Fascia Research

Friday, February 18, 2011
The explosion of fascia research

This posting is a modified version of an article I have written for a British cranial osteopathic publication.

Because I am actively involved in the organizational aspects of next year’s Fascia Research Congress in Vancouver I have had only a limited amount of time to give to writing for the blog – hence this recycled – but I hope interesting – update on fascia.

When I was studying osteopathy in the late 1950s (BCNO – now BCOM) fascia entered into the lessons and lectures as a somewhat mysterious part of the economy of the body. It featured large in the historical aspects of osteopathy’s evolution, with early pioneers referring to its all-pervading nature – it was everywhere, and there were theories and assertions as to its relevance, but there was very little that was rooted in science. (Still 1902)

So, the question remained – what did fascia do?

Clues were to be found in American osteopathic writing. For example, decades ahead of his time Cathie (1974) described fascia’s potential for contractility as well as its rich neural supply – features that would not be validated by research until very recently. (Schleip 2006, Stecco 2008).

Osteopaths – and others – in the USA (Little 1969, Taylor 1958, Rolf 1962) made it clear that that fascia was not just a background material, with little function apart from its obvious supporting role, but rather a widespread, tenacious, connective tissue involved deeply in almost all of the fundamental processes of the body’s structure, function and metabolism.

In therapeutic terms it became clear there can be little logic in trying to consider muscles and joints as separate structures from fascia, because they are so intimately related. Remove connective tissue from the scene and any muscle left would be a jelly-like structure without form or functional ability, and joints would quite simply fall apart. (Cantu et al 1992)

We now know that there exists a state of structural and functional continuity between all of the body’s hard and soft tissues, with fascia being the ubiquitous elastic–plastic, gluey, component that invests, supports and separates, connects and divides, wraps and gives cohesion, to the rest of the body – the fascial, connective tissue network. (Ingber 2008, Myers 2009)

Any tendency to think of a local dysfunction, as existing in isolation needs to be discouraged as we try to visualize a complex, interrelated, symbiotically functioning assortment of tissues, comprising skin, muscles, ligaments, tendons and bone, as well as the neural structures, blood and lymph channels, and vessels that bisect and invest these tissues – all given shape, form and functional ability by the fascia. (Schleip 2006, Ingber 2008, Solomonow 2009)

Fascial function and dysfunction revealed

Fascia, when healthy, forms a gliding interface with underlying muscle [allowing] free excursion of the muscle under the relatively immobile skin. A plane of potential movement exists in the form of the areolar tissue layer, apparently lined with a lubricant, hyaluronic acid. (McCombe et al 2001)

This process of ‘sliding fascia’ can now be visualised, using real-time ultrasound and elastography – as was demonstrated recently by Langevin (2010b). Dramatic video images demonstrated the free movement of lumbodorsal fascia in pain free individuals, contrasted with that of individuals with low back pain.

Similar images were displayed of myofascial trigger points, during the same panel presentation, that I co-chaired (Shah 2010). Both elastography and ultrasound images show trigger points to be denser than surrounding, normal, tissue.

When fascia is excessively mechanically stressed, inflamed or immobile, collagen and matrix deposition becomes disorganized, resulting in fibrosis and adhesions, and fascial ‘thickening’ (Langevin et al 2009), also described as ‘densification’ (Stecco et al 2009). This process involves distortion of myofascial relationships, altering muscle balance and proprioception. Consequent binding among layers, that should stretch, glide and/or shift on each other, potentially impairs motor function (Fourie 2009), and leads to chronic tissue loading, which contributes to ‘global soft tissue holding patterns’ (Myers 2009).

Cramer et al (2010) in rat studies showed that “hypomobility results in time-dependent adhesion development within the zygapophyseal joints”. Such adhesion development may have relevance to spinal manipulation, which could theoretically break up Z joint intra-articular adhesions”

Some therapeutic implications

A review by Schleip (2003) has documented both myelinated and unmyelinated fibers in fascia, including sympathetic endings. Stecco et al. (2008) found that the outer layers of the deep fascia contained a rich vascular and nerve supply, with intrafascial nerve fibres seen throughout. Some of these were presumed to be stretch receptors.

