The underrated tissue implicated in many cases of mysterious and persistent symptoms

Although I had degrees in both anatomy and physiotherapy and 20 years of clinical experience, I heard something at the 2007 World Congress on Low Back and Pelvic Pain that totally changed how I understand the human body.

German molecular biologist Professor Robert Schleip spoke about fascia – not as a passive tissue, but an active, responsive and integrated system. I sat enthralled, wondering why weren’t we taught this? This transformed my practice, and we’ve since discovered more about the crucial role of fascia – including how it helps explain pain patterns that don’t fit typical musculoskeletal or neurological models.

What is fascia – and why does it matter?

Fascia is everywhere. Ligaments, tendons, and the tissue just beneath the skin are all fascia. If you put your fingers on your forearm and move the skin from side to side, you’re feeling fascial glide. Restricted fascial glide often indicates pathology.

At a deeper level, every muscle is enveloped in fascia. If you picture a chicken breast wrapped in cling film, that outer covering is the epimysium. Within the muscle, each bundle of fibres (fascicle) is surrounded by fascia, and each individual muscle fibre has its own fascial sleeve.

Importantly, structures we once thought were confined to tendons, such as Golgi tendon organs, are actually located within fascial layers. There is constant communication between fascia and the brain. Fascia also surrounds and connects our organs, allowing them to glide over each other.

In other words, fascia is crucial for movement, communication and continuity throughout the body – which explains why it’s essential to consider pain through a fascial lens.

Fascia as a communication system

We tend to think of muscle as active and connective tissue more as passive support. But in reality, fascia is a responsive sensory tissue – it is highly vascular and densely innervated.

In fact, we receive around ten times more sensory input from fascia than from muscle. When a patient says they can’t bend any further because their hamstrings are tight, that signal is coming from fascia – not muscle fibres.

That’s why fascia plays such an important role in the proprioceptive system. Balance, coordination and movement efficiency all rely heavily on fascial feedback.

Layers, glide and hyaluronic acid

To allow smooth movement, fascia must be able to glide – which is enabled by its layered structure. A tougher, multilayered tissue (the aponeurosis) sits between superficial fascia and muscle. It is resistant to stretch but contains loose connective tissue between its layers, allowing movement.

These layers contain abundant hyaluronic acid (more correctly, hyaluronan). This glycosaminoglycan binds water and acts as a powerful lubricant. It is secreted along muscle borders specifically to facilitate glide between tissues.

If we don’t move enough, acidity in the extracellular matrix changes, increasing the viscosity of glycosaminoglycans. Then we can start getting stiffness when hyaluronan superaggregates.

Research has demonstrated that people with low back pain often have thicker thoracolumbar fascia with reduced interlayer glide. This may explain movement restriction even when clear structural pathology is absent.

Inflammation, densification and pain

We typically think of chronic soft tissue pain in terms of muscle shortening, or scarring/fibrosis. While these processes are important, they’re not the whole story.

During inflammation, fibroblasts in fascia respond to cytokines such as interleukin-1β, TNF-α and TGFB1 by increasing collagen production. Some fibroblasts turn into myofibroblasts, which have contractile capability. This is helpful for wound closure, but also tightens the extracellular matrix.

At the same time, mast cells degranulate, releasing histamine and inflammatory mediators that sensitise local nociceptors. Hyaluronan becomes more viscous, collagen cross-links increase, and the layers of fascia begin to stick together. This process is known as densification.

Densification is different to fibrosis as it is reversible – but only if it’s dealt with early. If not, reduced glide, altered mechanics and persistent nociceptive input can drive chronic pain long after the original tissue injury has healed, and may result in fibrosis. This can affect our tissues well beyond the original site of injury, leading to a systemic alteration in movement patterns.

Nerves, referred pain and chronic patterns

Nerves and blood vessels travel through fascia and are also wrapped in it. Nerves can lose their ability to glide if the tissue surrounding them densifies. This tethering can lead to hypersensitivity, ectopic firing and neuropathic-type pain – even when there’s no nerve lesion.

This helps explain why referred pain doesn’t always follow dermatomes and why pain often persists after structural healing. These issues are sometimes put down to conditions like fibromyalgia.

