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FASCIA COMPONENT

IN MYOFASCIAL PAIN SYNDROME

Stecco Antonio M.D.

University of Padua

TelescopeTelescope

ASTROMONYASTROMONY

Botanic gardenBotanic garden

BIOCHEMISTRYBIOCHEMISTRY

Anatomic theatreAnatomic theatre

ANATOMYANATOMY

SCIENTIFIC REVOLUTION (1543)

The university of The university of Padua foundation is Padua foundation is

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Disclosure

Stecco Antonio has no

relevant financial disclosures.

In separate sessions, 12 healthy subjects received ultrasound-guided bolus injections ofisotonic saline (0.9%) or hypertonic saline (5.8%) into the erector spinae muscle, thethoracolumbar fascia (posterior layer), and the overlying subcutis. Subjects were asked torate pain intensity, duration, quality, and spatial extent. Pressure pain thresholds weredetermined pre and post injection.

Injections of hypertonic saline into the fascia resulted in:

�significantly larger area under the curve of pain intensity over time than injections intosubcutis (P<0.01) or muscle (P<0.001),

�Pain radiation evoked by fascia injection exceeded those of the muscle (P<0.01) and thesubcutis significantly (P<0.05).

�Pressure hyperalgesia was only induced by injection of hypertonic saline into muscle, butnot fascia or subcutis.

TLF IS A PRIME CANDIDATE

TO CONTRIBUTE TO NON SPECIFIC LBP…

Schilder et al (2014) Pain 155 (2): 222-31

Sensory findings after stimulation of the thoracolumbar fascia with hypertonic saline suggest its contribution to low back pain.

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Patel and Lieber (1997) and Huijing (1999) have shown that:

•70% of the transmission of muscle tension is directed (in series) through tendons

•30% of muscle force is transmitted through the connective structures in parallel

WHAT IS FASCIA

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Origin of muscular fibers from the deep fascia that presents a thickening in correspondence with these insertions .

Insertion of the extensor carpi ulnaris at the antebrachialfascia

Insertion of the flexor carpi ulnarisat the antebrachial

fascia

MYOFASCIAL EXPANSIONS

Many muscles have myofascial

expansions. When these muscles

contract, they also stretch the

deep fascia connected with the

expansion.

Lacertus fibrosus (aponeurosis) continues from the biceps tendon and merges with the antebrachial fascia

MYOFASCIAL EXPANSIONS

The relationships between the expansions of the pectoral girdle muscles (i.e. pectoralis major, latissimus dorsi and deltoid) and brachial fascia were analyzed

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Specific spatial organization(Stecco et al, CTO, 2008)

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In the last years several researches have demonstrated the presence of many free and encapsulated nerve terminations, particularly Ruffini and Pacini corpuscles, inside the fasciae

WHAT IS FASCIA

Yahia L, at al. 1992; Stecco C, et al. 2007; Tesarz J, at al. 2011; Deising S, et al. 2012;

Pacini corpuscles (S100, 100x) Ruffini corpuscles (S100, 200x)

Structure of the fascia

“Hyaluronic acid is one of the chief components of the extracellular matrix.”

Frasher, J.R.E et al; 1997 Journal of Internal Medicine 242: 27–33.

Benetazzo L, et al; Surg Radiol Anat. 2011 Jan 4.

THE STRUCTURE OF THE FASCIA

Fiborus layer:

collagen fiber type I and III

LooseLoose layerslayers: :

adipose adipose cellcell; GAG; ; GAG; HyaluronicHyaluronic acidacid

FIBROSIS OR DENSIFICATION?

Fibrosis is similar to the process of scarring, with

the deposition of excessive amounts of fibrous

connective tissue, reflective

of a reparative or reactive process. It can obliterate

architecture and function

of the involved tissue.

FIBROSIS Densification indicates an increase in the density of

fascia. This is able to modify the mechanical proprieties

of fascia, without altering

its general structure.

DENSIFICATION

FIBROSIS OR DENSIFICATION?

In reality, in the majority of cases, it is not clear whether it is fascial densification or fascial fibrosis that

is involved. This lack of certainty causes not only confusion in terminology, but also implies that very

different treatment modalities can be applied to fascia in an attempt to relieve pain.

Adhesion could be

considered typical

examples of fascial fibrosis

FIBROSIS Thoracolumbar fascia shear strain was ~20%

lower in chronic low back pain Langevin HM et al; 2011.

