Review Article Open Access

Journal of Novel PhysiotherapiesJour

nal o

f Novel Physiotherapies

ISSN: 2165-7025

Petrogalli, J Nov Physiother 2020, 10:2

Volume 10 • Issue 2 • 1000425J Nov Physiother, an open access journalISSN: 2165-7025

Pathophysiology of Myofascial SyndromeNicola Petrogalli *Department of Mechanical Engineering, University of Brescia, Brescia, Italy

Keywords: Myofascial units, Myofascial syndrome, Homeostasis, Myofibroblasts, Muscles, Fascia, Nitric Oxide

Myofascial SyndromeIntroduction

The Myofascial System is a network for the managing of the biotensegrity of an organism and whose task is to maintain a tensional homeostasis, related to the concept of chemical homeostasis [1].

The human body is ‘kept in shape’ by a network of connective tissue and muscles forming the Myofascial System, arranged in Myofascial Units (MFU) which in turn can be subdivided in many different Myofascial Districts or, in simple terms, different muscles together with the myofascial layers associated to them.

The functions of many tissues and organs (e.g. the lungs, kidneys) are regulated by the internal stress state.

The fascia bears structural loads through a special modality of contraction which reveals to be central in maintaining the posture and in regulating the body movements [2].

The Interstitium is one of the biggest organs in the human body, since it is widespread in all the organism: under the skin and within the tissues that cover the digestive system, the lungs, the blood vessels and the muscles. It is made up by interconnected cavities full of liquid and sustained by collagen fibers [3,4] and elastin, which form a microvacuolar structure acting as a proper damper. Its presence could also explain a lot of biological phenomena such as the diffusion of tumors, the aging of the skin, the inflammatory degenerative diseases and the mechanism of acupuncture.

A recent study published on the Journal Scientific Reports by the New York University and by the Mount Sinai Beth Israel Medical Centre supports this statement. By means of a technique known as Laser Confocal Endomicroscopy, which enables to observe the living tissues directly inside the body – instead of picking them up and then fixing them on a slide - the real structure of the Interstitium has been found in all the parts of the body which undergo continuous movements and stresses.

The structural tensegrity is guaranteed by the disposition of the collagen fibers, which form aqueous structures inside the Extracellular Matrix (ECM) [5]. Such structures, called microvacuoles, are characterized by a high level of disorder and anisotropy. This is associated to a high level of entropy, which diminishes after the alignment along the main direction of stress - in the case that stress acts along preferential directions. The energy absorbed by the system causes an increase in the structural order along certain directions and a change in the shape. The Fascial System guarantees maximum efficiency in

managing the tensional homeostasis whenever the microvacuoles are disposed in the most entropic configuration.

The Collagen Fibers which support the interstitial cells contribute to the stiffening of the joints and to the progression of the inflammatory diseases related to the phenomena of Sclerosis and Fibrosis. The network of proteins supporting the interstitium generates an electrical current which follows the movements of the organs and muscles.

In the case of an external traumatic cause breaking such equilibrium, Pathological Myofascial Contractures are generated. A Contraction is a physiologic adaptive capability of the Fascial Connective Tissues which was discovered in the last years and seems to be favored by special contractile cells called Myofibroblasts (MFB), whereas the Pathological Myofascial Contracture is a pathological condition of fascial tissues shortening which determines the Myofascial Syndrome.

In this paper I put forward the hypothesis that the cause of the presence of Pathological Myofascial Contractures is, on one side, a loss of coherence of the biophotonic field within the Myofascial System and, on the other side, a gain in coherence, which determines phenomena of Nitric Oxide (NO) stasis characterizing the Myofascial Syndrome.

MyofibroblastsMyofibroblasts are mobile cells which are able to exert a contractile

force of 4, 1µN on the ECM - that is, four times the force exerted by common Fibroblasts - thanks to the presence of stress fibers made up of ASMA (α-Smooth Muscle Actin) (Figure 1).

The MFBs are arranged in linear syncytia from which the contractility of the fascia is guaranteed. They can exert a slower contraction (about 5-30 min for the activation) compared to the muscular contraction, developing prolonged traction actions (up to more than an hour) that contract collagen fibers and eventually cause the entire ECM to contract. This possibility of fascia to regulate and adapt its stiffness depending on different situations is an advantage for the organism: during fight-or-flight reactions, for example, a more rigid fascia prevents the body from physical traumas.

