last 20 years of pain science, that chronic pain is often a failure of nervous system itself. Many people with serious chronic pain problems — the same desperate patients who might try something riskier — are actually pathologically oversensitive. Pain can make us more sensitive to more pain.22 What happens if you “stress” a nervous system in that condition? Simple: the problem gets worse, not better.
And, finally, brand new research has shown quite conclusively (and graphically, on video!) that inflammation can be actively destructive to tissues: like a gang of insane firefighters, immune cells deliberately over-react and destroy healthy cells just in case there might be an infection.23 This response is exactly what we want for open wounds, but overkill for all minor internal injuries — like tendinitis. Indeed, it may be a major reason for the stubbornness of conditions like tendinitis. Any provocative, intense treatment unquestionably has the potential to provoke exactly this reaction.
Potentially dangerous treatments should never be sold to patients on the basis of scant data. We shouldn’t take risks without proven potential for benefit. There is no reason to think that it will necessarily go well to provoke tissue, and I just spelled out at least two theoretical reasons it could go badly. One of the only studies of scraping massage was a study in rats showed modest benefits.24 But what if, upon studying more rats, you found that some had a nasty reaction? What if all rats tolerate tendon scraping well … but one in a hundred humans is seriously injured?25 Different kinds of tendinitis won’t necessarily respond the same way to the same treatment, let alone completely different musculoskeletal conditions.
The safety of an aggressive treatment is something that should be tested thoroughly, to find out if the potential rewards outweigh the risks. Patients should be wary of overconfidence about these treatments.
Provocation therapy has always been a reasonable notion to test, but the devil is in the details: what constitutes the “right” amount and kind of stress is extremely hard to determine — it probably depends on some genetics, for instance — and consequently the results of such therapies have generally always been inconsistent. Probably some conditions/people benefit from “toughening up” while others don’t. Your mileage will vary! And naturally provocation therapies are inherently risky, some of them much more so than others. They are also usually among the more expensive therapeutic choices. Unreliable, a bit risky, and expensive is not a good combination — provocation therapies should be low on your list of treatments to try.
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About Paul Ingraham
I am a science writer in Vancouver, Canada. I was a Registered Massage Therapist for a decade and the assistant editor of ScienceBasedMedicine.org for several years. I’ve had many injuries as a runner and ultimate player, and I’ve been a chronic pain patient myself since 2015. Full bio. See you on Facebook or Twitter., or subscribe:
What’s new in this article?
Four updates have been logged for this article since publication (2012). All PainScience.com updates are logged to show a long term commitment to quality, accuracy, and currency. more
Like good footnotes, update logging sets PainScience.com apart from most other health websites and blogs. It’s fine print, but important fine print, in the same spirit of transparency as the editing history available for Wikipedia pages.
I log any change to articles that might be of interest to a keen reader. Complete update logging started in 2016. Prior to that, I only logged major updates for the most popular and controversial articles.
See the What’s New? page for updates to all recent site updates.
2017 — Added a great visual example of Woolf’s law at work on the arm bones of tennis players (Haapasalo).
2017 — An especially neat science update about changes in intervertebral discs in runners (Belavý).
2017 — Science update. Cited a new review of all relevant research so far (Cheatham et al). Also clarified the example of eccentric loading.
2016 — Science update. Cited a high quality new study of Graston technique, Crothers et al.
2012 — Publication.
Dr. Dr. Robert Zapolsky summarizes the hormonal dimension of it with flair:
Bones serve as the Federal Reserve for the body’s calcium, constantly giving and collecting loans of calcium to and from other organs. And part is for the sake of bone itself, allowing it to gradually rebuild and change its shape in response to need. How else do cowboys’ bow-legged legs get bowed from too much time on a horse?
From Why Zebras Don’t Get Ulcers .
- Haapasalo H, Kontulainen S, Sievänen H, et al. Exercise-induced bone gain is due to enlargement in bone size without a change in volumetric bone density: a peripheral quantitative computed tomography study of the upper arms of male tennis players. Bone. 2000 Sep;27(3):351–7. PubMed #10962345 ❐
- And, interesting additional point from the same passage: “the hormones of stress wreak havoc with the trafficking of calcium, biasing bone toward disintegration, rather than growth.”
