Hyaluronic acid and densification

Fascia creates a three-dimensional network in the body, of loose and dense connective tissue, which enables all cells and organ systems in the body to work together as an integrated whole. Fascia can simply be described as a solid part and a liquid part. The solid part consists of fibrous proteins, mostly collagen, and the liquid part of a water-binding gel that is largely made up of hyaluronic acid, but also other molecules. This solid and liquid part is collectively called the extracellular matrix (ECM), that is outside the cells and thus between each cell. Woven into the ECM are different kinds of cells, for example fibroblasts and fasciacytes. Fibroblasts produce fiber proteins like collagen and other components of the ECM, and fasciacytes produce hyaluronic acid (hyaluronan). The cells control the machinery by constantly communicating with the environment around and producing proteins and other molecules as needed.

The solid part, fiber proteins, contributes to structure and strength; controls the mechanical properties of fascia at a macro level. In the liquid gel, the properties of the fascia are controlled at the micro level; communication and transport between cells at the molecular level.

The fascia is incredibly adaptable, and is changing its composition and properties according to the load it is subjected to. This adaptation happens very quickly at the molecular level in the liquid gel. It responds to changes in load (excessive physical exercises or being sedentary), to injuries, overexertion, to physiological changes due to age, hormones, temperature, pH, and also to emotional strain and stress.

As described above, the cells are constantly communicating with the ECM. The cells are connected to, and have contact with the ECM through the cell membrane and further to the cell nucleus via the cytoskeleton. Every movement and change of load in the ECM directly signals to a complex chain of processes in the cells to adapt, and change their production of different molecules. The same applies in the other direction; changes in the function of the cell directly provide a signal for adaptation of the ECM and also signals to other cells. During wound healing, growth and new formation of tissue, a strong restructuring is needed locally in the ECM, on a micro level, to enable the adaptation and migration of cells needed for the new formation of tissue. All these changes in ECM result in changes in structure and homeostasis in tissues and organs.

Excessive and prolonged strain or direct trauma to the fascia, initiates micro and macro changes in the ECM to enable healing and repair. The immune system is also activated to take care of and phagocytize damaged cells. An acute inflammation process starts, which is a normal healing process that should end after a few days. The inflammation causes an increased sensitivity of nociceptors that signal pain to the brain, which promotes us to rest in the acute stage to give the body the opportunity to heal. If we then continue to expose the body to overload and harmful movement patterns or do not move at all, the inflammation can instead continue and become long-term or chronic. This creates proinflammatory molecules that can damage the tissue and can also form fibrosis in the long run.  

In the loose fascia, in the ground substance, there are large amounts of hyaluronan which binds water and creates a gel in the spaces between the collagen threads. Hyaluronan can occur in varying molecular sizes, with completely different properties depending on the molecular size. In a healthy, well-functioning fascia, there is plenty of hyaluronan with a high molecular weight, as it binds a lot of water and keeps the fascia well lubricated and provides an easy gliding function.

Hyaluronan is also a substance that participates in inflammatory processes and increases in concentration in case of injuries and then it also changes in molecular weight. Cowman et al. have shown that an increase in the concentration of hyaluronan can trigger a self-aggregation of the molecule, which leads to a dramatic reduction in water-binding capacity, which results in a reduced slide and glide function. It also results in an increased viscosity in ECM and a densification of the liquid fascia which increases the impact on the large number of nociceptors present there, reducing their stimulus threshold so that they over-signal pain to the brain. Luomala et al. has shown with ultrasound and elastography, that this densification coincides with movement dysfunction and also palpable stiffness in musculature and fascia.

Menon et al. have found, with a special MR technology (T1rho), that there is more unbound water in the loose fascia tissues where there is pain and functional impairment. The aggregated hyaluronan cannot bind water, but the water becomes unbound and trapped as in clusters like in a honeycomb. It was shown that the unbound water disappeared after manual treatment of the fascia, as did the pain, and the ability to move increased.

The densification is a reversible process that can be remedied with fascia treatment. If the process continues without treatment, the hyaluronan will eventually densify more and form a more dense endomysium and perimysium, around the muscle fibers, which reduces their ability to move. Eventually, more collagen will form, and a fibrosis has occurred, and the muscle fibers will atrophy. The fibrosis is now largely irreversible.


This process of densification, and eventually fibrosis, can develop in any type of tissue, not just muscles. It shows the importance of treating repeatedly in time, when the patient experiences pain and loss of movement, so that the hyaluronan can disperse and regain its water-binding and lubricating ability. The vibrations separate the aggregated hyaluronan molecules and the pressure on nociceptors disappears and movement is regained. Roman et al. have also shown that vibration effectively accelerates the flow of hyaluronan.

  • Cowman et al, 2015. Viscoelastic Properties of Hyaluronan in Physiological Conditions.
  • Luomala et al, 2014. Case study: Could ultrasound and elastography visualized densified areas inside the deep fascia?
  • Matteini et al, 2009. Structural behavior of highly concentrated hyaluronan.
  • Menon et al, 2019. Quantifying muscle glycosaminoglycan levels in patients with poststroke muscle stiffness using T(1ρ) MRI.
  • Menon et al, 2020. T1ρMapping for Musculoskeletal Pain Diagnosis: Case Series of Variation of Water Bound Glycosaminoglycans Quantification before and after Fascial Manipulation® in Subjects with Elbow Pain
  • Mense, S.; Hoheisel, U. Evidence for the existence of nociceptors in rat thoracolumbar fascia.
  • Roman et al, 2013. Mathematical Analysis of the Flow of Hyaluronic Acid Around Fascia During Manual Therapy Motions. 
  • Stecco et al, 2011. Hyaluronan within fascia in the etiology of myofascial pain.
  • Stecco et al, 2013. Fascial components of the myofascial pain syndrome.
  • Stecco et al, 2014. Ultrasonography in myofascial neck pain: Randomized clinical trial for diagnosis and followup.
  • Stecco et al, 2018. The fasciacytes: A new cell devoted to fascial gliding regulation