Dr. Ida Rolf Institute

Structural Integration: The Journal of the Rolf Institute – Winter/December 2004 – Vol 32 – Nº 04

Volume: 32

What happens in fascia when we touch it? According to Ida Rolf, fascia is a plastic medium capable of responding to manual pressure. Yet, we still don’t know where this adaptability comes from. When we feel a fascial release under our hands, which of the elements in fascia is responding? Is it the collagen or elastin fibers, the fibroblasts or perhaps the ground substance? Can fascia really change its tonus independent of the involved musculature? And finally, how does fascia respond to different types of pressure over varying amounts of time?

If these questions haven’t stirred up your interest or curiosity, take a look at Figure 1. What would you expect to feel when Rolfing this piece of living fascia?

Fascinating questions such as these motivated our group to conduct a basic research project, starting in August, 2003. Our goal was to understand more about fascial plasticity and about fascial responsiveness to manipulation in general. The experiment just described was a small playful excursion during our otherwise more serious scientific research work’. While we plan to publish our research in scientific journals in 2006, an interim report will be delivered at the 5th World Congress on Low Back and Pelvic Pain in November, 2004. This article is our way of sharing our experiences and insights with our bodywork colleagues.

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DRIVEN BY CURIOSITY

One of the scientific starting points of our project was a classic paper by Yahia, et al. on the biomechanical behavior of fascia2. Using the human lumbodorsal fascia, this extensive in vitro study explored the viscoelastic properties of dense connective tissues, such as stress relaxation, and creep. In other words, they measured the degrees of elastic and plastic changes of fascia in response to mechanical loading. During these tests, the researchers also discovered a new and unexpected behavior: When stretched at a constant length, the tensional resistance of the tissue slowly relaxed (as was expected); yet when the same tissue was stretched again after an appropriate time of rest, the tissue had not only regained its original strength, but it proved to be even stronger than before. Termed “ligament contraction,” this remarkable tissue behavior reminded the researchers of a similar stretch response in visceral organ tissue, and they recommended a histological study of the lumbodorsal fascia for contractile cells with smooth muscle properties.

While this particular histological study of fascia has not yet been done, smooth muscle cells (SMC) were discovered in the fascia of the lower leg a few years later; and it was suggested by Staubesand3 and others’ that these intrafascial cells might enable the fascia to contract and relax via the control of the autonomic nervous system, independent of the muscular tonus. While this explanation opens some exciting perspectives for myofascial body workers, it has never been proven, and questions have been raised as to whether the number of such contractile cells in fascia is sufficient to have any significant effects.5

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THE RESEARCH TEAMS

The original group began with two enthusiastic Rolfers fascinated by the diverse properties of fascia and inspired by the possibilities hinted at in the research of Yahia and Staubesand. The project was framed as a Ph.D. dissertation project in human biology. After several months of literature review and personal counseling by Rainer Breul, Ph.D. (a Munich University anatomy professor with a focus on fascia), Jochen Staubesand, Ph.D. (now emeritus professor of anatomy and the first person to discover intrafascial SMCs), and others, we decided to explore these questions following two main methodological approaches. The first approach consists of in vitro contraction tests of fresh fascia strips in response to chemical, electrical and mechanical stimulation, and the second approach is a histological study of contractile cells in human lumbar fascia.

Since those early days, the scope of the project has gained momentum and increased substantially, and now includes several research teams at different universities. Although more than a dozen people are involved, their activities are primarily coordinated by the three authors of this report.

The in vitro contraction test (IVCT) team now proudly runs a special “Fascia Research Lab” at the Department of Applied Physiology, University of Ulm, Germany (Fig. 3). Under the guidance of the head of the department, Frank Lehmann-Horn, Ph.D., we conduct in vitro tests with fresh strips of animal and human fascia. The histological team is led by Joerg Massmann, Ph.D., a former colleague of Dr. Staubesand and presently a leading researcher on SMC anomalies. Since October, 2003, his Munich team of histologists has been working regularly on our fascia research project (Fig. 2). Using monoclonal antibodies, more than 90 immunohistochemical analyses of fascia have been carried out so far, most of them with tissue sections from human lumbar fascia.

