There are a number of general and specific causes and processes involved when fascia becomes dysfunctional, whether due to trauma, inflammation, genetics, pathology, poor patterns of use (habitual postural or breathing patterns, for example), or the aging process.

To explain and discuss validated and/or suggested means of identifying, preventing, improving, or normalizing fascial dysfunction, even in cases of frank pathology, and even if symptomatic relief may realistically be the best possible outcome, it is necessary for us to give attention to some major forms of fascial dysfunction and pathology, whether acquired or inherited.

Adaptation: Overuse, Misuse, Disuse, and Trauma

Leaving aside fascia-related pathology, the effects of overuse, misuse, disuse, and trauma—resulting in pain and/or musculoskeletal dysfunction—are the features most likely to be brought to the attention of therapists and practitioners who employ manual and movement therapies.

Pain and dysfunction represent the acute or chronic effects of adaptation, compensation, decompensation, and maladaptive changes that manifest in the musculoskeletal system. Such changes almost always involve structural and functional changes in connective tissues. In some circumstances, the normally well-organized functioning of fascial sheets, planes, bands, and fibers will have modified their force transmission/load transfer activities, along with the reduced sliding potentials, possibly due to the evolution of areas of densification, adhesion, restriction, fibrosis, or scarring.¹

Klingler observes that “painful contractures and reduced range of motion are frequently associated with rigid collagenous tissue within and surrounding skeletal muscle, as well as other connective tissue involved in force transmission. The fascia/function, such as that involving joint capsules, tendons, or epi- and endomysium may be disrupted by trauma and/or inflammation.”²

Such changes may occur locally, or might involve more widespread, sometimes global, postural distortions, associated with a redirection of the vectors of mechanical force, potentially leading to musculoskeletal restrictions and pain, as well as modified circulatory and drainage effects.

While many other causative factors may also be involved in symptom production and maintenance, the major features of fascia-related dysfunction are likely to include:

• Modified, usually reduced (but sometimes increased) local or general ranges of motion associated with altered tissue viscoelasticity and resilience (potentially involving joints), as well as soft-tissue structures, and commonly associated with pain, usually perceived on movement.

• Altered load transfer features, potentially producing symptoms at a distance from the origins of the problem.

• Loss of sliding potential between tissue surfaces.

• Postural deviations and misalignments, frequently involving chain reactions of adaptation and compensation—commonly associated with impaired coordination and motor control—usually evident during the performance of normal daily activities.

• Myofascial (i.e., trigger-point related) pain.

• Autonomic imbalance, including sympathetic arousal or chronic fatigue.

All or any of these (and other) adaptive changes, signs, and symptoms might evolve gradually over time. However, they may also appear rapidly—for example, soon after inflammation-inducing events.

Causes, Effects, and Prevention

Now let’s talk about these examples of the evolution of fascia-related dysfunction and disease, under the following subheadings:

• Densification and loss of fascial sliding function

• Load transfer/force transmission issues

• Fascia and aging

• Myofascial pain

• Trauma and wounds

Densification and Loss of Fascial Sliding Function

A clinically underexplored function of many soft tissues involves their ability to slide, glide, and generally accommodate the movements of adjacent structures. Loose connective tissue (also known as areolar or superficial fascia) is relatively less structurally organized, as compared with dense connective tissue layers.

Pilat notes that the processes involved in the thickening and densification of the loose connective tissues and their extracellular matrix (ECM) appear to correspond to the loss (or reduction) of sliding potential between dense fascial layers and adjacent structures.³ This view is supported by Stecco et al., who note, “Ultrasound indicates that the main alteration in the deep fasciae is increased loose connective tissue between the fibrous sublayers. It is for this reason that, in indicating fascial alteration, we do not use the term fibrosis, which indicates an increase in collagen fiber bundles. We prefer the term densification, which suggests a variation in the viscosity of the fascia.”⁴

Luomala et al. demonstrate the presence of thicker (denser) layers of loose connective tissue in both the sternocleidomastoid and scalene muscles in individuals with chronic neck pain, compared with those without neck pain.⁵

