[libribook.com] Traumatic Scar Tissue Management 1st Edition

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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).

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).

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