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STARTING OUR OWN FASCIA RESEARCH LAB

After having conducted the initial test runs in a commercial lab over several months, Dr. Lehmann Horn’s offer to use his university lab for our research provided a giant step forward for our project. With technical assistance, we successfully modified the unique muscle-IVCT equipment, for which the department is well known, to suit our specific needs. With this state-of-the-art equipment we can perform computer-assisted tensional force measurements of fascia slips, which are suspended in equilibrated physiological solution, with controlled temperatures and a constant supply of 95% oxygen and 5%o carbon gas. These ideal physiological test conditions allow us to keep cellular responsiveness in fascia alive for up to six hours during our in vitro tests (Fig. 8).

About half of the fascia we use is pig tissue, which we collect early in the morning from the local slaughterhouse. Our other samples are from lab mice, and since September 2004 we have had the privilege of acquiring fresh samples of human fascia lata once a week from the surgery.

INTERNATIONAL NETWORKING CONTACTS

We are working in conjunction with Myron Spector, Ph.D., and his group at the Harvard-M.I.T. Division of Health Sciences in Boston. Their research is focused on the ability of connective tissue cells to become contractile6. It was their suggestion to use the cytokine TGF-beta as a contraction stimulant in our current in vitro studies. We have also received the support of Jochen Staubesand, Ph.D., from Freiburg, Germany, and Giulio Gabbiani, Ph.D., from Geneva, an international authority on myofibroblasts.

Our collaboration with Priscilla Barker’s team at Melbourne University, which is studying the innervation of the human lumbar fascia, has been another source of inspiration. Currently they are repeating and expanding on an earlier histological study by Bednar’, who found no evidence of sensory nerve endings in the lumbar fascia in low back pain patients as compared with healthy people. While this finding may concur with the observed lack of proprioceptive accuracy in low back pain patients’ experience of their pelvis and lower back position’, it is also reminiscent of a similar correlation between diminished peripheral sensation and a distorted cortical perception in phantom pain and tinnitus9″0. If verified, these insights could open exciting avenues and further research into proprioceptive training as well as a specific manual stimulation of fascial mechanoreceptors to facilitate an increased development and function in these receptors. Barker’s research group will also present their results at the upcoming world congress in Melbourne and both teams are eagerly anticipating exchanging their experiences.

LEARNING FROM OTHERS

An important part of our research project has been and continues to be a thorough review of all the current literature in our field. This is how we learned that connective tissue cells are now considered to be quite similar to fetal stem cells, i.e., they are cells which are still fairly undifferentiated and therefore maintain the ability to adapt their nature to different functional needs. All fibroblasts (FB), for example, maintain the ability to become contractile by expressing smooth muscle (SM) actin stress fibers as well as special focal adhesions on their membrane. Not only FBs, but also chondroblasts and osteoblasts can change their morphology to become “connective tissue cells with muscle”6. For FBs this hap-pens regularly in wound healing as well as in pathological tissue contractures, such as palmar fibromatosis (Dupuytreri s disease), frozen shoulder”, Peyronie’s disease, plantar fibromatosis, or club foot12.

Yet the same kind of contractile cells have also been found to make up a significant portion of the FBs in healthy people: e.g., in the anterior cruciate ligament of the knee 13, the Achilles tendon, the periodontal ligament, or in digital flexor tendons. When taking the maximum contraction force of such cells as determined in a cell culture and multiplying that by their reported density, it seems clear to us that the outcome could be sufficient to allow a significant and palpable effect on local tissue tension.

Our original hypothesis, which is shared by Professor Staubesand, was that the contractile cells in fascia would probably have the same physiology and innervation as visceral or vascular SMCs. This hypothesis had a certain appeal to the manual therapists in our team, since its verification would nicely support Staubesand’s credo of an intimate two-way connection between fascia and the autonomic nervous system. Nevertheless, this hypothesis now appears unlikely to be substantiated in the light of recent advances in FB research. Here’s why: FBs exist in a certain heterogeneity. Those phenotypes which contain SM-actin stress fibers are often called myofibroblasts (MFB), and many of those have several features in common with SMCs. Yet MFBs have been clearly shown to express different proteins and to use different messenger substances and energy processes for contraction than SMCs. While most SMCs can be easily influenced by input from either sympathetic or parasympathetic nerves, contraction of MFBs is regulated by specific cytokines (like TGF, or fibronectin) and by mechanical tension.14

