[libribook.com] Traumatic Scar Tissue Management 1st Edition
Clinical ConsiderationRecall from Chapter 4: lateral or tangential forces appear to have a morenotable impact on Ruffini endings, which are known to interface with theANS. SNS activation tends to activate transforming growth factor beta-1(TGF-β1) expression (and likely other cytokines), which has a stimulatoryeffect on MFB contraction, increasing fascial tone and stiffness. Inaddition, shifts in the ANS state can induce changes in pH, which alsoaffects MFB contraction. Skillful, manual stimulation of mechanoreceptorsin fascia, particularly of Ruffini or free nerve endings, can induce favorablechanges in ANS tone (Chaitow 2014).
Pathophysiological considerationCompromised vascularity, local ischemia and resultant hypoxia are primaryfactors in poor wound healing. Oxygen plays a key role in every healingphase including epithelialization, angiogenesis, collagen deposition,inflammation and bactericidal activity. Fibroblasts require a partial pressureof oxygen of 30–40 mmHg to synthesize collagen and enzymaticremodeling of collagen occurs between 20 and 200 mmHg. In comparison,chronic wounds have been measured to have a partial pressure of oxygen of5–20 mmHg (Sheffield 1988, Franz et al. 2007, Gordillo & Sen 2003,Schreml et al. 2010, Gantwerker & Hom 2012).
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- Page 697 and 698: Scar scalesScar scales can be used
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- Page 705 and 706: Table 9.1Comparative of normal and
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- Page 709 and 710: Myofascial meridian exampleSuperfic
- Page 711: Clinical ConsiderationKnee and back
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- Page 721 and 722: Safety FirstMT appears to have few
- Page 723 and 724: Deep workThe deep techniques noted
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- Page 753 and 754: TechniquesCommonly employed techniq
- Page 755 and 756: Treatment outcomesThe later stages
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- Page 775 and 776: Pressure Level 4 - Strong pressure/
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- Page 779 and 780: Neutralize pHFacilitate healing pro
- Page 781 and 782: Manual Lymphatic TechniquesEarly ma
- Page 783 and 784: Table 9.4Treatment guideline summar
- Page 785 and 786: Clinical ConsiderationEdema, excess
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Pathophysiological consideration
Compromised vascularity, local ischemia and resultant hypoxia are primary
factors in poor wound healing. Oxygen plays a key role in every healing
phase including epithelialization, angiogenesis, collagen deposition,
inflammation and bactericidal activity. Fibroblasts require a partial pressure
of oxygen of 30–40 mmHg to synthesize collagen and enzymatic
remodeling of collagen occurs between 20 and 200 mmHg. In comparison,
chronic wounds have been measured to have a partial pressure of oxygen of
5–20 mmHg (Sheffield 1988, Franz et al. 2007, Gordillo & Sen 2003,
Schreml et al. 2010, Gantwerker & Hom 2012).