Bialowski (2008) has hypothesised that mechanical force (soft tissue & manipulative) initiates neurophysiological responses – peripheral and central – possibly evoking and explaining the clinical outcomes of manual therapy. These hypotheses have been expanded on by Simmonds et al (2011) who suggest that HVLA manipulative therapies (i.e. rapid) stimulate fascial tissues (as in the Z-joint example described earlier), while myofascial therapies (such as myofascial release and muscle energy technique) deliberately stimulate fascial tissues

Langevin’s in vivo and in vitro studies have shown that loose connective tissue responds to light tissue stretch, which “may be key to the therapeutic mechanism of treatments using mechanical stimulation of connective tissue” (Langevin & Sherman 2006, Langevin 2010a)

Myers (2010) suggests that stretching can be applied not only to ‘length’ problems, but also to ‘stuck layer’ problems, using shear stress to allow the restoration of increased relative movement between the adjacent planes of fascia (Schwind 2004)

In Germany, Pohl (2010) has demonstrated, using real-time ultrasound imaging, changes in collagen density in various layers of skin before and after connective tissue massage (CTM) involving skin rolling

Mechanotransduction and strain transmission

What has now been established is the remarkable degree to which muscular effort depends on the multiple links that muscles have with connective tissue structures.

These connections mean that – for example – a hamstring stretch will produce 240% of the resulting strain in the Iliotibial tract – and 145% in the ipsilateral lumbar fascia – compared with the hamstrings.

The process of strain transmission that occurs during stretching, involves many other tissues beyond the muscle that is being targeted, largely due to fascial connections, making the use of the word ‘isolated’ – together with ‘stretching’ – difficult to justify. (Franklyn-Miller et al 2009)

A fascial hydraulic effect?

Klingler & Schleip (2004), at the University of Ulm, measured wet & dry “freshly harvested” human fascia and found that during an isometric stretch, water is extruded, refilling afterwards. As water extrudes temporary relaxation occurs in the longitudinal arrangement of the affected collagen fibres. If only moderate strain is involved there are no micro-injuries, and water soaks back into the tissue until it swells, becoming stiffer again. It therefore seems that some tissue responses to manual therapy may relate to this sponge-like squeezing and refilling in the semi-liquid ground-substance, with its water binding glycosaminoglycans and proteoglycans.

Fascia related therapeutic approaches

The range of methods and modalities that focus attention on fascial dysfunction are proliferating. A few of those where a degree of supporting validation exists are summarised below :

· Heat in the therapeutic range, relaxes many fascial contractures associated with myofascial dysfunction. External heat has been shown to be beneficial in low back pain (Klingler 2011)

· Graston Technique® (GT) is an instrument-assisted soft tissue assessment and mobilization method delivering load deformation via stainless steel instruments. Mechanical deformation influences the extracellular matrix (ECM,) modulating the synthesis of proteoglycans and collagen by fibroblasts, increasing collagen formation (Hammer 2007)

· Neurologically active scars can restrict back flexion, which the patient feels as low back pain. This can be relieved by treatment of scars on the abdomen and/or below the symphysis (Kobesová, 2007)

· Fryer & Fossum have suggested that apart from the influence of mechanoreceptors on pain (via both ascending and descending pathways), Muscle Energy Techniques induce in-vivo mechanical stretching of fibro-blasts that both alters interstitial osmotic pressure as well as increasing blood flow, so reducing concentrations of pro-inflammatory cytokines, reducing sensitization of peripheral nociceptors.

· Standley & Meltzer (2008) have demonstrated – on a cellular level – the beneficial effects, on fibroblasts, of both myofascial release and positional release (Strain/counterstrain) methods. “……strain direction, frequency and duration, impact important fibroblast physiological functions known to mediate pain, inflammation and ROM….”