IN VITRO FASCIAL CONTRACTION

Now we’d like to share some of our discoveries with you, starting with our first line of approach, the in vitro tests at our Fascia Research Lab. Similar to the classic experiments of Yahia, we suspend strips of lumbar fascia in a physiological organ bath (Fig. 5). Both ends of the strip are attached to a computerized testing apparatus, which can both elongate the strip in a controlled fashion and also measure the resistance force with a precision of 100 nano-Newtons. When working with pig fascia, we use strips of 40 mm x 5 mm x 1 mm; when testing the lumbar fascia in humans or mice, our strips are about half that size (Fig. 4).

We were able to show that Yahia’s observed “ligament contraction” not only happens in human fascia, but also in mice and pigs; i.e., when we stretch a fascial strip for 15 minutes, allow it to rest for 30 minutes, and then stretch it again, the tissue resistance tends to be stronger the -second time. In May of this year, we began to repeat the same tests with fascia in which the cells had been destroyed by deep freezing in liquid nitrogen and subsequent rapid thawing. We wondered if we still could get a similar “Yahia effect” of a relative contraction at the repeated stretch with these tissue samples? And yes, we clearly did, although to a slightly lesser degree. This now leads us to believe that the observed contraction does involve, at least partially, some non-cellular factors.

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WATER,THE SURPRISING ELEMENT

Based on the contributions of Alfred Pischingerl3, James Oschman16 and MaeWan Ho17, we began to look at the water content in the ground substance. By carefully measuring the wet weight of our fascial strips at different experimental stages, plus the final dry weight (after later drying the strips in an oven), we found the following pattern: during the isometric stretch period, water is extruded, which is then refilled in the following rest period. Interestingly, if the stretch is strong enough and the following rest period long enough, more water soaks into the ground substance than before. The water content then increases to an even higher level than before the stretch.18

Could this be the explanation for the observed “ligament contraction” in both Yahia’s and our experiments? In the literature we found mixed information on the effect of increased hydration on connective tissues: some studies (e.g., with cartilage) show that increased hydration leads to an increase in stiffness, others show an opposite tendency. To clarify the effect of hydration on our tissues, we performed a series of tests in which we replaced our usual physiological solution with distilled water (which tends to increase tissue hydration) or with 251/,, sucrose (which dehydrates the tissue). The results were quite clear: Increased hydration increases the elastic modulus, i.e. the stiffness.

The picture starts to look like this to us. When fascia is being stretched, water is being extruded from the ground substance and simultaneously there are some temporary relaxation changes in the longitudinal arrangement of the collagen fibers. When the stretch is finished, the longitudinal relaxation of the fibers takes a few minutes to revert (provided the strain has not been too strong and there have been no microinjuries); yet the water continues to be soaked up into the tissue, to the degree that the tissue even swells and becomes stiffer than before.

One possible and profound conclusion is that: fascia seems to adapt with very complex and dynamic water changes to mechanical stimuli, to the degree that the matrix reacts in smooth-muscle-like contraction and relaxation responses of the whole tissue. It seems likely that much of what we do with our hands in structural integration and the tissue response we experience may not be related to cellular or collagen arrangement changes, but to sponge-like squeezing and refilling effects in the semiliquid ground substance with its intricate scrub-like arrangement of water-binding glycosaminoglycans and proteoglycans. Since age-related tissue changes are associated with a decreased water content, this brings up the question: could slow but strong tissue draining moves that are a part of our work prove to increase hydration?

Future studies with in vivo measurements of the tissue water content, taken hours and days after such treatments, might offer interesting “anti-aging” perspectives for our field.