Langevin also confirms that the density of superficial thoracolumbar fascia is markedly increased (25 percent thicker) in individuals with low-back pain, as compared with those without low-back pain.⁶ The process of thickening and densification appeared (in ultrasound video images) to correspond with a marked reduction in the sliding potential of the deeper layers of the thoracolumbar fascia in individuals with low-back pain. “Thoracolumbar fascia shear strain was ~20 percent lower in human subjects with chronic low-back pain. This reduction of shear plane motion may be due to abnormal trunk movement patterns and/or intrinsic connective tissue pathology.”⁷

The changes in thickness of the deep fascia in such cases have been found to correlate with an increase in the quantity of loose connective tissue—lying between dense collagen fiber layers—with no increase of the collagen fiber layers themselves.⁸ The clinical relevance of the sliding features of fascial sheets cannot be overemphasized. Using ultrasound imaging, Wong et al. demonstrated that changes in the mechanical properties of the posterior lumbar fascia (PLF) could be observed and evaluated (quantified) in real time, in healthy individuals, before and after a manual therapeutic intervention such as myofascial release.⁹ Their conclusion was simple: “After myofascial release, the stiffness of the PLF decreased in healthy men.” The authors expressed the hypothesis that similar changes could be evaluated in individuals with dysfunctional symptoms, as in chronic low-back pain.

This hypothesis had already been confirmed in an earlier study by Chen et al. (2016), who used ultrasound imaging to identify the increased thickness of the transversus abdominis, as well as limited sliding function, in men with chronic low-back pain (LBP).¹⁰

Gracovetsky reported that “Franchi et al. (2010) [used] electron microscopy to study the changes in the collagen fiber organization when the tissues are put under stress and demonstrated that the well-ordered fibrils become disorganized under stress, thereby interfering with an orderly sliding motion. [The resulting] ‘hardening’ may explain why repeated massage, and/or the application of myofascial release techniques, can reduce the amount of disorganization within the collagen fibrils and permit freer movement.”¹¹

Further Objective Evidence

There is objective evidence that changes such as densification/stiffness and loss of slide/glide functions are commonly related to pain, and dysfunction may be improved by a variety of manual methods.

Barnes et al. conducted a study to measure hysteresis (changes in fascial stiffness) in response to different manual methods.¹² These osteopathic researchers adopted the following protocol:

1. Areas of cervical articular somatic dysfunction (SD) were identified in 240 subjects using carefully controlled palpation assessment methods involving the STAR palpation protocol. Tissue stiffness was measured prior to treatment (or sham treatment) using an instrument designed for that purpose (a durometer).

2. Four different techniques—balanced ligamentous tension, muscle energy technique, high velocity manipulation, and strain-counterstrain—and a sham technique were randomly applied in a single application to the most severe area of identified somatic dysfunction, after which (10 minutes posttreatment) the “changes in tissue stiffness” (i.e., hysteresis) were reassessed using a durometer.

3. The durometer measurement of the myofascial structures overlying each cervical segment (pre-- and postintervention) used a single, consistent piezoelectric impulse. This quantified four different characteristics—fixation, mobility, frequency, and motoricity (described as “the overall degree of change of a segment”)—including resistance as well as the range of motion.

4. When baseline pretreatment and posttreatment findings were compared for all restricted (dysfunctional) segments, the results showed that strain-counterstrain produced the greatest changes in overall tissue stiffness, as compared with the other methods used (all of which resulted in beneficial changes) and with sham treatments.

Of particular importance in relation to findings of stiffness, such as those noted by Barnes et al., are observations by Dennenmoser et al. that “stiff/hard” muscles/fascia respond differently to tissue manipulation, “depending on gender, age, pain history and activity level, and particularly to hydration levels.”¹³

Using electrical impedance assessment and elastography imaging, after soft-tissue treatment greater degrees of fascial softening were observed in physically active, middle-aged females, with little or no pain compared with those with back pain, who showed more fascial and less muscular changes. Of interest is the observation that the researchers considered “tissue hydration effects” to be significant in their findings.