DENSIFICATION

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• The deep fasciae are a complex structure formed by at least two components:

• two or three layers of parallel collagen fibre bundles

• Loose connective tissue interposed

FIBROSIS OR DENSIFICATION?

An alteration of the collagen tissue

could give a fascial fibrosis,

An alteration of the loose connective

tissue a fascial densification

• Song Z, Banks RW, Bewick GS. Modelling the mechanoreceptor's dynamic behaviour. J Anat. 2015 Jun 25.

• Bell J, Holmes M. Model of the dynamics of receptor potential in a mechanoreceptor.;Math Biosci. 1992 Jul;110(2):139-74.

• Suslak TJ, Armstrong JD, Jarman AP. A general mathematical model of transduction events in mechano-sensory stretch receptors. Network. 2011;22(1-4):133-42.

• Loewenstein WR Skalak R; Mechanical transmission in a Pacinian corpuscle. An analysis and a theory.;J Physiol.1966 Jan;182(2):346-78.

• Swerup C, Rydqvist B. A mathematical model of the crustacean stretch receptor neuron. Biomechanics of the receptor muscle, mechanosensitive ion channels, and macrotransducer properties. J Neurophysiol. 1996 Oct;76(4):2211-20.

• Husmark I, Ottoson D.;The contribution of mechanical factors to the early adaptation of the spindle response.;J Physiol. 1971 Feb;212(3):577-92.

Tissue viscoelasticity shapes the dynamic response of

mechanoreceptors

FIBROUS COMPONENT OF THE DEEP FASCIA

The deep fasciae

are formed by

collagen fibres

type I and type

III, disposed in

many directions.

Lateral region of the tight

APONEUROTIC FASCIAE:

from an irregular fibrous tissue

to a multilayer organization

Layer I

Layer II

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The fascia is not an elastic tissue, the elastic fibres are less than 1%

THE MULTILAYER STRUCTURE PERMITS TO

FASCIAE TO ADAPT TO VOLUME VARIATIONS

Van Gieson stain, 200x

As a fishing-net, the fascia could adapt to

muscular volume variations and to

stretches, but over a cut-off the fascia

becomes tensioned and consequently is

able to transmit the forces at a distance.

Hypodermidis

SUPERFICIAL FASCIA

DEEP FASCIA

MUSCLE

EPIMYSIUM

Fascia lata

Hypodermidis

SUPERFICIAL FASCIA

DEEP FASCIA

MUSCLE

EPIMYSIUM

Fascia lata THE MULTILAYER STRUCTURE PERMITS TO FASCIAE

TO TRANSMIT THE FORCES AT A DISTANCE

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The multilayer structure of the deep The multilayer structure of the deep The multilayer structure of the deep The multilayer structure of the deep fasciae of the limbs fasciae of the limbs fasciae of the limbs fasciae of the limbs

Medial region of the elbow

The presence of loose connective tissue interposed between adjacent layers permits

local sliding, and so from a mechanical point of view the single layers could be

considered independently.

Deep fascia

Muscle

AlcianAlcian Blu 12.5 XBlu 12.5 X

Hypodermis Layers of loose connective tissue

are present between the various

sublayers of aponeurotic fasciae,

between fascia and muscle and

inside muscle

THE ADATTABILITY IS PERMITTED ONLY IF

THE EXTRACELLULAR MATRIX

WHERE THE COLLAGEN FIBRES ARE EMBEDDED IS FLUID.

The loose connective tissue is composed by:

�Water

�Ions

�Glycosaminoglycans (with a prevalence of hyaluronan)

• Hyaluronan is secreted by specific cells inside the fascia, which are called fasciacytes.

• Hyaluronan is a lubricant that allows normal gliding of joint and connective tissue.

• Hyaluronan occurs both as individual molecules, and as macromolecular complexes that contribute to the structural and mechanical properties of fascia.

THE ADATTABILITY IS PERMITTED ONLY IF

THE EXTRACELLULAR MATRIX

WHERE THE COLLAGEN FIBRES ARE EMBEDDED IS FLUID.