· Borgini et al (2010) have demonstrated the influence of direct compressive force on dense fascial restrictions, using the Italian modality developed at the University of Padua, Fascial Manipulation®

· The benefits of Connective Tissue Massage have been demonstrated in a number of clinical trials – notably in relation to chronic pelvic pain (Fitzgerald 2009)

· The methods used in structural integration (Rolfing) are directed mainly at fascia and connective tissue, which are treated with fingers, open hands, clenched fists, and elbows, with pressure directed to release adhesions between what should be freely sliding structures. (Findley & Schleip 2007)

· Fernandez-de-las-Penas and Pilat (2010) have described the successful use of neuromuscular technique (NMT) in treatment of myofascial pain

Much more to learn

What has emerged from the first two Fascia research conferences – Boston 2007 and Amsterdam 2009 – suggests that there is far more yet to learn.

These conferences brought clinicians of all schools, together with scientific researchers, in the hope and expectation that this would lead to a cross-fertilization, in which the clinical needs, confusions and questions of practitioners and therapists would inform researchers, who in turn would help clinicians to better understand the real nature of fascial structure and function, in relation to their patient’s problems and their own therapeutic efforts. It was further hoped that researchers would be spurred to new directions of study fascia.

And this has happened, and continues, with studies emerging at a remarkable pace, that have further clarified the nature and multiple functions and roles of fascia in the body.

The theme of the 3rd Fascia Research Congress (Vancouver, Canada, March 28 – 30, 2012) will be: Fascia: What do we know? What do we feel? Continuing the Scientist/Clinician Dialogue.

As the organising committee have said : The 2012 Fascia Congress will centre on the latest and best research on human fasciae. Additionally—and recognizing the interests of clinicians in gaining insights that will bear on practical applications—the program will be designed to include more presentation time to relating the research findings to clinical issues, particularly the practical applications of fascial layers.”

The conference proper will be preceded (March 23-27) by a Fascial Dissection Workshop, with a range of additional pre and post-conference workshops, on March 27th and March 31st .

At this early stage the planning for the Vancouver conference is already advanced.

For example, among the confirmed keynote speakers are:

· Cesar Fernandez de las Penas DO PhD : Muscular and fascial aspects of myofascial Pain

· Al Banes PhD : Mechanical Loading and Fascial Changes – Tendon Focus

· Karen Sherman PhD : Existing trials on fascia in the context of manual therapies

· Carla Stecco MD : Fascial Anatomy Overview

· Dr. Rolf K. Reed : Fluid Dynamics and fascia (lymph, circulation etc)

· Mary Francis Barbe : Changes in Fascia Related to Repetitive Motion Disorders

A number of panel sessions are also in the planning stage that will highlight the needs and interests of all clinicians – including exploration of modern imaging methods

· The conference website is http://www.fasciacongress.org/2012/

· A call for Abstracts will soon be displayed on that website

Proceeding books and DVDs from the 2007 and 2009 congresses can be purchased via this link

British Osteopathic representation in fascia research?

There has to date been little evidence of interest from British osteopaths in current fascial research or the Research Congresses. In contrast, senior members of the American osteopathic profession (including Brian Degenhardt, Michael Kuchera, Frank Willard) are active in research as well as promotion of this trend via participation in the organisation of the 3rd Congress (Vancouver 2012). For example Dr Kuchera is co-chair of the Scientific Committee, of which I am a member, as are several US based chiropractic researchers.

The possibilities for active involvement in the next congress, via submission of abstracts, is something I would encourage British DOs to consider. In my studies of cranial concepts, the intercranial structures (Tentorium cerebelli, Falx cerebri and others) were always central considerations. Has there been any cranial research that could stand scrutiny in the form of an abstract – and/or possible oral presentation? Are there perhaps a series of cases that could be described, written up, presented?

And if not now – when?


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