AbstractThis paper analyzes the pathophysiological mechanism which is responsible for the arisen of the myofascial tensions

which characterize the Myofascial Syndrome. The mechanism involves gain and loss of coherence of the biophotonic field within the myofascial tissues. The paper also takes into account the physiological alterations of some important molecules, among which the most important is Nitric Oxide (NO).

*Corresponding author: Nicola Petrogalli, Department of Mechanical Engineering, University of Brescia, Brescia, Italy; E-mail: n.petrogalli@studenti.unibs.it

Received January 20, 2020; Accepted June 17, 2020; Published June 24, 2020

Citation: Petrogalli N (2020) Pathophysiology of Myofascial Syndrome. J Nov Physiother 10: 425.

Copyright: © 2020 Petrogalli N. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: Petrogalli N (2020) Pathophysiology of Myofascial Syndrome. J Nov Physiother 10: 425.

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Volume 10 • Issue 2 • 1000425J Nov Physiother, an open access journalISSN: 2165-7025

A lot of MFBs are situated near capillary blood vessels, from which they can easily get all the chemicals needed for their functioning, including:

Inflammatory molecules (e.g. TGF-β1, cytokines, histamine and oxytocin) which stimulate contraction;

Nitric Oxide (NO) stimulating relaxation.

On the contrary, MFBs are not responsive to other neurotransmitters such as Acetylcholine and Adrenaline and not even to molecules blocking the calcium channels (e.g. angiotensin, caffeine). Besides being the main chemical regulatory agent of MFBs’ activity as it promotes the intracellular accumulation of contractile proteins in Fibroblasts, TGF-β1 promotes a greater collagen density within tissues.

With regard to histology, MFBs are a sort of link between smooth and connective muscle tissue; several MFB phenotypes exist, ranging from cells which are very similar to smooth muscle to cells which are more similar to fibroblasts. The maximum density of MFBs in the Fascial System can be found in the Perimysium. Within the ECM, Myofibroblasts are located between Smooth Muscle Cells, innervated by the autonomous nervous system, and a common fibroblast, acting as a linking element. The control of this type of cells is involuntary (Figure 2).

When a fibroblast is solicited by a non-physiological mechanical stress, it differentiates into a proto-myofibroblast, which produces filaments of ASMA-actin in order to form adhesion complexes and structural fibers so as to guarantee the external anchorage to ECM. If stress persists, the complete differentiation in MFB will take place with the formation of an organized network of connections with the ECM through the cellular membrane, due to the presence of ASMA filaments directly connected with the cytoskeleton.

The phenomenon of Myofibroblasts’ differentiation depends on:

the mechanical stress in the tissues;

the proinflammatory chemical milieu;

the chemical acidity, since a lower pH level than the physiological one stimulates the Contraction of MFBs.

The Myofascial SyndromeThe Myofascial Syndrome is characterized by imbalances of

the internal stresses of the Myofascial System due to the presence of Myofascial Pathological Contractures.

When a phenomenon of structural imbalance affects the human body, it is continuously corrected with compensations by the Myofascial System, which modifies the distribution of the internal stresses changing its proper geometry and constitutive nature in terms of chemical, structural and morphological composition of the tissues and the cellular population in order to react to the imbalance of the internal tensional homeostasis. Such an adaptation is caused by variations in the chemical homeostasis following the mechanical mutations which become constitutive for the organism over time.

In turn, this is due to epigenetic modifications of the molecules that make up tissues, which react either by getting stiffer or contracting depending on the tensional tenso-bending or compressive stresses which they undergo.

If we consider the role of fascia as a structural constituent along with the Myofascial Continuum, we can see that it adapts to the behavior of the muscular fibrocells with which it is in contact. In particular:

where the muscle is contracted, fascia is extended, causing a Tendinous MFU, i.e. a Myofascial Pathological Contracture;

where the muscle is in traction, Fascia is contracted, resulting in a Granulomatous MFU.

Tendinous MFUs

Following a trauma, an entire MFU enters a state of continuous contraction. When a deformation is imposed, the stress relaxation in those visco-elastic tissues tends to diminish the internal stress and, even if the intensity of stress falls below the threshold perceived by the muscular mechanoreceptors - also due to the damping caused by a more and more rigid ECM - the deformation over time becomes chronic, so that the gaps between the contracted and circled muscle fibers are covered by the application of new connective tissue. Should the contraction persist over time, it takes the name of Myofascial Pathological Contracture.

The aim of this paper is to explain the mechanism by which such tissutal modifications occur and feed themselves, for which a gain of coherence of the biophotonic field within such tissues is postulated [6-8].

