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[libribook.com] Traumatic Scar Tissue Management 1st Edition
Clinical ConsiderationThe presence of higher than normal concentration of MFBs in injured andscarred fascia further accentuates its ability to contract/influence tension(e.g. contractures, fibrosis) resulting in subsequent pain and dysfunction.It is suggested that MFBs also play a role in issues associated with decreasedmyofascial tension or hypermobility (e.g. peri-partum pelvic pain due to pelvicinstability, sacroiliac joint force closure dysfunction or back pain due to spinalsegmental instability) (Schleip et al. 2012).MFBs are also present in normal healthy fascia implying a valid – homeostatic –functional purpose (Wilson & Dahners 1988, Murray & Spector 1999, Ralphs etal. 2002). For example, MFBs provide fascia with the ability to remodel itself inresponse to normal daily movement and activity demands (adaptation). Recallfrom page 12: fibrocollagenous tissue morphology is shaped by tensionalloading. Demand (mechanical/tensile forces) invokes MFB proliferation andtherefore (normally) higher concentrations of MFBs are typically present indense presentations of fascia commonly subjected to higher tensional demands(e.g. those that play a significant role in stability and support, fascia lata, plantar,crural and thoroacolumbar fascia, perimysium).Biomechanically, interactions between MFBs and the ECM contribute to wholebody mobility and tensional integrity or biotensegrity (Schleip et al. 2005,Guimberteau 2007, Ingber 2008, Levin & Martin 2012).Fibrous ProteinsFascia is constructed from two predominant fiber types:• Collagen• Elastin.
CollagenCollagen is the most abundant fiber type found throughout fascia. Various typesof collagen occur in the human body (Type I is the most predominant) (Gelse etal. 2003, Gartner & Hiatt 2007, Gordon & Hahn 2010, Ross & Pawlina 2011,Kumka & Bonar 2012).Collagen cross-linking, a chemical bond between adjacent collagen fibers, playsa significant role in tissue integrity. Physiological linkage augments mechanicalstability, however excessive (pathological) cross-links can interfere with slidepotential and contribute to mobility restrictions. Conversely, insufficient orunstable bonds can result in diminished tissue integrity.Collagen provides tensile strength, guards against over extension and can ‘storeand release’ energy (can store and release an equal amount of energy whilestretching only 100th the amount of elastin) (Zorn 2011). This is often referred toas catapult or rebound effect. Collagen fibers are somewhat firm yet pliant andable to yield to force (e.g. they can bend, twist and lengthen). Collagen’s elasticstiffeningpotential (viscoelastic property) is considered to be one of its definingfeatures (Zorn & Hodeck 2011). Normal healthy collagen fibers display adistinctive ‘wavy/crimped’ formation which factors into normal healthyfunctioning (e.g. force transmission and energy facilitation).Adequate hydration is vital to collagen health and functioning. Dehydration hasbeen identified as an initiator of inflammatory response in collagen and oncepresent, inflammatory mediators can contribute to tension held in collagenoustissues (e.g. skin and fascia). As previously noted, dehydration also decreases thefluid-bulk of GS which can result in pathological collagen cross linking,diminished lubrication and reduced tensile strength.Type I collagen is the fiber type typically laiddown during tissue remodeling.Under healthy normal circumstances, collagen turnover (reconstruction phase ofhealing) lasts from 300 to 500 days, meaning it takes that length of time forcollagen to fully mature – an important consideration in post-trauma recoveryand rehabilitation (van den Berg 2010).Kumka and Bonar (2012) note that if function changes (e.g. increasedmechanical strain, insufficient mechanical strain or prolonged immobilization),
- Page 205 and 206: Therapeutic relationshipEncompasses
- Page 207 and 208: Trait anxietyA more intense degree
- Page 209 and 210: TraumaInsult or injury to the physi
- Page 211 and 212: Traumatic scarPathophysiological sc
- Page 213 and 214: ViscoelasticityThe ability of a med
- Page 215 and 216: Nowadays it is common to see massag
- Page 217 and 218: A Reasonable NexusPrecise etiologic
- Page 219 and 220: integration of art and science are
- Page 221 and 222: Diamond M (2012) Scars and adhesion