Load Transfer/Force Transmission Issues

There are many ways in which force/load is transmitted via fascial pathways; for example, from contracting hamstring muscles to the ipsi- and contralateral thoracolumbar fascia¹⁴ and from latissimus dorsi contraction to the contralateral gluteal muscles, and onward to the knee.¹⁵ Dysfunction may emerge from unbalanced, excessive, and/or inefficient load transfer.

For example, Joseph et al. have demonstrated that an excessive anterior translation of the humeral head occurs in the contralateral glenohumeral joint, due to altered force transmission from the posterior oblique sling tissues in individuals with sacroiliac joint dysfunction (SJD).¹⁶ The oblique muscle sling/train/chain that lies on the posterior aspect of the trunk involves muscles such as the biceps femoris, gluteus maximus, thoracolumbar fascia, latissimus dorsi, and upper trapezius (Image 1). Joseph et al. have identified similar imbalances involving anterior myofascial force transmission, comprising the hip adductors, transversus abdominis, internal and external obliques, the anterior fascia of the trunk, and the pectoralis major running from the hip-lumbopelvic region to the contralateral glenohumeral joint.¹⁷ Note: the clinical effects of this chain remain to be substantiated (Image 2). Vleeming has demonstrated that the thoracolumbar fascia transfers load from the trunk to the legs, and that stability of the SI joint depends on these forces, acting across the joint (“force closure”).¹⁸

Fascia and Aging

The aging process leads to marked changes in the fascia of the body:

• Creases and wrinkles on the surface relate to reduced numbers of fibroblasts and, therefore, collagen fibers. Three important factors affect skin aging. These are the natural chronological process, decreased estrogen (post-menopause), and harmful environmental factors such as poor nutrition, ultraviolet radiation, excess alcohol consumption, and smoking.¹⁹

• All these changes are aggravated by inadequate hydration.²⁰

• Fibrosis, a major feature of the aging process, is a common phenomenon (characterized by excessive extracellular matrix accumulation) involving effector cells, such as myofibroblasts, that are activated following inflammatory injury.²¹ AMPK (5’-AMP-activated protein kinase) is an enzyme that plays a key role in cellular energy homeostasis, and can both prevent or delay the process of fibrogenesis, as well as encourage fibrogenesis in certain situations. It remains the focus of research to unravel its apparent contradictory roles.²²

• Glycosaminoglycans are found in the skin, together with collagen and elastin, and are essential for its hydration, as they bind large volumes of water. As glycosaminoglycan levels decrease with age, the skin’s hygroscopic properties also diminish.²³

• As these changes occur, elastic fibers also reduce or become frayed or thickened.

• The remaining collagen fibers—particularly in the superficial fascia—gradually become disorganized, tangled, lose shape, and contribute to sagging and ptosis.

• Fat cells in the superficial fascia atrophy and distort in shape, presenting as cellulite. Simultaneously, changes in sebaceous and sweat glands lead to dryness of the skin.

• These changes can be seen from the third decade of life and are accelerated by conditions such as diabetes.²⁴

• Age-related changes also affect muscle fascia, with endomysial and perimysial tissues developing tangled cross-linkages, which has clear health implications, as these structures act as “pathways for myofascial force transmission.” Reduced mobility is the result.²⁵

• Proprioceptive functions are inevitably affected as fascia ages, with implications for balance, motor control, and stability.

Myofascial Trigger-Point Pain

Myofascial pain and dysfunction, associated with active and latent trigger points, have been shown to be linked to misuse activities (poor posture, repetitive overuse patterns, etc.); therefore, alteration of such patterns to less stressful ones should reduce trigger-point activity.²⁶

For example, Bradley has reported that her preference for deactivating active intercostal trigger points in individuals with habitual upper-chest breathing patterns is to evaluate their sensitivity over time (by noting the degree of algometer pressure required to produce symptoms).²⁷ She notes that during rehabilitation, as breathing patterns revert to a more diaphragmatic pattern over time, trigger points become less active until they are no longer identifiable.

A range of manual and other methods have also been shown to be capable of reducing myofascial pain, albeit temporarily.