Such a gain of coherence causes muscular contractions to perpetuate over time, leading to the formation of ordered fascial structures which disrupt the histological structure and functionality of fascia and eventually to a Myofascial Pathological Contracture which limits the relative sliding within the fascia itself.

The muscular fibers which belong to Tendinous MFU are contracted because of a malfunctioning in the behavior of the neuromuscular joint and of the biochemical milieu, with a state of Hypoxia causing:

the cells to release HIF-α (Hypoxia Induced factor-1α), a protein acting as a transcription factor for pro-inflammatory molecules (e.g. VEGF, Vascular Endothelial Growth Factor);

the production of lactate (i.e. Lactic Acid HLa), acting as a proinflammatory agent within healing processes, and promoting the deposition of collagen fibers and angiogenesis, thus increasing the release of VEGF by Macrophages (Figure 3).

The reduced oxygen supply causes a situation of metabolic alkalosis which feeds the concomitant isto- and angio-flogosis.

In particular, blood vessels are dilated due to phenomena of nitric oxide stasis within the Myofascial System [9,10].

Figure 1: Myofibroblast with stress fibers highlighted in red, marker 20 µm.

Citation: Petrogalli N (2020) Pathophysiology of Myofascial Syndrome. J Nov Physiother 10: 425.

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Volume 10 • Issue 2 • 1000425J Nov Physiother, an open access journalISSN: 2165-7025

This supports the thesis that after manual treatment on myofascial contractures an increase of nitric oxide in the blood is observed [11].

In the case of a Myofascial Contracture, a more and more fibrous, extended and more liquid ECM is generated because of a continuous and reiterative remodeling process characterized by an inappropriate and excessive apposition of collagen fibers within the ECM. The excess of water, in particular, is responsible for the inflation of the tissues.

The metabolites produced in this district by the continuous contraction of the fibers accumulate and trigger stasis phenomena of acid substances. This, in turn, determines a condition of Metabolic Acidosis and a proinflammatory milieu, since the TRL-Toll Like Receptors warn the presence of non-self toxins (e.g. ATP, Uric Acid) within the extracellular milieu.

The presence of an acid milieu also alters the muscular function,

since a high concentration of H+ inhibits the myofibrillar and sarcoplasmic ATPase and reduces the release and the re-uptake of Ca2+ ions.

Such contractures are accompanied by an overall increase of the myofascial stiffness of the affected districts; furthermore - given the continuous and unceasing activity of gravity on each living organism over the whole life - the situation on a biostructural level can only get worse due to the phenomenon of Hyperstatic Call: since the Myofascial System is a hyperstatic structure, the stiffest parts tend to bear most of the structural loads during exercise.

Granulomatous MFUs

The Muscular Fibers of a Granulomatous MFU are subject to the opposite traction forces coming from Tendinous MFUs and to the loss of coherence of the biophotonic field within the tissue.

Figure 2: Differentiation of a myofibroblast.

Figure 3: Model for the myofascial pathological contracture.

Citation: Petrogalli N (2020) Pathophysiology of Myofascial Syndrome. J Nov Physiother 10: 425.

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Volume 10 • Issue 2 • 1000425J Nov Physiother, an open access journalISSN: 2165-7025

This determines an increase in the concentration of the following substances [12]: bradikynin, a peptidic neurotransmitter locally produced within tissues - often after a physical trauma – which helps increase the permeability of blood vessels and relax the smooth muscle cells and plays as an important role in Nociception, P Substance, Serotonin, Noradrenalin, Interleukins (e.g. IL-6, IL-8) and Histamine.

In a Granulomatous MFU, Nitric Oxide is absent [13] and blood vessels are contracted due to the contraction of the fascial tissues.

Dynamical functioning

Due to the fact that sarcomeres are at a length higher than the resting physiological one l0, Granulomatous MFUs are not able to dispatch their proper functions in moving the bones, forcing the organism to use the elastic return of the elastic fibers in the contracted ECM of the antagonist Tendinous MFUs. For the simple maintenance of the internal tensional homeostasis, the presence of residual stresses within the Myofascial continuum alters the mutual role of Antagonist MFUs in the following manner:

in the Granulomatous MFU, supposing to examine an extensor muscle, the Muscular Fibers are extended so as to reach the neutral position in the body, whereas Fascia is disorganized due to its contraction. As a result, the contribution of Myofascial transmission to the force exerted by the eccentric and tetanic contraction of muscles in extension which is transmitted to bones is almost zero;

in the Tendinous MFU, supposing to examine a flexor muscle, the Muscular Fibers are contracted and exploit the elastic energy stored in the elastic fibers in order to make up for the lack of both the Myofascial antagonist force in a Granulomatous MFU and their Myotendinous force component.

