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

Clinical Consideration
During wound healing, continuous or cyclical loading (brief, light stretch
or compression) of mechanosensitive tissues stimulates resident fibroblasts
to secrete collagenase (Tortora et al. 2007) reducing the potential of excess
collagen formation (fibrosis and pathological cross-linking). Cyclical
stretch and/or compression – involving approximately 10% of available
tissue elasticity – doubles collagenase production, whereas continuous
stretching appears to be 50% less productive (Carano & Siciliani 1996,
Langevin 2010).
Stage 4: Remodeling
In this stage, regression of capillary hypervascularity occurs, ensuring a return to
normal vascular density and the wound continues to undergo contraction
(mediated by MFBs), which contributes to the formation of a mechanically
sound scar (Hinz et al. 2001, Hinz et al. 2012, Hinz 2013). Adequate amounts of
TGF-β1 and mechanical tension (produced by MFBs) play an important role in
assuring this stage culminates in the restoration of normal physiological (i.e. as
close to pre-trauma) ECM and tissue architecture (Desmoulière et al. 2005).
However, even physiological scars exhibit slightly out of the ordinary features
(e.g. smaller Type I collagen than that seen in undamaged tissue and the fiber
arrangement is less orderly or somewhat ‘non-specific’) (Bran et al. 2012,
Profyris et al. 2012, Bordoni & Zanier 2014).
The increase in scar matrix strength can somewhat impact tissue elasticity;
however, with healthy scars this will not result in pain or dysfunction. Normal
scar tissue progresses from being weak and easily broken down, to being red and
prominent, to finally becoming thin, pale and stable. The strength of the scar
tissue increases gradually, and reaches a plateau about 7 weeks after wounding
(Huang et al. 2013). As long as the scar appears redder than normal, remodeling
is still under way.
If the wound is healing normally, this stage should be relatively painless and