Trigger Points Defined

• Simons et al. have defined a trigger point as: “a hyperirritable spot in skeletal muscle that is associated with a hypersensitive palpable nodule in a taut band.”²⁸

• Dommerholt summarizes the background: “Usually, trigger points develop as a result of local muscle overuse and are frequently associated with other dysfunctions, such as pain diagnoses with peripheral and central sensitization, joint dysfunction, dental or otolaryngic diagnoses, visceral and pelvic diseases and dysfunctions, tension-type headaches and migraines, hypothyroidism, systemic lupus erythematosus, infectious diseases, parasitic diseases, systemic side effects of medications, and metabolic or nutritional deficiencies or insufficiencies.”²⁹

• Shah et al. have studied the environment of trigger points and report that oxygen deficit (hypoxia) is a feature, as is the presence of inflammatory markers, such as substance P and bradykinin.³⁰ The tissues surrounding trigger points are also excessively acidic.

• LeMoon proposes a “fasciagenic” pain model in which prolonged, unremitting fascial thickening and stiffening seems to be responsible for generating myofascial pain symptoms.³¹ Local ischemia appears to be a precursor to such changes in muscles that have been constantly or repetitively overused, possibly involving inflammation, microtrauma, and mechanical strain.

• Bron and Dommerholt expand on the inflammation model, noting that fascial inflammation may occur when motor endplates release excessive acetylcholine, shortening sarcomeres locally, disrupting cell membranes, damaging the sarcoplasmic reticulum, leading to local inflammation.³²

• Stecco et al. report that reduced sliding function between fascial layers and coincidental stiffness of the deep fascia are due to changes in the loose connective tissue layers that separate the dense fascial sheets.³³ They have demonstrated that these changes (stiffness/thickening) are common predictors of myofascial pain.

• Ball observes that “Fibrotic myofascial change can vary in severity both in terms of area(s) affected and degree of ensuing restriction and dysfunction,” resulting in unrelenting, debilitating myofascial pain, particularly in the flexor muscle groups.³⁴

• Salavati et al., using sonoelastography imaging, have demonstrated that fascial thickness in the upper trapezius—as measured by ultrasonography—reliably correlates with myofascial pain syndrome, involving active trigger points in that muscle.³⁵ “Measurement of the upper trapezius muscle and fascia/thickness by ultrasound imaging is a good to excellent method in participants with myofascial pain syndrome.”

Trauma and Wounds

When tissue damage occurs, dormant fibroblasts (and, to a lesser extent, other local cells) respond to mechanical stress and acquire contractile properties, becoming myofibroblasts.

These then form architectural scaffolding by synthesizing the ECM, including various types of collagen, in order to support the healing wound. Under normal conditions, as healing continues, these processes slow down and cease.

• Hinz has summarized the relationship between tissue damage and wound healing: “Myofibroblasts regulate connective tissue remodeling. During normal tissue repair, such as skin wound healing, controlled and transient activation of myofibroblasts contributes to restoration of tissue integrity by forming a mechanically sound scar.”³⁶

• Quite simply, the success of wound healing depends on the new tissue matrix that the myofibroblasts create, including the collagen they produce.

• Among the factors required for this process to proceed smoothly are the adequate presence of TGF-Pl, and most importantly from a mechano-transduction perspective, adequate mechanical tissue tension.³⁷

• In a landmark study, Hinz et al. showed that “mechanical tension is a prerequisite for the development and maintenance of myofibroblast differentiation and hence of granulation tissue contraction. Given the reciprocal relationship between fibroblast contractility and the mechanical state of the matrix, the modulation of extracellular and intracellular tension may help to influence wound healing and development of fibro-contractive diseases.”³⁸

• When the usually well-choreographed process of wound healing goes wrong and becomes excessive, “beneficial tissue repair turns into the detrimental tissue deformities.” These may include hypertrophic scarring, fibromatoses, and fibro-contractive diseases.

• There is a surprising connection between the individual’s breathing pattern and how well wounds heal.

• Inadequate healing results in the likelihood of adhesion development, reduced flexibility, and excessive scarring, preventing free movement between usually mobile tissues.

