Wound healing

The process of wound healing may be best understood by dividing it into phases.1-4 These phases are somewhat arbitrary, as they overlap in time, physiology, and cell type, with each phase not entirely completed before the next begins. Our knowledge of these phases is constantly improving, resulting in additional revision of our understanding of how these different aspects of healing interact. In addition, not all wounds heal in precisely the same manner due to differences in the etiology of the wound, presence or absence of infection, and medical or surgical interventions. Which of these components predominates depends on whether the wound is closed immediately (first intention), allowed to granulate (secondary intention), or has delayed primary closure (third intention). These processes remain more similar than different regardless of how the wound is managed. Medical and surgical interventions primarily change the time course of events. For the purposes of the present discussion, the healing process will be divided into the five components of hemostasis, inflammation, proliferation, contraction, and remodeling (Figure 1.1).

FIGURE 1.1 The process of wound healing may be considered to consist of five overlapping stages. Some authors combine one or more of these stages under a single category. The time course of these stages depends upon methods of treatment and metabolic status of the injured individual.


Healing begins the instant the wound is made. When the skin is cut, the body responds with a complex mechanism that protects us from exsanguination. Vasoconstriction is almost immediate to decrease blood loss, but enough blood is released in the wound to stimulate Hageman Factor (XII) to initiate the clotting cascade.3-5 Collagen, present in all tissues of the body and ironically the major protein of wound healing, is exposed in the wound, resulting in stimulation of the alternate complement pathway as well as platelet adherence and degranulation.346 Along with complement and Hageman pathway stimulation, numerous additional vasoactive and chemotactic components are released. Blood fibrinogen quickly converts to fibrin, which, along with platelets, helps form what is commonly called a scab.3 78 The scab ultimately provides a temporary protective barrier. The fibrin forms a pathway to aid cell migration, especially for the fibroblast, one of the major cells of the proliferative phase of wound healing.9

One of the most active components of the hemostatic phase of wound healing is the platelet. Platelets are present in the blood; they rapidly aggregate and degranulate in the wound. With degranulation, numerous cytokines, such as PDGF (platelet-derived growth factor) are released (Table 1.1).346-8 PDGF is a potent cytokine with numerous functions, including being a chemoattractant for neutrophils, one of the dominant cells of the inflammatory phase (Figure 1.1).

The stage of hemostasis does more than just stop exsanguination. It also initiates the process of healing by creating a protective layer to minimize the infection risk while providing both a biochemical milieu and physical framework for the stages that follow.

Thus, the hemostatic stage prepares for and influences the onset of the next stage of healing — inflammation.


Overlapping with the stage of hemostasis is the stage of inflammation (Figure 1.1). While fibrin is forming and platelets are aggregating, leukocytes are coming into

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