All wounds heal through the same orderly process. By understanding that process, you can facilitate wound care and spot potential problems. There are three phases of wound healing: the inflammatory, fibroblastic, and maturation stages.

WOUND WITHOUT SKIN LOSS
Consider first the simple laceration, a well-studied wound. Inflammation begins after injury and peaks at three to five days. The wound site swells as the biochemical ingredients needed for healing gather: leukocytes and monocytes for bacterial phagocytosis and lysis, fibrinogen for adherence of wound edges, histamine, prostaglandins, and vasoactive substances for hemostasis. This initial healing period was in the past known as the "lag phase" - based on the mistaken notion that nothing significant was occurring, since the wound remained mechanically weak. However, a great deal happens during this stage, and today, it is known as the substrate or inflammatory phase. This must occur to prepare the wound for the succeeding phases of healing. Therefore, drugs which limit inflammation, such as non-steroidal anti-inflammatories or steroids, will slow the healing of a wound.

After the biochemical components of healing are assembled, fibroblasts begin to proliferate and position themselves for their principal task, collagen synthesis. As collagen content increases, the wound site strengthens. Sutures may be removed in three to fourteen days, depending on their location. However, the wound's tensile strength and collagen content increase over the next several weeks; collagen turnover within the wound continues indefinitely. This second stage of wound healing is often called the fibroblastic or collagen phase.

Ascorbic acid plays an essential role in collagen formation. Without vitamin C, proline cannot be hydroxylated to hydroxyproline, meaning that collagen synthesis stops. Recall that Herman Melville's scorbutic sailors in chase of Moby Dick witnessed their old wounds break open. Today, we explain why this happened. Without ascorbic acid, collagen synthesis stops while collagen resorption continues at a normal pace, leading eventually to wound breakdown.

The third and final stage of wound healing lasts the longest. This maturation, or remodeling phase, may continue for several years, with concomitant improvements in wound appearance. During this interval, progressive collagen replacement yields a softer, less conspicuous scar. Plastic surgeons depend on maturation for the gradual improvement of postoperative scars.

WOUNDS WITH LOSS OF SKIN
Acute, traumatic injuries that result in loss of skin - such as a full-thickness burn, a deep abrasion, or avulsion - will pass through the same phases of healing. However, wound closure requires two additional biological mechanisms: epithelial migration and wound contraction.

a. Epithelialization

As soon as the biochemical and cellular substrates for healing are assembled and bacterial contamination falls below 10⁵ organisms/gm, the epithelium begins to proliferate and migrate across the wound surface. If the wound is a superficial burn or abrasion, the epithelium will spread quickly from sweat glands and hair follicles, covering entire wound surface within 10 to 14 days. When full thickness skin has been lost, epithelium can migrate only from the wound margins. Epithelialization is very slow process, and is often insufficient for timely wound closure. Furthermore, epithelium migrates without an accompanying dermal layer, and is therefore vulnerable to injury.

The histology of migratory epithelium often appears neoplastic. A chronic wound that is not closed for many years might in time become a malignant ulcer, named for the French surgeon, Marjolin, who first described this complication of a longstanding surface defect.

Reconstructive surgeons who manage extensive wounds learn not to depend exclusively on epithelialization, except for the smallest or most superficial of injuries. Instead, they use grafts or flaps for wound closure.

b. Wound Contraction

With time, open wounds attempt to close themselves through internal forces. When a wound "granulates," this means that its surface fills with granulation tissue, an appropriate name for the pebbly surface appearance that results from capillary/fibroblast proliferation. The formation of granulation tissue in an open wound corresponds to the fibroblastic phase of primary wound healing.

After granulation, the wound edges pull to the center, a shift that cannot be explained by epithelialization alone. This gradual shrinking of a wound's surface is known as contraction. Today, it is believed that contraction is due to myofibroblasts, highly specialized fibroblasts that behave like smooth muscle cells.

This process is the basis for burn scar contractures, Dupuytren's contracture, and cirrhotic hepatic fibrosis, as well as many other problems characterized by uncontrolled contraction.

Neither epithelial migration nor contraction will proceed in the presence of heavy bacterial contamination (more than 10⁵ organisms/gm). Contraction can be slowed by application of split-thickness skin grafts, and very nearly stopped with full-thickness grafts or a skin flap. Certain synthetic membranes such as Biobrane^TM can also inhibit contraction.

Therefore, large wound defects are best treated by surgical closure, and should not be allowed to heal by spontaneous or natural means.