• Chapelle and Bove summarize the process of adhesion formation in the abdominal viscera as:

“Adhesions form following a number of injuries to the peritoneum, including mechanical trauma, drying, blood clotting, and foreign object implantation. The inflammation caused by peritoneal trauma from any etiology leads to a disruption of the balance between the fibrin-forming and fibrin-dissolving capacities of the peritoneum, favoring the deposition of a fibrin-rich exudate on the damaged area. If the fibrin is not resolved by the fibrinolytic system within days, adhesions form…. Persistent adhesions can prevent the normal sliding of the viscera during peristalsis and movements of the body, such as respiration. Adhesions become both innervated and vascularized.”³⁹

• Almost all surgery, even minor “keyhole” versions, results in adhesion formation with the potential for chronic pain and possible obstruction as a result.⁴⁰

• Scars have been shown to predispose toward formation of myofascial trigger points in adjacent tissues, with the potential for initiating pain in distant structures—an appendectomy scar, for example—causing low-back pain.⁴¹

• Cramer et al. have confirmed in animal studies that inactivity and immobilization result in the development of adhesions in the zygapophy-seal (facet) joints.⁴² They found that the duration of immobility was directly linked (“small, medium, large”) to the size and frequency of these spinal adhesions. They hypothesize that such adhesion development may have relevance to higher velocity spinal manipulation, which could theoretically break up Z-joint intra-articular adhesions.

Fibrosis and Keloids

Chronic inflammation leads to fibrosis, which may occur in soft tissues or organs as a result of excessive build-up of connective tissue.⁴³

As Fourie explains: “Fibrosis represents a pathologic excess of normal tissue repair. Excessive or sustained production of TGF-fil is a key molecular mediator of tissue fibrosis. It consistently and powerfully acts on cells to encourage the deposition of extracellular matrix. The connective tissue response to the internal (inflammatory mediators and growth factors) and external (motion and directional strain) stresses applied will determine how the scar matures. Thus, the scar can become either dense and unyielding or pliable and mobile. Remodeling is not restricted to the injured area only. Neighboring, noninjured tissue also changes its collagen production rate in response to inflammation.”⁴⁴

Welshhans and Homs report that factors that predispose an individual toward poor wound healing and excessive scarring, including irregularly shaped keloid scars that may progressively enlarge, include the following:

• Ethnicity may be a feature, with African, Hispanic, and Asian Indian individuals being more likely to have hypertrophic scar formation.

• Previous exposure to radiation results in excessive fibrosis and poor cellular replication during scar healing.

• Individuals who smoke or are being treated with corticosteroids and/or chemotherapy agents have increased risk for scarring.

• Poor nutritional status, particularly involving vitamins C and K and zinc, impedes normal healing.

• Having hyperplastic (hypermobile) joints due to increased levels of elastin.

• In younger (pre-puberty) individuals, remodeling takes longer than in adults, leading to more lengthy erythema and hypertrophy.

• Infection of foreign-body presence increases likelihood of excessive scarring.

• Conditions such as diabetes, collagen vascular disease, hypothyroidism, immunocompromised states, and diseases with delayed healing, have an increased risk for scarring.⁴⁵ 

Notes

1. H. M. Langevin et al., “Reduced Thoracolumbar Fascia Shear Strain in Human Chronic Low Back Pain,” BMC Musculoskeletal Disorders 12 (2011): 203.

2. W. Klingler, “Temperature Effects on Fascia,” in Fascia: The Tensional Network of the Human Body, eds. R. Schleip et al. (Edinburgh: Churchill Livingstone Elsevier, 2012): 421–4.

3. A. Pilat, “Myofascial Induction,” in Practical Physical Medicine Approaches to Chronic Pelvic Pain (CPP) and Dysfunction, eds. Chaitow et al. (Edinburgh: Elsevier, 2011). 

4. A. Stecco et al., “Fascial Components of the Myofascial Pain Syndrome,” Current Pain and Headache Reports 17, no. 8 (2013): 352; A. Stecco et al., “Ultrasonography in Myofascial Neck Pain: Randomized Clinical Trial for Diagnosis and Follow-Up,” Surgical and Radiologic Anatomy 36, no. 3 (2014): 243–53.