In the presence of Pathological Myofascial Contractures in a Tendinous MFU the activity of an α-Motoneurons is increased [14], since the Sarcomere are at a length outside the plateau line corresponding to the maximal force of contraction; more Acetylcholine is provided for their contraction and, in addition, they tend to dispose in parallel rows, because such a configuration allows the fibrocells to exert an overall force which equals the sum of the forces produced by every single Sarcomere, as shown in the figure below (Figure 4).

This condition causes a bulking of the muscular fiber due to an increase of the muscular mass (hypertone). The role of Fascia, disposed in parallel to sarcomeres, is to permit the volumetric dilatations of the muscle during contractions and - given the increase in the intrinsic muscular volume - it undergoes extra physiological dilatation that overstress the collagen fibers in crimped configuration (Figure 5).

The increased activity of α-Motoneurons makes the Tendinous MFUs completely equivalent to spastic muscles, i.e. atrophic muscular districts due to a disused atrophy and hypertrophy of the Fascia due to an increase of Collagen Apposition triggered by a gain of coherence in the local biophotonic field.

It can be assumed that the traction of Connective Fascial Tissue within Tendinous MFU occurs through the contraction of Fascia, following a decrease in Nitric Oxide (NO) due to alterations in the myoendothelial coupling between muscular fibrocells and blood vessels [15] (Figure 6).

On a cytomechanical level, Myofibroblasts have a central role in the Fascial Contractures, since the increase of the MFBs density in the perimysium is associated to fibrocontractive disorders of the myofascial system and an increase in the stiffness of the tissues is observed [16].

Persisting stresses within the tissues generate a chemotensile milieu which promotes the differentiation of Fibroblasts in MFBs and the migration of MFBs from neighboring zones. Such an increase in cellular density of the MFBs population in that district may happen in few hours or in a few days and may generate pathological contractures of Fascial Tissues. In the long run, this condition may extend to the Extracellular Matrix until it determines a different pattern of remodeling.

Myofascial Contractures persist also without the action of MFBs, since they are only caused by changes in the anatomo-functional relation between the fascial and the muscular elements that made up the myofascial continuum, i.e. due to structural and morphological modifications of the MEC, of the collagen fibers and of the elastic fibers.

Examples of myofascial syndrome

Let’s suppose to observe a patient who has been operated (osteosynthesis) and then plastered after a multiple fracture of the left radius. Let’s suppose the course of the operation turns pathological because of the iron inserted for osteosynthesis damaging the tendon of one or more lateral muscles of the forearm (e.g. Brachioradialis) and causing an inflammation which is treated by numerous medications in the insertion area of such muscles (medial area of the wrist).

Since the inflammation persists, the surgeon chooses to remove the plaster after twenty days instead of a month and the inflammation goes away within few days thanks to the structural compensation which takes place at Fascial level. As a consequence, a Myofascial Pathological Contracture of the antagonist MFUs (e.g. Flexor Ulnaris Carpi, Palmaris Longus, Flexors of the fingers...) occurs.

This may be a case study in which tensional imbalances are generated as a result of surgical operations - therefore labeled as ‘traumatic’ - which have not been carried out to perfection. In such cases the Brachioradialis Muscle features a Granulomatous MFU, along with the Synergistic MFUs (e.g. the MFUs in the Extensor Pollicis and Radia and the Brachial Muscle). On the other hand, the Flexor Ulnaris Carpi (FUC) works as a Tendinous MFU in which the contracted muscular fibrocells of the FUC remain in a state of contraction during the contraction of the MFU, since the movement is mainly realized

Figure 4: In-Parallel disposition of the muscular fibrocells to increase the force generated.

Figure 5: Crimped and uncrimped collagen fibers.

Citation: Petrogalli N (2020) Pathophysiology of Myofascial Syndrome. J Nov Physiother 10: 425.

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Figure 6: Dynamical functioning of muscles hit by myofascial syndrome.

Figure 7: Example of myofascial syndrome in which a muscle is stretched due to an eccentric load whereas another one is shortened due to a concentric load.

thanks to the elastic return of the contracted elastic fibers and the collagen fibers.