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CELLULAR CONTRACTION

Nevertheless, at this time we believe that there is probably also a cellular effect, which may allow a slow fascial contraction. Our reasoning behind this is based on the literature study of such fairly common fascial contractures as frozen shoulder, palmar fibromatosis, or club foot. Recent studies have shown that these aberrations are due to cellular contraction within fascia; and that the amount of contraction is a response to mechanical stress as well as specific chemical messengers. If such adaptive processes show up pathologically in different parts of the body, it seems also probable – although not certain – that there also exists a span of different degrees of fascial contracture among normal healthy people. Interestingly, palmar fibromatosis rarely disappears without any intervention, whereas such spontaneous improvements are quite common in frozen shoulder. This makes us wonder whether similar fascial contractures exist to a minor degree in normal people and that some of these may have the same temporary nature and spontaneous responsiveness as was observed in the examples of frozen shoulder.

It was our advisor, Professor Breul, who made the suggestion to build a testing apparatus in which. we could perform IVCTs with fresh pig fascia to test the response to several chemical stimulatory transmitters (Fig. 6). Based on Staubesand’s suggestion that the contractile cells within fascia would most likely be sympathetically innervated and may work like SMCs, we conducted our first test rows with the addition of the sympathetic neurotransmitter adrenaline.

Although three of our first tests did appear to elicit a contractile response (and we consequently toasted one evening with a small bottle of Champagne), more than 30 tests later we now believe that those results were mere statistical deviations and that adrenaline does not have any significant effect on fascial contraction, at least not within a time period of up to 45 minutes.

After gathering suggestions from several different experts, we then tested other substances and solutions, such as acetylcholine, caffeine, and a depolarizing potassium solution – all without any significant statistical effect. Since each substance needed to be tested on different samples and protocols, the testing with just these three solutions kept us busy for several weeks.

We also got some positive responses. When we tested two SM relaxants that are known as vasodilators (nifedipin and glyceroltrinitrate), we got a significant relaxation effect with the second one (Fig. 7). This second substance works as a NO-donator, i.e. it produces nitrous oxide, which acts as a gaseous transmitter and can pass through most of the body’s membranes. Additionally, we got a significant effect in response to electrical stimulation: a frequency of 5 Hz showed a clear force increase, and a stimulation with 20 Hz a decrease.

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Since by then we had become obsessed with constantly questioning our results and checking for possible experimental artifacts, we observed one day how in most of the 20-Hz applications there was a slightly stronger turbulence in the solution than without electrical stimulation. While such processes, known as electrophoresis, are hard to prevent, we finally came up with an idea to check their effect upon our force measurements with a piece of thin elastic rubber replacing our fascial strips. Would we still get a similar response pattern from the different electrical stimulations? Yes, we did. We therefore concluded that our previously observed electrical effect on fascia was a mere experimental artifact of the electric stimulation, and not due to a change it cellular contraction.

Currently we are following Gabbiani s suggestions by checking our fascial strips with one-hour-long protocols for a response to the agents endothelin-1, histamine, and angiotensine, as well as with a four-hour long protocol with the cytokine TGF-beta. While we have not completed these time-consuming tests, our preliminary results already indicate a contractile effect of histamine.

OUR HISTOLOGICAL DISCOVERIES

What did we find out with our second line of approach, the tissue analysis via immunohistology (IH)? With good luck, enthusiasm, private money, patience, and a lot of paperwork we managed to establish a clinical support network in Munich and to obtain fresh tissue sections from human autopsies. Within one day after death, small samples of fascia are taken out, put in formaldehyde and brought by courier to our histology lab. Here they are first embedded in paraffin and then stored until we start our IH procedure. Consisting of 18 steps, the IH treatment includes the application of a special antibody that marks only those cells that contain alpha-SM-actin stress fibers and are considered to be contractile. The really interesting part for us is in the following days, as we watch those cells under special microscopes. Our sense of excitement in this particular part of our work comes from the fact that this is, to our knowledge, the first time that contractile cells in fascia have been systematically observed in normal people, and that patterns in the arrangement and density of these cells can be recognized.

Fig. 9 shows the results of IH analysis of the lumbar fascia from eleven human cadavers. We found FBs containing alpha-SMactin in all specimens. Mean density of these cells in longitudinal sections was 79 per mm’. Assuming the known potential force of MFBs, the amount of cells could be sufficient to result in significant fascial contractions, such as in compartment syndrome. Interestingly, the density of contractile cells was statistically higher in our younger age group (<32 yrs) than in the two older groups. However, one cadaver of an elderly person exhibited a high number of stained FBs. Unfortunately there is no information on the physical activity of this individual.

