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Integrated Bodywork

By Leon Chaitow, ND, DO

About the Columnist
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Newly Identified Self-Repair Methods

Implications for manual therapists.

In June of 2009, Massage Today published my article titled "Research in Water and Fascia: Micro-tornadoes, hydrogenated diamonds & nanocrystals." In this issue, I will describe important new evidence of fascia's ability to self-regulate, maintain and repair itself, as it performs its' multiple vital tasks – with the stabilizing contribution of water, forming part of the process. For readers who are unfamiliar with fascia's many roles, I have summarized some of the more important of these in Box 1 - with notes on one aspect – mechanotransduction in Box 2.

Fascia Self-healing

Fascial/connective tissue – which is made up of the triple-helix of fibrillary collagen (Figure 1), the primary building block of connective tissue/fascia - organizes itself into a supporting scaffolding that supports, separates and shapes the extracellular matrix, tendons, bones, and other load-bearing structures.

Newly Identified Self-Repair Methods - Copyright – Stock Photo / Register Mark The triple helix of collagen fibrils, showing the cross-links that, together with external tension, and water. support them. These fibrils have cleavage sites, 1 millionth of a meter apart, that can buckle and self-repair, when stabilizing tension features are inadequate - as described in the text.
(Dittmore 2016)
New research by Dittmore, et al., (2016) has been able to describe experimental evidence as to how collagen operates a self-healing process. These researchers have identified what they call "cleavage-vulnerable binding regions" on collagen fibrils, at tiny intervals of 1 micron (a millionth of a meter) apart.

It seems that when collagen fibrils are lined up, with their molecules in a more-or-less straight conformation (demanding high energy to resist the tendency to uncoil) the fibrils periodically accumulate so much internal strain, that "buckling" occurs at the cleavage sites. This exposes collagen, so allowing enzymes (specialized matrix metallo-proteinases or MMPs) to bind to and degrade the collagen, before an almost immediate process (taking seconds) starts, of repair and remodeling.

This research suggests that fibrillar collagen self-regulates its own maintenance in this way, by constantly repairing collagen on a cellular level. They – and other researchers - have observed the importance of tissue tension in this process, suggesting that the self-repair, remodeling sequence is tension-dependent, meaning that repair may be delayed (i.e. made less necessary) if stabilization tension in the tissues is adequate.

Other researchers, such as Susilo, et al. (2016), have also reported that, "mechanical loading induces stabilizing changes internal to the fibrils themselves, or in the fibril-fibril interactions."

Box 1
FASCIA (Chaitow 2014):

  • Binds, packs, protects, envelopes and separates tissues.
  • Invests and connects structures, providing scaffolding that permits and enhances transmission of forces.
  • Has sensory functions – neural and biomechanical (see Box 2) - from the microscopic level (e.g. cell to cell communication) to large fascial sheets, such as the thoracolumbar fascia (TLF), that transfers load - for example from the legs to the shoulders, and beyond.
  • Facilitates tissues sliding and gliding on each other.
  • Allows energy-storage – acting in a spring-like manner via fascial structures - e.g. large tendons and aponeuroses of the leg.
  • Supports the multiple functions of the connective tissue matrix, combining strength and elasticity – biotensegrity.
Bhole, et al. (2009), have noted that "contractile forces of the cell, stresses exerted through changes during development, interstitial fluid pressure, and physical activity, alter the strain on fibrils and reinforce collagen in the direction of loading." We should also consider the role of respiration, and other rhythmic mechanical features – such as the cardiac pulse, intestinal contractions, etc., as these all generate movement, and might therefore influence local collagen cleavage sites (Gracovetsky 2016).

Collagen fibrils contain billions of minute sites that are vulnerable to buckling, if internally or externally derived forces fail to maintain optimal tension. A triple helix collagen fibril that is not under adequate external tension spontaneously forms buckling (cleavage) sites at approximately 1 micron intervals. However, if the fibril is under appropriate tension, the number of buckling sites decreases, and if tension is sufficiently high, there are no buckling (cleavage) sites.