From a histological point of view, the tendinous MFUs are homologous to spastic muscle cells as they are both subject to the overstimulation of α moto-neurons (cause of spasticity), to the limited articular ROM and to the altered curves of Hill’s Relation.

The following image describes a further example in which the patient keeps his head forward with the chest bending inwards due to the curved back (Figure 7).

The upper muscle fascicles of the Trapezium Muscle undergo a displacement due to an eccentric load caused by the weight of the head, while the single fibrocells are subject to extra physiological stresses of traction; we can observe, in this district, a clear example of Granulomatous MFU. The muscular fascicles of the Front Deltoid are contracted due to a concentric load and show a Pathological Contracture, causing the district to become a Tendinous MFU.

DiscussionMyofascial diseases, also called Somatic Disfunctions [8], are

characterized by pain, reduced articular mobility and damage to neighboring tissues (e.g. skin, muscles and tendons). Such discomforts, especially in case they are particularly serious, can lead to modifications in the constitutive morphology of tissues and in the shape of the organism – and eventually in its physiology. In other words, because of the imbalance of the tensional homeostasis which characterize the somatic dysfunctions the neuroendocrine activity may undergo modifications which affect the functioning of the internal organs controlled by a retroaction feedback regulated by chemical mediators such as hormones and neurotransmitters.

To sum up, in a state of complete relaxation the Tendinous MFUs (where a Pathological Fascial Contracture occurs) are short, while the Granulomatous MFUs are extended. The Tendinous MFUs are in a condition of local metabolic acidosis, while the Granulomatous MFUs experience alkalosis; the two biochemical thrusts in opposite direction with respect to pH, are counterbalanced according to the concept of Allostasis, without giving rise to systemic alteration of pH values.

The chronical interstitial inflammation characterizing the Generalized Myofascial Syndrome allows the pathology to feed itself: as a matter of fact, TGF-β1 [17], Nitric Oxide (NO) [18] and P Substance have a crucial role in triggering and maintaining a proinflammatory status.

The presence of zones with an increased coherence impairs the biomechanical functioning of Myofascial Units; in addition, the continuity of the Myofascial Network often they affect districts belonging to different muscles. In particular, within the same muscle can exist areas pathologically contracted and areas pathologically extended (e.g. tensed fibers at the proximal insertion and contracted fibers at the distal insertion of long muscles).

ConclusionThe compression of the neurovascular tract in fascial disfunctions

contributes to the imbalance of the chemical homeostasis, not only from a functional point of view – that is, the biochemical milieu altered by chemical stress alters in turn the behavior of certain organs - but also mechanically, with circling (following extra physiological stresses of traction) or bulking (following extra physiological stresses of compression) of the biological structures in the extracellular matrix.

If an inflammation affects the vertebral tissues, this may be caused by the difficulty of the lymphatic system in compensating the biomechanical malfunctioning of the Diaphragm. This condition leads to a chronic inflammatory status which continuously feeds itself. When the diaphragm is forced to bear a postural overload, it subtracts part of the mechanical energy which it is able to provide and which should physiologically be designated for the respiratory function.

In the presence of Chronic Myofascial Contractures, the abdominal and lumbar areas are weak because of the weakness of the Diaphragm which determines a smaller thoracic expansion and an altered central control of breathing. Fibrocontractive diseases can also cause adhesions of the structure which make up the abdominal wall.

From a biomechanical perspective, the diaphragmatic disfunctions determine a decreased articular ROM of the cervical tract and a more marked tensional state in crural Fascia. This condition affects the whole Fascial System with a chronic state where an increase of Nociceptive Fibers and a loss of the motor coordination without apparent causes of neurological type occur. From the endocrinological point of view, on the

Citation: Petrogalli N (2020) Pathophysiology of Myofascial Syndrome. J Nov Physiother 10: 425.

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other hand, the altered mobility of the Diaphragm within a Generalized Myofascial Syndrome can generate a hormonal disorder, given the close relationship of the muscle with the hypothalamic pituitary adrenal axis (HPA) which controls the whole endocrine production of the organism. As a result of imbalances and structural compensations, the behavior of the paravertebral muscles and, consequently, of the fascia profunda of the trunk, are altered. This alters the proprioception and nociception, determining the disfunction of the Autonomous Nervous System and an impairment of the functioning of the afferent autonomous post ganglia fibers, thus resulting in alteration of such phenomena as the blood vessels vasoconstriction and the hyperhidrosis of sweat glands.

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