We also discovered that there is a positive correlation between the density of contractile cells and the amount of crimp formation (waves) in collagen fibers. That is, in areas with a more straight fiber arrangement, hardly any contractile cells are found; whereas their density is much higher in areas with more wave-like collagen fibers (Fig. 10). At this stage we do not know the causal relationship behind this correlation. It could be that the cellular contraction creates the waves (which is what some authors suggest for the contractile FBs in tendons”); and it could be also that a FB suspension between waves increases tensional input to the FBs in everyday usage, so that these cells are stimulated to become more contractile.

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Interestingly, when doing the same IH analysis with the lumbar fascia of two of our young lab mice, we found an amazing density of FBs; yet none of them had any SM-actin stress fibers. Before jumping to any premature conclusions, we decided to wait for the IH results from the following tissues, which we had already collected: lumbar fascia and fascia lata of five more mice; lumbar fascia and fascia lata of six pigs; and fascia lata and plantar fascia of five humans. We expect that the results will help us to understand more about the general function of contractile cells in fascia. It is possible that we may discover that the existence of such cells is primarily related to micro-injuries and resultant repair processes. On the other hand, it is also possible that they will suggest that density of such cells is mainly driven by everyday tensional stimulation (as our observed correlation with the amount of collagen crimp seems to indicate). This would support the notion that fascial contractility serves indeed as a secondary and adaptable tension control system in the body.

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TREASURES AHEAD

This research project continues to feel like a real “treasure hunt” to all of us involved. Already at this stage we are certain that our results will contribute towards shifting the traditional concept of fascia as a passive tension-transmitter to a new picture of fascia as a dynamically adaptable organ. Together with the work of Barker, et al. on the sensory innervation of fascia, our findings support the notion of both Andrew Taylor Still and Ida Rolf that fascia is much more alive and responsive than commonly assumed and that working through this adaptable medium can have profound effects on the whole organism.

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Additionally, our research may shed some light upon – and open new therapeutic avenues for – pathological conditions that are associated with an increased or decreased fascial tone. Examples include: plantar fasciitis; fibromyalgia; compartment syndromes (including those in lower arms and erector spinae); carpal tunnel syndrome; flat foot; fascial contractures (as in frozen shoulder, Dupuytreri s disease, plantar fibromatosis, or club foot); and several of the common muscular contractures, such as tensional headache, low back pain, tennis or golfer’s elbow, etc.

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As far as we know, we are currently the only experimental research group on fascial contractility in normal (healthy) people. Unless we stumble unintentionally onto some pharmaceutically marketable insights, it is unlikely that we will receive any government or industry funding. And although it may be partially disappointing, it is indeed understandable and reasonable that the Rolf Institute’s research committee feels obliged to the membership to invest their funds in clinical research that proves the efficiency of structural integration, rather than into basic research. By definition, the outcome of basic research is unpredictable. Yet we feel that finding out more about what is still unknown about our work is most needed in our field, and that that is how we can best foster the development or our work.

Fig.11: Happy Brainstormers at the “Berlin Think Tank”: Divo Gitta Muller, Robert Schleip, Adjo Zorn Ph.D.

Currently our research is driven entirely by our personal passion. It is financed out of our own private practices, and supported by a lot of volunteer work and free service from other people and institutions, whom we have managed to infect with our enthusiasm. Our sincere appreciation also goes to the European Rolfing Association, which continues to support us in many helpful ways.

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We feel quite honored and privileged to be invited to present our interim results at the upcoming 5th Interdisciplinary World Congress on Low Back and Pelvic Pain’, and we expect this to attract some attention and networking contacts for our project. We feel that this remarkable invitation is also reflective of a general increase in interest in fascia among low back pain researchers. We plan to publish our results in scientific journals in 2006, and will of course also continue to share our discoveries and questions with you, our fascial bodywork colleagues. If you, dear reader, know of any private person or a foundation with the means and willingness to support such a unique research project, please do connect them with us 20. And yes, we love to have more people join in our efforts and network with us in what feels like an important and exciting journey of discovery (Fig. 11).