Buckling exposes collagen to specific enzymes (MMPs) at these cleavage site, initiating the enzyme-related degradation and subsequent repair process that strengthens and maintains the fibrils. These findings raise the possibility that externally applied load via exercise, or the application of compression/shear force/stretching, might be capable of influencing this apparently constant operation.

Box 2
Mechanotransduction (Chaitow 2014):

  • The shape & architecture of cells determines their function – independent of neural influences.
  • Loading and unloading tissues modifies cellular architectural/shape features, and changes gene expression and function.
  • Different degrees, durations and directions of biomechanical load applied to soft-tissues (compression, stretch, friction, shear-force etc) can have quite different effects – possibly inducing relaxation, or increased tension, or production of inflammatory products, or reductions of these – as examples.
  • The effects of modelled myofascial release (loading) and counterstrain (unloading), on human fibroblasts (the precursors of fascial molecules), leads to biochemical cellular responses - including changes in gene expression, interleukin secretion and myoblast differentiation.
This leaves open the question of the implications to self-regulation of what happens to the process (and to collagen) if there is excessive tension, for lengthy periods? It is of interest to note that these self-regulating processes operate via mechanisms that are independent of the nervous system - being dependent on force transmission/load transfer, fluid dynamics and mechanotransduction mechanisms (amongst others) (Humphrey et al., 2014) Many  studies have observed that tightly bound water helps to stabilize the triple-helix collagen fibrils (Leikin 1997, Bella 2016, De Simone et al 2008).

Clinical Relevance

Rather than speculating – it may be safer to ask a few questions – to which answers will eventually be found (if not already obvious):

  • In what ways might exercise, and/or movement therapies (Yoga, Tai chi, Pilates, Feldenkrais, etc.) influence the tension status – and therefore the repair mechanisms -  of associated collagen fibrils?
  • In what ways do externally applied loads, via manual therapies (massage, osteopathy, chiropractic, physical therapy etc) and active exercise, influence the tension status – and therefore the repair mechanisms - of associated collagen fibrils?
  • If collagen self-repair is tension-dependent - as suggested by Dittmore et al - in what ways might the "unloading" of excessively tense tissues – as applied in osteopathic functional and counterstrain methodology, or forms of kinetic taping, as examples or relaxation of tense tissues via massage influence the self-regulating mechanisms potentially enhancing collagen maintenance, repair?
  • How important is hydration in collagen self-repair maintenance and how can we best influence this?

Specific and detailed answers need to wait for further research, but what is clear is that massage/movement and manual therapies can and do influence the vital self-regulation and maintenance of these foundational tissues.

The challenge will be to identify optimal types, degrees, directions, durations and frequency of applied load, in particular clinical situations, involving different body-types, age groups etc - whether this involves manual or movement methods.


  1. Bella J 2016 – Collagen structure: new tricks from a very old dog – Biochemical journal, 473 (8) 1001-1025  DOI: 10.1042BJ20151169l.
  2. Bhole, A., et al., 2009. Mechanical strain enhances survivability of collagen micronetworks in the presence of collagenase: implications for load-bearing matrix growth and stability. Philos. Trans. R. Soc. Lond. A Math. Phys. Eng. Sci. 367 (1902), 3339-3362.
  3. Chaitow L 2014 Fascial Dysfunction. Handspring Publishers, Scotland
  4. De Simone A et al 2008 Role of hydration in collagen triple helix stabilization. Biochemical and biophysical research communications 372.1:121-125.
  5. Dittmore, A., et al., 2016. Internal Strain Drives Spontaneous Periodic Buckling in Collagen and Regulates Remodeling.
  6. Gracovetsky S 2016 Can fascia's characteristics be influenced by manual therapy?. Journal of Bodywork & Movement Therapies. 10.1016/j.jbmt.2016.08.011
  7. Humphrey, J., et al., 2014 Dec. Mechanotransduction and extracellular matrix homeostasis. Nat. Rev. Mol. Cell Biol. 15 (12):802-812.
  8. Leikin S. et al. 1997 Raman spectral evidence for hydration forces between collagen triple helices. Proceedings of the National Academy of Sciences94.21:11312-11317.
  9. Susilo, M.E., et al., 2016. Collagen Network Strengthening Following Cyclic Tensile Loading.
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