The process of wound healing of the skin is classically described as either a primary or secondary union. Healing by primary union (frst intention) occurs after surgical in-cisions in which wounds that are usually clean and unin-fected have their edges approximated by surgical sutures. The healing by secondary union (secondary intention) occurs in traumatic wounds with separated edges, which are characterized by more extensive loss of cells and tis-sues. Wound healing in such cases involves generating a large amount of granulation tissue, which represents a specialized type of tissue formed during the repair process. The repair of an incision or laceration of the skin requires stimulated growth of both the dermis and the epidermis. Der-mal repair involves (1) blood clot formation, (2) removal of damaged collagen fibers, primarily through the effort of macrophage activity that is associated with inflammation, (3) formation of granulation tissue, (4) reepithelialization of the exposed surface, (5) proliferation and migration of fibroblasts and differentiation of myofibroblasts involved in wound contraction, and (6) deposition and remodeling of the extracellular matrix of underlying connective tissue. Healing by primary union following application of sutures reduces the extent of the repair area through maximal closure of a wound, minimizing scar formation. Surgical incisions are typically made along cleavage lines; the cut tends to parallel the collagen fibers, thus minimizing the need for excess collagen production and the inherent scarring that may occur. Repair of the epidermis involves the proliferation of the basal keratinocytes in the stratum basale in the undamaged site surrounding the wound (Fig. F15.6.1). Mitotic activity is markedly increased within the first 24 hours. In a short time, the wound site is covered by a scab that represents dehydrated blood clot. The proliferating basal cells of the stratum basale begin migrating beneath the scab and across the wound surface. The migration rate may be as much as 0.5 mm/day, starting within 8 to 18 hours after wounding. Further proliferation and differentiation occur behind the migration front, leading to restoration of the mul-tilayered epidermis. As new cells ultimately keratinize and desquamate, the overlying scab is freed with the desqua-mating cells, which explains why a scab detaches from its periphery inward. In cases in which the full thickness of the epidermal layer is removed either by trauma or in surgery, the parts of hair follicles, the follicular bulge that contains niche of the epidernal stem cells, will produce cells that migrate over the exposed surface to reestablish a complete epithelial (epidermal) layer. Massive destruction of all of the epithelial structures of the skin, as in a third-degree burn or extensive full-thickness abrasion, prevents reepithelialization. Such wounds can be healed only by grafting epidermis to cover the wounded area. In the absence of a graft, the wound would, at best, reepithelialize slowly and imperfectly by ingrowth of cells from the margins of the wound. FIGURE F15.6.1 • Photomicrograph showing a late stage in the epidermal repair of a skin wound. The initial injury was caused by an incision through the full thickness of the skin and partially into the hypodermis, which contains adipose cells (A). The epidermis has re-formed beneath the scab. The asterisk marks an artifact where epithelium separated during specimen preparation. The scab, which contains numerous dead neutrophils in its inferior aspect, is close to the point of release. The dermis at this stage shows little change during the repair process but will ultimately reestablish itself to form a continuous layer. 110. LLLL L*scabL*scabL*scabL *scabA A * scab
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