- Page 223 and 224: General HistologyExtracellular Matr
- Page 225 and 226: Clinical ConsiderationVitamin C has
- Page 227 and 228: Ground substanceGround substance (G
- Page 229 and 230: Pathophysiological ConsiderationIn
- Page 231 and 232: HyaluronanThis hydrophilic, viscous
- Page 233 and 234: Clinical ConsiderationHA and its fr
- Page 236 and 237: Figure 2.1Layers and components of
- Page 238 and 239: Skin HistologyThe skin comprises:
- Page 241 and 242: Figure 2.2The delicate, well-hydrat
- Page 243 and 244: DermisThe dermis is made up of laye
- Page 245 and 246: Fascia Structure and FunctionsIn th
- Page 247 and 248: fundamental characteristic is its c
- Page 249 and 250: tensional properties co-exist in bo
- Page 251 and 252: HistologyFascia comprises:• ECM (
- Page 253 and 254: Clinical ConsiderationManual therap
- Page 255: Clinical ConsiderationTransforming
- Page 259 and 260: Clinical ConsiderationSignificant c
- Page 261 and 262: Fascia Layers and FunctionsFascia t
- Page 263 and 264: Clinical ConsiderationSuperficial a
- Page 265: Clinical ConsiderationWhen thickene
- Page 268 and 269: LinkingLinking fascia is sub-divide
- Page 270 and 271: FascicularFascicular fascia augment
- Page 272 and 273: Clinical ConsiderationMuscle spindl
- Page 274 and 275: SeparatingSeparating fascia provide
- Page 276 and 277: Clinical ConsiderationFascia suppor
- Page 278 and 279: Andrade C-K (2013) Outcome-based ma
- Page 280 and 281: Ingber D (2008) Tensegrity and mech
- Page 282 and 283: tendons: organisation in vivo and r
- Page 284 and 285: Zorn A, Hodeck K (2011) Walk with e
- Page 286 and 287: Discovery of the Lymphatic SystemTh
- Page 288 and 289: Hematic SystemThe heart, blood vess
- Page 290 and 291: Lymphatic System Structure and Func
- Page 292 and 293: Clinical ConsiderationNerves, blood
- Page 295: Figure 3.1Lymph tissue structure.In
- Page 298 and 299: Lymphoid OrgansThe lymphoid organs
- Page 300 and 301: ThymusThe thymus is a lymphoid glan
- Page 302 and 303: Lymphatic Drainage and TransportIn
- Page 304 and 305: SuperficialThe superficial layer is
Collagen
Collagen is the most abundant fiber type found throughout fascia. Various types
of collagen occur in the human body (Type I is the most predominant) (Gelse et
al. 2003, Gartner & Hiatt 2007, Gordon & Hahn 2010, Ross & Pawlina 2011,
Kumka & Bonar 2012).
Collagen cross-linking, a chemical bond between adjacent collagen fibers, plays
a significant role in tissue integrity. Physiological linkage augments mechanical
stability, however excessive (pathological) cross-links can interfere with slide
potential and contribute to mobility restrictions. Conversely, insufficient or
unstable bonds can result in diminished tissue integrity.
Collagen provides tensile strength, guards against over extension and can ‘store
and release’ energy (can store and release an equal amount of energy while
stretching only 100th the amount of elastin) (Zorn 2011). This is often referred to
as catapult or rebound effect. Collagen fibers are somewhat firm yet pliant and
able to yield to force (e.g. they can bend, twist and lengthen). Collagen’s elasticstiffening
potential (viscoelastic property) is considered to be one of its defining
features (Zorn & Hodeck 2011). Normal healthy collagen fibers display a
distinctive ‘wavy/crimped’ formation which factors into normal healthy
functioning (e.g. force transmission and energy facilitation).
Adequate hydration is vital to collagen health and functioning. Dehydration has
been identified as an initiator of inflammatory response in collagen and once
present, inflammatory mediators can contribute to tension held in collagenous
tissues (e.g. skin and fascia). As previously noted, dehydration also decreases the
fluid-bulk of GS which can result in pathological collagen cross linking,
diminished lubrication and reduced tensile strength.
Type I collagen is the fiber type typically laiddown during tissue remodeling.
Under healthy normal circumstances, collagen turnover (reconstruction phase of
healing) lasts from 300 to 500 days, meaning it takes that length of time for
collagen to fully mature – an important consideration in post-trauma recovery
and rehabilitation (van den Berg 2010).
Kumka and Bonar (2012) note that if function changes (e.g. increased
mechanical strain, insufficient mechanical strain or prolonged immobilization),
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