- Fritton SP, Weinbaum S. Fluid and Solute Transport in Bone: Flow-Induced Mechanotransduction. Annu Rev Fluid Mech. 2009 Jan;41:347–374. PubMed #20072666 ❐ PainSci #52978 ❐
Astronauts lose about 20% of their leg bone mass in a three-month stay in space, no matter how hard they work out on the Stair Master®. Why? To figure it out, scientists needed to crack a century-old mystery. We’ve known since the late 1800s that bone’s microscopic structure is perfectly adapted for the stresses it has to endure — but how does it do it? Bone cells are trapped deep in rigid bone. How do they know what’s going on? Sheldon Weinbaum is one of the scientists who cracked the bone code; he was interviewed by Robyn Williams on Australia’s excellent The Science Show in 2009:
“Bone cells live in caves. The mystery has always been how a tissue that’s as stiff as bone can communicate that it’s being loaded to the cells that live within it.”
And the solution to the mystery is “tiny little tubes.” Just like your inner ear uses fluid-filled tubes to detect motion, bone uses (much, much smaller) microscopic tubes to detect forces on bone: “a flow-induced system of mechanotransduction.” Under stress, fluid in the teensy tubes triggers a reaction in the bone cells. This process was identified only in the 90s, and Sheldon Weinbaum has been trying to figure out exactly how it works ever since. They made a major breakthrough: “we showed that the bone cell processes were actually tethered along their length and attached to these rigid canalicular walls.” It is these “tethers” that are responding to the fluid motion, tugging ever-so-slightly on the cell in response to gravity.
No wonder it took a hundred years to figure it out.
So, astronauts lose bone mass because the tube system simply doesn’t work in zero-G: the fluid floats randomly in the tubes! Precisely the same reason that astronauts get dizzy in zero-G, and have to learn how to orient themselves visually.
- No one seems to know who Davis was. Whoever he was, I was only dimly aware of his law before preparing this post. The Wikipedia entry for Davis’ law is anemic.
- If not entirely, at least substantially. It seems like some physical adaptation must be occurring in the examples of gymnast, contortionists and martial artists. But for most people, most of the time, simple stretch tolerance is a strong candidate theory to explain modest increases in flexibility with stretching. I cover this in considerable detail in the second half of my main stretching article, Quite a Stretch.
- Venkataraman VV, Kraft TS, Dominy NJ. Tree climbing and human evolution. Proceedings of the National Academy of Sciences of the United States of America. 2012 Dec. PubMed #23277565 ❐ PainSci #54672 ❐
The Twa people of Africa and you will earn amazingly limber calves that allow your ankles to bend half way (45˚) to the shin — two to four times greater than the average urban person! A good video of this flexibility has unfortunately disappeared from YouTube.
- Belavý DL, Quittner MJ, Ridgers N, et al. Running exercise strengthens the intervertebral disc. Scientific Reports. 2017 Apr;7:45975. PubMed #28422125 ❐ PainSci #53606 ❐
- As a general rule, placebos are always more powerful when people think a medicine is more “potent,” and we all assume that potency correlates with harshness. Things that taste bad, hurt, or feel awful at first must be powerful medicine … right?
From a prominent description of prolotherapy by The American Osteopathic Association of Prolotherapy Regenerative Medicine:
Prolotherapy works by stimulating the body’s natural healing mechanisms to lay down new tissue in the weakened area. This is done by a very directed injection to the injury site, “tricking” the body to repair again. The mild inflammatory response which is created by the injection encourages growth of new, normal ligament or tendon fibers, resulting in a tightening of the weakened structure. Additional treatments repeat this process, allowing a gradual buildup of tissue to restore the original strength to the area.
- For instance, low back pain does not correlate at all with the “looseness” of ligaments, and therefore logically it cannot in general benefit from “tightening” them.