5. T. Luomala et al., “Case Study: Could Ultrasound and Elastography Visualize Densified Areas Inside the Deep Fascia?” Journal of Bodywork and Movement Therapies 18, no. 3 (2014): 462–68. 

6. H. M. Langevin et al., “Reduced Thoracolumbar Fascia Shear Strain.”

7. H. M. Langevin et al., “Reduced Thoracolumbar Fascia Shear Strain.”

8. A. Stecco et al., “Fascial Components of the Myofascial Pain Syndrome.”; A. Stecco et al., “Ultrasonography in Myofascial Neck Pain: Randomized Clinical Trial for Diagnosis and Follow-Up.”

9. K. K. Wong et al., “Mechanical Deformation of Posterior Thoracolumbar Fascia After Myofascial Release in Healthy Men: A Study of Dynamic Ultrasound Imaging,” Musculoskeletal Science & Practice 27 (2017): 124–30.

10. Y. H. Chen et al., “Increased Sliding of Transverse Abdominis During Contraction, After Myofascial Release, in Patients with Chronic Low Back Pain,” Manual Therapy 23 (2016): 69–75.

11. S. Gracovetsky, “Can Fascia’s Characteristics be Influenced by Manual Therapy?” Journal of Bodywork and Movement Therapies 20 (2016): 893–7.

12. P. L. Barnes et al., “A Comparative Study of Cervical Hysteresis Characteristics after Various Osteopathic Manipulative Treatment (OMT) Modalities,” Journal of Bodywork and Movement Therapies 17, no. 1 (2013): 89–94. 

13. S. Dennenmoser, R. Schleip, and W. Klingler, “Clinical Mechanistic Research: Manual and Movement Therapy Directed at Fascia Electrical Impedance and Sonoelastography as a Tool for the Examination of Changes in Lumbar Fascia After Tissue Manipulation,” Journal of Bodywork and Movement Therapies 20 (2015): 145.

14. A. Franklyn-Miller et al., “The Strain Patterns of the Deep Fascia of the Lower Limb,” in Fascial Research II: Basic Science and Implications for Conventional and Complementary Health Care (Munich: Elsevier GmbH, 2009).

15. A. Stecco et al., “The Anatomical and Functional Relation Between Gluteus Maximus and Fascia Lata,” Journal of Bodywork and Movement Therapies 17 (2013): 512–7.

16. L. Joseph et al., “Myofascial Force Transmission in Sacroiliac Joint Dysfunction Increases Anterior Translation of Humeral Head in the Contralateral Glenohumeral Joint,” Polish Annals of Medicine 21 (2014): 103–8.

17. L. Joseph et al., “Effect of Lumbopelvic Myofascial Force Transmission on Glenohumeral Kinematics—A Myofasciabiomechanical Hypothesis,” Polish Annals of Medicine 24 (2017): 276–82.

18. A. Vleeming, “The Thoracolumbar Fascia,” in Fascia: The Tensional Network of the Human Body, eds. R. Schleip et al. (Edinburgh:  Churchill Livingstone Elsevier, 2012): 56.

19. N. Avery and A. Bailey, “Restraining Cross-Links Responsible for the Mechanical Properties of Collagen Fibers; Natural and Artificial,” in Collagen: Structure and Mechanics, ed. P. Fratzl (New York: Springer, 2008): 81–110.

20. K. Sven and F. Josipa, “Interstitial Hydrostatic Pressure: A Manual for Students,” Advances in Physiology Education 31 (2007): 116–7.

21. S. Jiang et al., “AMPK Orchestrates an Elaborate Cascade Protecting Tissue from Fibrosis and Ageing,” Ageing Research Reviews 38 (2017): 18–27.

22. S. Jiang et al., “AMPK Orchestrates an Elaborate Cascade.”

23. L. Baumann, “Skin Ageing and its Treatment,” Journal of Pathology 211, no. 2 (2007): 241–51.

24. V. Macchi et al., “Histotopographic Study of Fibroadipose Connective Cheek System,” Cells Tissues Organs 191 (2010): 47–56.

