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Chapter 3: Wound Healing and Care

Regarding Fig. 3-1, which of the following statements is correct?



FIGURE 3-1. Phases of wound healing.


(A) Lymphocytes play a minor role during inflammation

(B) Wound healing is complete by 6 months

(C) Epithelialization occurs during maturation

(D) Granulation tissue develops during proliferation

(E) Myofibroblasts produce contracture of the wound during proliferation

(D) Wound healing can be divided into three phases: inflammation, proliferation, and maturation. The inflammatory phase is characterized by hemostasis, inflammation and increased vascular permeability. Platelet aggregation and activation are stimulated by exposure to collagen and intravascular and extravascular proteins. Platelet adhesion to the endothelium is mediated through the interaction between high-affinity glycoprotein receptors and the integrin receptor glycoprotein IIb/IIIa. Platelet alpha granules contain histamine, serotonin, and other vasoactive amines that cause vasodilation and increased vascular permeability and cytokines including PDGF and TGF-α. Complement factors promote neutrophil chemotaxis and adhesion. Macrophages also play a key role during the inflammatory phase; cleaning debris, releasing cytokines, and promoting chemotaxis.

A provisional extracellular matrix soon forms in the wound, composed primarily of fibrin and fibronectin, which form the scaffold for the migration of inflammatory, endothelia, and mesenchymal cells. By 48 h, the wound is completely epithelialized (and the surgical dressing can be safely removed). Cellular proliferation continues, as epidermis is reconstructed. The inflammatory phase resolves after 72 h, and macrophages begin to outnumber neutrophils.

The appearance of fibroblasts marks the beginning of the proliferative phase, which predominate after 2 to 4 days. This phase is mediated by cytokines, including PDGF, epidermal growth factor, TGF-β, and insulin-like growth factor. Angiogenesis reconstructs damaged vasculature, stimulated by high lactate levels, acidic pH, and low oxygen tension mediated by FGF-1 and VEGF.

Collagen is produced by fibroblasts beginning 3 to 5 days after injury and gradually replaces fibrin in the wound. After 4 weeks, synthesis rates decline to match the rate of collagen degradation by collagenase. Granulation tissue formation is characteristic of the proliferative phase and serves as bridge for wound maturation, especially in open wounds. The migration and revascularization of endothelial cells are facilitated by the formation of a new extracellular matrix formation of new capillary vessels.

Wound contraction begins 4 to 5 days after injury, and maximal wound contraction continues for up to 15 days. Myofibroblasts are modified fibroblasts that interact with extracellular matrix, leading to wound contraction. It appears that wound contraction is more dependent on myofibroblasts than collagen synthesis.

Approximately 21 days after injury, maximal collagen content is reached and maturation begins. During the ...

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