- Yelland MJ, Sweeting KR, Lyftogt JA, et al. Prolotherapy injections and eccentric loading exercises for painful Achilles tendinosis: a randomised trial. Br J Sports Med. 2011 Apr;45(5):421–8. PubMed #19549615 ❐
This is a trial of 40 patients, comparing eccentric loading exercises and prolotherapy, or a combination of the two. It looks like a win, and the evidence is worth noting, particularly about prolotherapy, but there are several caveats and the results must be taken with a grain of salt: it’s a small study with no control group, the short-term effect size is modest, and the long-term results were scarcely distinguishable. With a control group, for all we know, untreated individuals would have done just as well, or even better.
“Tendinitis” versus “tendonitis”: Both spellings are acceptable these days, but the first is the more legitimate, while the second is just an old misspelling that has become acceptable only through popular use, which is a thing that happens in English. The word is based on the Latin “tendo” which has a genitive singular form of tendinis, and a combining form that is therefore tendin. (Source: Stedmans Electronic Medical Dictionary.)
“Tendinitis” vs “tendinopathy”: Both are acceptable labels for ticked off tendons. Tendinopathy (and tendinosis) are often used to avoid the implication of inflammation that is baked into the term tendinitis, because the condition involves no signs of gross, acute inflammation. However, recent research has shown that inflammation is actually there, it’s just not obvious. So tendinitis remains a fair label, and much more familiar to patients to boot.
- ScienceBasedMedicine.org [Internet]. Hall H. The Graston Technique: Inducing Microtrauma with Instruments; 2009 Dec 29 [cited 12 Oct 11].
Dr. Harriet Hall reviews the minimal science of Graston Technique for ScienceBasedMedicine.org, with her usual dry wit.
- Wilson JK, Sevier TL, Helfst R, Honing EW, Thomann A. Comparison of Rehabilitation Methods in the Treatment of Patellar Tendinitis. Journal of Sports Rehabilitation. 2000;9(4):304–314. PainSci #54747 ❐
It’s doubtful that this tiny trial was actually of high quality. However, it is notable for being one of the only clinical trials of provocation therapy with instrument massage, and the results were positive. Noted … with a huge grain of salt.In science, positive evidence from a single source, even a high quality source, doesn’t count for much. This is just too little data to take to the bank.
- McCormack JR, Underwood FB, Slaven EJ, Cappaert TA. Eccentric Exercise Versus Eccentric Exercise and Soft Tissue Treatment (Astym) in the Management of Insertional Achilles Tendinopathy. Sports Health. 2016;8(3):230–237. PubMed #26893309 ❐ PainSci #53623 ❐
A tiny, flawed test of scraping massage (Astym) for Achilles tendinopathy, comparing it to exercise (eccentric contractions). With just eight subjects given Astym, this is a seriously underpowered study, and Astym did not reduce pain significantly. The good news is that Astym results were better as measured by a questionnaire and the (notoriously unreliable) “global rating of change” scale. However, Astym subjects spent much more time with therapists, so there’s a strong chance they benefitted from those interactions — a well known effect — and not the Astym. The modestly positive results here simply cannot be trusted without backup.
- Crothers AL, French SD, Hebert JJ, Walker BF. Spinal manipulative therapy, Graston technique® and placebo for non-specific thoracic spine pain: a randomised controlled trial. Chiropr Man Therap. 2016;24:16. PubMed #27186365 ❐ PainSci #53346 ❐ This study bills itself as the first “fully powered” trial comparing Graston technique® to a placebo (a fair claim to the best of my knowledge). The experiment was fairly careful, large (143 patients), and long term (a year). Disability and pain were the primary outcomes. The results were resoundingly negative: everyone got slowly better, whether they received Graston or a placebo.
- Burke J, Buchberger DJ, Carey-Loghmani MT, et al. A pilot study comparing two manual therapy interventions for carpal tunnel syndrome. J Manipulative Physiol Ther. 2007 Jan;30(1):50–61. PubMed #17224356 ❐
A small clinical trial comparing treatment of carpal tunnel syndrome with standard “soft-tissue mobilization” to “instrument-assisted soft-tissue mobilization” (specifically Graston Technique tools). Both appeared to have modest benefits, but using tools was no better: “the clinical improvements were not different between the 2 manual therapy techniques.”
(See more detailed commentary on this paper.)