Last but not least: our research has changed our Rolfing work. Our insights about the scrub-like water binding nature of the semifluid matrix now bring up images and a more detailed caring for the sponge-squeezing and refilling effects of our work. It suddenly makes new sense why a repeated slow-draining stroke, followed by appropriate rest, sometimes makes all the difference. And why such treatment often works wonders in rejuvenating dried-out tissues. On the other hand, having observed thousands of spindle-shaped cells floating in the collagenous matrix in our microscopes, our working fingers now frequently feel like they are contacting similar fish-like creatures under our hands (Fig. 12). Such beautiful and enriching touch perceptions already make the whole journey worthwhile for us. Yet they also foster our growing curiosity. Wouldn’t it be nice to understand even more about these subtle tissue responses under our hands?

NOTES

1. Our subjective impression in this experiment was that we felt a similar responsiveness to our experience of working with fascia in the living human body. Of course, aside from the obvious possibility of human interaction, we were also missing the response transmission from many external factors, such as connected musculature, breathing, etc.

2. Yahia L, et al. 1993: “Viscoelastic properties of the human lumbodorsal fascia.” J Biomed Eng 15 (9): 425-429.

3. Staubesand J, et al. 1997: “La structure fine de l’aponevrose jambiere.” Phlebologie 50(l):105-113.

4. Chaitow L 2004 “Signposts” (Editorial), Journal of Bodywork and Movement Therapies 8 (2): 77-79.

5. Gaggini L, Beech M 1998: “How Rolfing° Produces Change.” Rolf Lines 26 (5): 30-34.

6. Spector M 2001: “Musculoskeletal connective tissue cells with muscle: expression of muscle actin in and contraction of fibroblasts, chondrocytes, and osteoblasts.” Wound Rep Reg 9: 11-18.

7. Bednar DA, et al. 1995: “Observations on the pathomorphology of the thoracolumbar fascia in chronic mechanical back pain.” Spine 20(1): 1161-64.

8. Radebold A 2001: “Impaired postural control of the lumbar spine is associated with delayed muscle response times in patients with chronic idiopathic low back pain.” Spine 26(7): 724-30.

9. Karl A 2004: “Neuroelectric source imaging of steady-state movement-related cortical potentials in human upper extremity amputees with and without phantom limb pain.” Pain, 110(1-2):90-102.

10. Bauer CA 2004: “Mechanisms of tinnitus generation.” Curr Opin Otolaryngol Head Neck Sur 12(5): 413-7.

11. Bunker TD, Anthony PP 1995 “The pathology of frozen shoulder – a Dupuytrenlike disease.” J Bone Joint Surg 77B(5)67783.

12. Sano H et al. 1998: “Pathogenesis of softtissue contracture in club foot.” J Bone Joint Surg 80B(4): 641-44.

13. Murray MM, Spector M 1999: “Fibroblast distribution in the anteromedial bundle of the human anterior cruciate ligament: the presence of alpha smooth muscle actin-positive cells.” I Orthop Res 17: 18-27.

14. Hinz B, Gabbiani G 2003: “Mechanism of force generation and transmission by fibroblasts.” Curr Opin Biotechn 14: 538-546.

15. Pischinger A 1991: “Matrix and matrix regulation: basis for a holistic theory in medicine.” Medicina Biologica, Brussels.

16. Oschman J 2003: Energy Medicine in Therapeutics and Human Performance. Butter worth-Heinemann/Elsevier, Amsterdam.

17. Ho M-W 1999: The Rainbow and the Worm – The Physics of Organisms. World Scientific Publ., Singapore.

18. Using a 6% tissue elongation over 15 minutes, followed by rest, we got the following average weight changes (compared with the state before the stretch; n=21): at end of stretch: -11.8%; after 30 min. rest: – 0.3%; after one hr.: 0%; after two hrs.: +2.1’/r,; after three hrs.: +3.6%.

19. Ralphs JR, et al. 2002: “Actin stress fibres and cell-cell adhesion molecules in tendons.” Matrix Biol 21: 67-74.

20. Internet: www.fasciaresearch.com Email: [email protected]

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