Fascial damage (i.e. surgery or trauma) alwayscauses an inflammatory reaction thatpromotes the healing process. Threesequential, yet overlapping, phases of thereparative healing process occur:

�inflammation

�proliferation (fibroblasts grow and form anew, provisional ECM by excreting collagentype III and then type I collagen andfibronectin. In this phase, the collagen formsan irregular connective tissue that has themain function of closing the wound gap)

�Remodeling (for the correct healing of thedeep fascia it is fundamental that collagenfibres remodel and realign according thelocal tensile stress. Only now the connectivetissue can transmit forces at a distance)

INFLAMMATORY REACTION

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ENT

Male, 65 ys, diabetic, amputation after 10 months of immobility following

trauma

Normal

Pathological

Remodeling can last for years, depending on the size

and nature of the wound. In actuality, this process is

fragile and susceptible to interruption or failure.

In particular, it seems that a fundamental role is

played by the mechanical stress acting on the injury

site, that guides the neuroinflammatory response.

If the tissue in which tensile state can be observed

was previously in an unbalanced condition or is

immobilized, the remodeling process does not lead to

physiological spatial reconstitution, but instead causes

random deposition of collagen fibers.

Control

SKIN

DEEP FASCIA

MUSCLE

HYPODERMA

Male, 65 ys, diabetic, amputation after 10 months of

immobility following trauma

For example, in the leg, a horizontal scar causes a tensile state three times greater than

a vertical scar.

REMODELING OF THE FASCIAL

FIBROUS COMPONENT

CAUSES OF ALTERATIONS

IN THE FIBROUS COMPONENT: IMMOBILIZATION

Slimani et al (2012) demonstrated that immobilization causes pronounced muscle connective tissue thickening.

During early recovery there are sustained increased expression of markers of CT remodeling and increased nuclear apoptosis.

• Duffin et al (2002) demonstrated that patients withtype I diabetes have a plantar fascia significantlythicker compared to normal controls.

• Li et al (2013) demonstrated that diabetes alter thephysical properties of collagen structures and tissuebehavior:

• reduce tissue stress relaxation (p<0.01)

• Reduce drastically fiber-sliding with acompensatory increase in fiber-stretch.

All of these changes were demonstrated for tendons,but it is probable that this also applies to fasciae,causing loss of fascial viscoelasticity. This haspotentially important implications for tissueremodeling and mechanically regulated cell signaling.

CAUSES OF ALTERATIONS

IN THE FIBROUS COMPONENT: DIABETES

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• Trindade et al (2012) demonstrate that the humandeep temporal fascia is stiffer in older than in youngerpersons. Thus, increasing age creates stiffer, strongerand more stable connective tissues, although muchless flexible.

• Wojtysiak (2013) demonstrated that in newborn pigsthe perimuscular collagen fibrils of the longissimuslumborum muscle have a wavy disposition and form aloose network. Only with increasing age do thearrangement of collagen fibrils becomes denser andmore regular. These factors can influence the shearforce value of connective tissue and the underlyingmuscles.

CAUSES OF ALTERATIONS

IN THE FIBROUS COMPONENT: AGING

�The strain patterns in fasciae may not be uniform, so it is probably that overuse andunderuse sites inside fasciae exist.

�Connective tissues exhibit adaptive responses to conditions of increased loading anddisuse.

�If the adaptive response is inadequate, the fasciae hoard local alterations that change thedistribution of the lines of force inside fasciae.

CAUSES OF ALTERATIONS

IN THE FIBROUS COMPONENT: OVERUSE

Stecco A et al; RMI study and clinical correlations of ankle retinacula damage and outcomes of ankle sprain. Surg Radiol Anat. 2011 Dec

ROLES OF THE LOOSE CONNECTIVE TISSUE:

DENSIFICATION

The loose connective tissue assures the autonomy of adjacent fibrous layers.

Only if the loose connective tissue has low viscosity the fibrous layers can:

� transmit forces along different directions without interfering with each other

� adapt to volume variations of the underlying muscles during contraction.

The densification of the loose connective tissue, represented with a red flash, alters the

gliding between the two fibrous layers.

The transmission of the forces can be altered in a way that is not easily defined.

The tissue around the densification point can be subjected to intense mechanical stress.

ROLES OF THE LOOSE CONNECTIVE TISSUE:

DENSIFICATION

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CAUSES OF DENSIFICATION:

STRENUOUS EXERCISES

Piehl-Aulin et al (1985) demonstrate a

transient accumulation of hyaluronan

following exercise. Similarly to a synovial

joint, increased production of HA is the

initial attempt to increase the gliding

efficiency between two surfaces.

