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

Figure 5.1
Hypertrophic scar example.
The Four Stages of Wound Healing (Marieb 2003; see
Also Table 5.1)
Stage 1: Homeostasis
The healing process begins within seconds after injury when tissue and blood
vessels are disrupted. Vessel wall rupture results in the release of blood-borne
cells, proteins and platelets into the periphery (ECM). Platelets are activated
upon coming into contact with collagen and other ECM constituents outside of
the blood vessels. Activated platelets adhere together, forming an initial plug to
slow or stop blood loss. The platelet coagulation cascade results in the
production of a stable fibrin-reinforced clot and provisional matrix. A
provisional matrix, comprising fibrin and Type III collagen, provides structural
support for cellular attachment and subsequent cellular proliferation within the
wound (Tredget et al. 1997). Once bleeding is controlled, various signaling
molecules (e.g. pro-inflammatory cytokines and growth factors, such as TGF-β1;
epidermal growth factor – EGF; insulin-like growth factor – IGF1; and platelet
derived growth factor – PDGF), stimulate chemotaxis, the migration of
inflammatory and reparative cells (e.g. neutrophils, macrophages, epithelial and
endothelial cells, mast cells and fibroblasts) to the wound, initiating the next
stage (Gauglitz et al. 2011, Guo & DiPietro 2010, Bordoni & Zanier 2014, Zhu
et al. 2013).
Stage 2: Inflammation
In this stage, specific types of cells perform specific tasks. Neutrophils, mast
cells and macrophages clean up potentially contaminating micro-organisms,
degrade surplus components and rid the area of waste material.
Macrophages also secrete a variety of chemotactic and growth factors (e.g.