- Blanchette MA, Normand MC. Augmented soft tissue mobilization vs natural history in the treatment of lateral epicondylitis: a pilot study. J Manipulative Physiol Ther. 2011 Feb;34(2):123–30. PubMed #21334545 ❐
A small clinical trial comparing treatment of tennis elbow with augmented soft tissue mobilization (tool massage) to “advice on the natural evolution of lateral epicondylitis, computer ergonomics, and stretching exercise.” Both helped a bit, and tools were no better.
- Cheatham SW, Lee M, Cain M, Baker R. The efficacy of instrument assisted soft tissue mobilization: a systematic review. J Can Chiropr Assoc. 2016 Sep;60(3):200–211. PubMed #27713575 ❐ PainSci #53642 ❐
This is the first review of studies of an unusual and controversial massage technique: using tools to “scrape” soft tissue. The authors evaluated seven studies, five of which were controlled, and “the results of the studies were insignificant with both groups displaying equal outcomes.” Although there’s not much good evidence to review, the research so far “challenges the efficacy of IASTM as a treatment for common musculoskeletal pathology.”
One slightly positive note was that there is “some evidence supporting its ability to increase short term joint ROM,” for whatever it’s worth (not much — short term increases in ROM have no clear clinical value in and of themselves). As always, more study is needed, and some benefits might be discovered by studying the right people in the right way, but the first several tests have failed to show any obvious benefit.
- I’m often asked what I think of a treatment that supposedly has a “100% success rate.” Or any percentage over 90, really. It’s the same answer, every time: hyperbolic treatment claims in health care are bollocks (and are almost always part of a sales pitch). Most painful problems are not really one problem. Perfect treatment results are nonsense due to co-morbidities & multiple overlapping etiologies alone. Nothing can treat everything. In fact, nothing can treat anything reliably.
- Woolf CJ. Central sensitization: Implications for the diagnosis and treatment of pain. Pain. 2010 Oct;152(2 Suppl):S2–15. PubMed #20961685 ❐ PainSci #54851 ❐
Pain itself often modifies the way the central nervous system works, so that a patient actually becomes more sensitive and gets more pain with less provocation. That sensitization is called “central sensitization” because it involves changes in the central nervous system (CNS) in particular — the brain and the spinal cord. Victims are not only more sensitive to things that should hurt, but also to ordinary touch and pressure as well. Their pain also “echoes,” fading more slowly than in other people.
For a much more detailed summary of this paper, see Sensitization in Chronic Pain.
- McDonald B, Pittman K, Menezes GB, et al. Intravascular danger signals guide neutrophils to sites of sterile inflammation. Science. 2010 Oct;330mcd(6002):362–6. PubMed #20947763 ❐
Researchers at the University of Calgary Faculty of Medicine are using an innovative new imaging technique to study how white blood cells (called neutrophils) respond to inflammation, and have revealed new targets to inhibit the response. Basically this research explains why neutrophils unnecessarily “swarm” sterile injury sites, causing damage and pain with no direct benefit — a biological glitch with profound implications. Collateral damage!
- Davidson CJ, Ganion LR, Gehlsen GM, et al. Rat tendon morphologic and functional changes resulting from soft tissue mobilization. Med Sci Sports Exerc. 1997 Mar;29(3):313–9. PubMed #9139169 ❐
This small study of rats attempted to demonstrate the possible relevance of Graston Technique to tendon healing. It is cited as the sole example of scientific research supporting the clinical use of Graston Technique. Although it does provide some interesting and positive findings, it is a small study of rats, so it has major limitations. Rat tendons were injured with a collegenase injection, allowed to heal for three weeks, and then some were treated with Graston Technique. Their gait allegedly improved more quickly than in the untreated rats. The authors claim that the results “suggest” that scraping “may promote healing via increased fibroblast recruitment.” Such cautious phrasing is appropriate: although promising, the effect of treatment on five rats is hardly conclusive.
- A 1% rate adverse effect rate is high — but you could do five human studies, using treatment groups of 20 each, encounter only a single example, and you still wouldn’t have a clue about the real statistical risk. Graston Technique poses a real potential danger, yet its safety hasn’t been studied at all. This is precisely the kind of thing that makes peoples heads explode about drugs — foisting serious side effects on the public, no matter how rare, is the stuff of scandal!