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

size/depth, anatomic region, and local mechanical tension all factor into wound
healing process and subsequent nature of the scar (Niessen et al. 1999, Cho et al.
2014).
Multiple studies on hypertrophic and keloid scar formation have been conducted
over several decades, leading to many therapeutic strategies to prevent or
attenuate excessive scar formation. Most therapeutic approaches remain
clinically unsatisfactory, however, with an agreement that there is a meager
understanding of the complex mechanisms underlying the processes of scarring
and wound contraction and fibroproliferative disorders in general (Gauglitz et al.
2011, Rabello et al. 2014).
Scar pathogenesis involves cellular and extracellular matrix (ECM) components
in both the epidermal and dermal layers that are regulated by a wide array of
interfering factors in the inflammation, proliferation, and remodeling stages of
healing (Huang et al. 2013).
Hypertrophic scarring after deep or partial-thickness wounds is common. A
review of the literature on the prevalence of hypertrophic scarring found that
females, children, young adults, and people with darker, more pigmented skin
are particularly at risk and, in this subpopulation, the prevalence is up to 75%
(Engrav et al. 2007). Hypertrophic scars are morphologically characterized by
(Linares 1996, Cho et al. 2014):
• Abnormal collagen
• Reduced elastin
• Persistent cellularity
• Alterations in proteoglycan composition and amount
• Prolonged inflammatory reaction resulting in persistent hypervascularity and
excess deposition of ground matrix.
Feature
Hypertrophic scar
(HS)
Keloid scar (KS)
Demographic prevalence Pigmented skin Age 10–30, rare in elderly
Regional prevalence
Risk factors
Across areas of high
stress/tension (e.g.
joints)
Common complication
Anterior chest,
shoulders, earlobes,
upper arms and
cheeks
Both