Because fascia connects the entire body, problems in one area can cause symptoms elsewhere. An ankle injury, for example, can lead to knee pain, hip pathology and spinal issues years later. I liken this effect to a spider’s web: disturb one strand and the entire web responds.

Movement and mood

Fascia plays a key role in a negative feedback loop that can perpetuate pain and mental health issues. You don’t move as well when you’re tired, stressed, depressed, anxious, or cold, which can put you at risk of injury. Pain then leads to reduced movement and social participation, which can increase anxiety and depression. In turn, altered mood affects movement quality and proprioceptive input.

Why movement matters

Fascia requires regular, varied mechanical load to align collagen and maintain function. Without it, the extracellular matrix becomes more acidic, hyaluronan thickens and densification increases. This is why prolonged immobility worsens pain. In one study, a healthy young adult was immobilised for three weeks, after which MRI studies showed profound disorganisation of muscle and fascial tissue.

It also helps explain delayed onset muscle soreness – much of the stiffness is not just lactic acid or muscle damage, but transient fascial densification. Athletes recover quickly because continued movement restores normal glide.

Sustained postures create another problem: fascia that stays in one position for hours has less ability to recoil. Without sufficient recovery time (usually about 24 hours), its proprioceptive capacity degrades, which can increase injury risk.

Moreover, restricted, repetitive movement can lead to densification even without acute injury.

Hydration, nutrition and fascia

Happy fascia is wet fascia. Adequate hydration is essential for maintaining hyaluronan quality.

There is insufficient evidence to recommend other nutritional interventions to support fascial health, although vitamin C’s role in collagen synthesis is established. Emerging research is exploring collagen supplementation before loading activity.

For patients with low dietary collagen intake such as vegans, adequate mechanical loading is especially important. Fascia adapts to demand. We are not born with an iliotibial band, for example – it develops as we crawl and walk. The “use it or lose it” principle is highly applicable to fascia.

Lymphatics, inflammation and recovery

Lymphatic vessels are embedded within fascia. They rely on movement to function. Lymphatic drainage is compromised in areas experiencing oedema and densification, which can perpetuate inflammation.

This challenges the traditional advice to manage acute injuries with rest, ice, compression and elevation. Acute inflammation is necessary for healing, although chronic inflammation is problematic. Gentle, graded movement within pain limits supports normal fascial behaviour and recovery. Some people benefit from support such as a bandage to give them more confidence to move.

Diagnosis, imaging and treatment

You don’t need a long consultation to see things through a fascial lens. A history of fractures, injuries or surgeries provides important clues that fascia may be involved, as do scars. Occupational posture, sedentary behaviour and recreational activity all influence fascial health.

Palpate the painful area but be sure to compare it with the other side and remote regions. Feel for tissue glide and texture, not just tenderness.

Observing how a patient walks, stands or guards against certain movements can give you a lot of information. For example, slow, guarded movement is common in depression. This may not be purely psychological – it can be correlated with fascial stiffness and reduced glide.

High-resolution ultrasound and MRI can identify fascial thickening and reduced glide. As awareness grows, it will be critical to train sonographers and clinicians to recognise these patterns.

Management-wise, refer early to a physiotherapist or osteopath who uses manual therapy techniques.

Most importantly, remember many ‘difficult’ pain presentations can be a sign of real, modifiable tissue dysfunction. Looking at pain through a fascial lens can change how you understand patients – and provide an important tool for helping them.

Key takeaways:

• Fascia is a highly innervated, vascular-rich tissue that plays a key role in movement and proprioception.
• Regular, varied movement and adequate hydration are essential for maintaining normal fascial function.
• Restricted fascial glide can cause pain and stiffness even when imaging shows no clear pathology.
• Inflammation can lead to fascial densification, a potentially reversible process different to fibrosis that contributes to chronic pain.
• Reduced fascial glide can tether nerves, explaining referred and neuropathic-type pain without nerve injury.
• Prolonged immobility, sustained postures and repetitive movements can increase fascial stiffness and pain.
• Many complex, unusual or persistent pain presentations indicate fascial dysfunction which can benefit from manual therapy and graded movement.