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

Box 5.1
Factors that drive excessive collagen proliferation
During the remodeling stage, premature or anomalous mechanical
strain/tensional loading can exaggerate scar tissue formation (Akaishi et al.
2008, Wolfram et al. 2009, Bordoni & Zanier 2014).
Rubbing or friction, for example, due to a wound dressing or bandage
being too tight, can also result in an over-stimulation of inflammatory
response and subsequent pathological scar formation (Akaishi et al. 2008).
According to Bordoni & Zanier (2014) the direction of the lesion may also
be a consideration as those that lie horizontal to a body segment (e.g. calf)
induce three times greater tensional pull (i.e. mechanical strain) on the
developing scar (Miyamoto et al. 2009). Although it seems plausible, it has
not been confirmed whether lesion direction predisposes one to a higher
incidence of pathophysiological scar formation or has an effect on the scar
once the healing process has concluded.
Pathophysiological scars can perpetuate aberrant signaling (e.g. neuroinflammatory
and neurogenic signaling). This in turn can create a viscous
cycle of persistent presence of pro-inflammatory and pain agents (e.g.
substance P, calcitonin, cytokines and growth factors) further driving
excessive/pathological scar formation.
Inflammatory mediated disruption in the balance of fibrin-forming and
fibrin-dissolving capacities, favoring un-checked fibrin deposition
(Chapelle & Bove 2013).
Breathing patterns, acidic pH and anxiety have also been identified as other
potential contributing factors (Chaitow 2014).
CT and fascia’s response to the internal (inflammatory mediators and
growth factors) and external (mechanical strain) stresses applied will
determine how the scar matures. The scar can become either dense and