Tadmor et al (2002) show that when

hyaluronan is organized into layers,

viscosity increases considerably with

increasing distance between the two

surfaces.

The increased viscosity of The increased viscosity of

the loose connective tissue the loose connective tissue

inside the fascia may cause inside the fascia may cause

decreased gliding between decreased gliding between

the layers of collagen fibers the layers of collagen fibers of the deep fasciae. of the deep fasciae. This This

may be perceived by may be perceived by

patients as an increase in patients as an increase in

fascialfascial stiffness.stiffness.

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The hypoechoic and stiffer nodules

Sikdar S et al 2009

The LBP group had approximately 25% greater fascia thickness

Langevin HM et at 2009

Trigger points and fascial densification

Chronic neck pain group had an hypoechoic and thicker fascia Stecco A et al 2013

The three-dimensional superstructure of HA chains breaks down progressively when temperature is increased, with a consequent decrease in viscosity (Gabor et al, 2003)

This may explain the effects of many physical therapies that increase temperature (laser, etc.) and with warming up in general.

CAUSES OF DENSIFICATION:

LOW TEMPERATURE

7.36 –

7.44

CAUSES OF DENSIFICATION:

LOW pH

The hyaluronan shows stable condition in

alcaline solution, but in acid solution its

viscosity increases drammatically (Gatei 2005).

After strenuous exercises the muscles pH

can reach a value of 6.60 with an increase

of approximately 20% in HA viscosity

This may be perceived by patients as an This may be perceived by patients as an

increase in increase in fascialfascial stiffness.stiffness.

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Pipelzadeh (1998) demonstrated that,

when superperfused with lactic acid,

the contraction of the myofibroblasts of

the superficial fascia of rats was

significantly increased.

Trabold et al (2003) demonstrated that

lactate stimulates collagen synthesis

The pH induces The pH induces

also an increase also an increase

of the fibrosis of the fibrosis

and of the and of the

fascialfascial tension tension

CAUSES OF DENSIFICATION:

LOW pH

The loose connective tissue is an important reservoir of water and salts for surrounding tissues. But it also has the capacity to accumulate varieties of waste products.

The biomechanical properties of loose connective tissue may be altered depending upon water content and waste products accumulation.

CAUSES OF DENSIFICATION:

DEHYDRATION AND WASTE PRODUCTS

CAUSES OF DENSIFICATION:

IMMOBILIZATION

Hyaluronan is a thixotropic substance. Dintenfass (1966) demonstrates that synovial fluid has thixotropic and elastic (instantaneous dilating) properties. He finds that its viscosity decreases with an increase in shear rate, but it is pressure-resistant under sudden impacts.

This property can be assumed also for the key element of the fascial loose connective tissue and explains why immobility reduces fascial gliding and consequently, range of motion. Besides, the movements and massages can reduce its viscosity.

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FIBROSIS OR DENSIFICATION?

DensificationDensification

• Alteration of loose connective tissue

• Alter the gliding

FibrosisFibrosis

• damage of the fibrous component

• affects the capacity of loading

transmission

The two alterations cause different problems for the fascial function

and need different treatments

FIBROSIS OR DENSIFICATION?

DensificationDensification

• It is easily curable by increasing the temperature, or increasing local strain

with a (controlled) mechanical stimulus

FibrosisFibrosis

• This alteration is difficult to modify because only a local inflammatory process can

destroy the pathologic collagen fibers and

permit deposition of new collagen fibers.

The two alterations are not incompatible: a chronic altered gliding

modifies the distribution of the forces inside the fibrous layers

DENSIFICATION

calcal

Kg

This water-mediated supramolecular assembly

was shown to break down progressively when the

temperature was increased to over ∼40 °CMatteini P. 2009

DENSIFICATION

Luomala T et al. 2014

Stecco A et al. 2013

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It is more difficult to modify because:

- only a local inflammatory process can destroy the pathologic collagen fibers and permit deposition of new collagen fibers.

FIBROSIS

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nStern R. 2006

“Under conditions of stress hyaluronan becomes

depolymerized and lower molecular mass

polymers are generated” Noble P.W, 2002

It is only with a clear understanding of fascial anatomy

and structure that it will be possible to make accurate

differential diagnoses;

Only then it will be possible to prescribe correct

treatments.