25. P. P. Purslow, “Intramuscular Connective Tissue and its Role in Meat Quality,” Meat Science 70 (2005): 435–47.

26. J. Dommerholt, “Trigger Point Therapy,” in Fascia: The Tensional Network of the Human Body, eds. R. Schleip et al. (Edinburgh: Churchill Livingstone Elsevier, 2012): 297–302. 

27. Bradley, personal communication with author (2010)

28. D. G. Simons et al., Travell & Simons’ Myofascial Pain and Dysfunction: The Trigger Point Manual (Baltimore: Williams & Wilkins, 1998). 

29. J. Dommerholt, “Trigger Point Therapy.”

30. J. P. Shah et al., “Biochemicals Associated with Pain and Inflammation are Elevated in Sites Near to, and Remote from Active Myofascial Trigger Points,” Archives of Physical Medicine and Rehabilitation 89, no. 1 (2008): 16–23.

31. K. LeMoon, “Clinical Reasoning in Massage Therapy,” International Journal of Therapeutic Massage & Bodywork 1, no. 1 (2008): 12–18.

32. C. Bron and J. D. Dommerholt, “Etiology of Myofascial Trigger Points,” Current Pain and Headache Reports 16, no. 5 (2012): 439–44.

33. A. Stecco et al., “Fascial Components of the Myofascial Pain Syndrome.”; A. Stecco et al., “Ultrasonography in Myofascial Neck Pain.”

34. T. Ball, “Scleroderma and Related Conditions,” in Fascia: The Tensional Network of the Human Body, eds. R. Schleip et al. (Edinburgh: Churchill Livingstone Elsevier, 2012): 225–32.

35. M. Salavati et al., “Reliability of the Upper Trapezius Muscle and Fascia Thickness and Strain Ratio Measures by Ultrasonography and Sonoelastography in Participants with Myofascial Pain Syndrome,” Journal of Chiropractic Medicine 16, no. 4 (2017): 316–23. 

36. B. Hinz, “Wound Healing and the Extracellular Matrix,” presentation at Touro College of Osteopathic Medicine (August 18, 2013). 

37. A. Desmoulière, C. Chaponnier, and G. Gabbiani, “Tissue Repair, Contraction, and the Myofibroblast,” Wound Repair and Regeneration 13, no. 1 (2005): 7–12.

38. B. Hinz, “Mechanical Tension Controls Granulation Tissue, Contractile Activity and Myofibroblast Differentiation,” American Journal of Pathology 159, no. 3 (2001): 1009–20.

39. S. L. Chapelle and G. M. Bove, “Visceral Massage Reduces Postoperative Ileus in a Rat Model,” Journal of Bodywork and Movement Therapies 17, no. 1 (2013): 83–8.

40. T. S. Lee et al., “Prognosis of the Upper Limb Following Surgery and Radiation for Breast Cancer,” Breast Cancer Research and Treatment 110, no. 1 (2009): 19-37.

41. K. Lewit and S. Olsanska, “Clinical Importance of Active Scars: Abnormal Scars as a Cause of Myofascial Pain,” Journal of Manipulative and Physiological Therapeutics 27, no. 6 (2004): 399–402. 

42. G. D. Cramer et al., “Zygapophyseal Joint Adhesions after Induced Hypomobility,” Journal of Manipulative and Physiological Therapeutics 33, no. 7 (2010): 508–18.

43. T. A. Wynn, “Cellular and Molecular Mechanisms of Fibrosis,” Journal of Pathology 214, no. 2 (2008): 199–210.

44. W. J. Fourie, “Surgery and Scarring,” in Fascia: The Tensional Network of the Human Body, eds. R. Schleip et al. (Edinburgh: Churchill Livingstone Elsevier, 2012): 233–44. 

45. J. L. Welshhans and D. B. Homs, “Soft Tissue Principles to Minimize Scarring: An Overview,” Facial Plastic Surgery Clinics of North America 25 (2017): 1–13.