Painful Connections: Densification Versus Fibrosis of Fascia

Deep fascia has long been considered a source of pain, secondary to nerve pain receptors becoming enmeshed within the pathological changes to which fascia are subject. Densification and fibrosis are among such changes. They can modify the mechanical properties of deep fasciae and damage the function...

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Published inCurrent pain and headache reports Vol. 18; no. 8; p. 441
Main Authors Pavan, Piero G., Stecco, Antonio, Stern, Robert, Stecco, Carla
Format Journal Article
LanguageEnglish
Published Boston Springer US 01.08.2014
Springer Nature B.V
Subjects
Online AccessGet full text
ISSN1531-3433
1534-3081
1534-3081
DOI10.1007/s11916-014-0441-4

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Abstract Deep fascia has long been considered a source of pain, secondary to nerve pain receptors becoming enmeshed within the pathological changes to which fascia are subject. Densification and fibrosis are among such changes. They can modify the mechanical properties of deep fasciae and damage the function of underlying muscles or organs. Distinguishing between these two different changes in fascia, and understanding the connective tissue matrix within fascia, together with the mechanical forces involved, will make it possible to assign more specific treatment modalities to relieve chronic pain syndromes. This review provides an overall description of deep fasciae and the mechanical properties in order to identify the various alterations that can lead to pain. Diet, exercise, and overuse syndromes are able to modify the viscosity of loose connective tissue within fascia, causing densification, an alteration that is easily reversible. Trauma, surgery, diabetes, and aging alter the fibrous layers of fasciae, leading to fascial fibrosis.
AbstractList Deep fascia has long been considered a source of pain, secondary to nerve pain receptors becoming enmeshed within the pathological changes to which fascia are subject. Densification and fibrosis are among such changes. They can modify the mechanical properties of deep fasciae and damage the function of underlying muscles or organs. Distinguishing between these two different changes in fascia, and understanding the connective tissue matrix within fascia, together with the mechanical forces involved, will make it possible to assign more specific treatment modalities to relieve chronic pain syndromes. This review provides an overall description of deep fasciae and the mechanical properties in order to identify the various alterations that can lead to pain. Diet, exercise, and overuse syndromes are able to modify the viscosity of loose connective tissue within fascia, causing densification, an alteration that is easily reversible. Trauma, surgery, diabetes, and aging alter the fibrous layers of fasciae, leading to fascial fibrosis.
Deep fascia has long been considered a source of pain, secondary to nerve pain receptors becoming enmeshed within the pathological changes to which fascia are subject. Densification and fibrosis are among such changes. They can modify the mechanical properties of deep fasciae and damage the function of underlying muscles or organs. Distinguishing between these two different changes in fascia, and understanding the connective tissue matrix within fascia, together with the mechanical forces involved, will make it possible to assign more specific treatment modalities to relieve chronic pain syndromes. This review provides an overall description of deep fasciae and the mechanical properties in order to identify the various alterations that can lead to pain. Diet, exercise, and overuse syndromes are able to modify the viscosity of loose connective tissue within fascia, causing densification, an alteration that is easily reversible. Trauma, surgery, diabetes, and aging alter the fibrous layers of fasciae, leading to fascial fibrosis.Deep fascia has long been considered a source of pain, secondary to nerve pain receptors becoming enmeshed within the pathological changes to which fascia are subject. Densification and fibrosis are among such changes. They can modify the mechanical properties of deep fasciae and damage the function of underlying muscles or organs. Distinguishing between these two different changes in fascia, and understanding the connective tissue matrix within fascia, together with the mechanical forces involved, will make it possible to assign more specific treatment modalities to relieve chronic pain syndromes. This review provides an overall description of deep fasciae and the mechanical properties in order to identify the various alterations that can lead to pain. Diet, exercise, and overuse syndromes are able to modify the viscosity of loose connective tissue within fascia, causing densification, an alteration that is easily reversible. Trauma, surgery, diabetes, and aging alter the fibrous layers of fasciae, leading to fascial fibrosis.
ArticleNumber 441
Author Pavan, Piero G.
Stern, Robert
Stecco, Carla
Stecco, Antonio
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  fullname: Stecco, Carla
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Issue 8
Keywords Load
Densification
Lines of forces
Loose connective tissue
Overuse syndrome
Stress–strain curves
Connective tissue
Hyaluronan
Fibrosis
Aging
Mechanics
Fascia
Hysteresis
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PublicationTitle Current pain and headache reports
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Snippet Deep fascia has long been considered a source of pain, secondary to nerve pain receptors becoming enmeshed within the pathological changes to which fascia are...
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StartPage 441
SubjectTerms Connective tissue
Connective Tissue - pathology
Connective Tissue - physiopathology
Fascia - anatomy & histology
Fascia - pathology
Fascia - physiopathology
Fibrosis - diagnosis
Humans
Internal Medicine
Mechanical properties
Medicine
Medicine & Public Health
Musculoskeletal Physiological Phenomena
Myofascial Pain (R Gerwin
Myofascial Pain Syndromes - pathology
Myofascial Pain Syndromes - physiopathology
Myofascial Pain Syndromes - psychology
Pain
Pain Medicine
Section Editor
Topical Collection on Myofascial Pain
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Title Painful Connections: Densification Versus Fibrosis of Fascia
URI https://link.springer.com/article/10.1007/s11916-014-0441-4
https://www.ncbi.nlm.nih.gov/pubmed/25063495
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