Remodeling Phase
July 22, 2007 on 7:51 am | In Surgery |David J. Terris
In the remodeling or maturation phase, the inflammatory response has resolved, angiogenesis diminishes, and the intense fibroplasia begins to subside. The process of collagen lysis, which is perpetual, reaches equilibrium with the level of collagen synthesis. This dynamic balance between collagen synthesis and lysis is responsible for the maturation of the wound.
The net gain in tensile strength undergoes an exponential growth phase that plateaus in a prolonged period of gradually increasing wound strength. This is reflected in classic studies using a rat model. However, the scar tissue never regains the breaking strength of normal skin, reaching a maximum strength of approximately 80% of unwounded skin.
Wounds that are left open to heal by secondary intention rely heavily on epithelialization and wound contraction. Epithelialization begins within 24 hours after wounding by migration of basal keratinocytes either from the edges of the wound or from within the wound if they are still intact. This migration, as well as the concomitant proliferation of keratinocytes, is stimulated by several cytokines. Another proposed stimulant for keratinocyte migration and proliferation is the “free-edge” effect, whereby these activities are precipitated by the absence of adjacent cells at the margin of the wound.
The second important element of secondary healing, which is often exploited by surgeons but can be deleterious, is wound contraction. This process occurs by the stretching of surrounding skin to close the defect rather than by production of new skin. The mechanism of this contraction remains poorly understood. There is evidence to support the role of a specialized fibroblast called the myofibroblast, which contains abundant actinomyosin and behaves like smooth muscle. The granulation tissue of contracting wounds contains as much actinomyosin as the uterus, for instance, and these myofibroblasts are capable of causing contraction of granulation tissue in vitro. Wound contraction is inhibited when anti-smooth muscle agents are applied topically. Additional studies, however, suggest that collagen and the ground substance may contribute to the process of wound contraction. It may be that the combination of both a specialized cell (the myofibroblast) and a material susceptible to contraction (the ground substance) is necessary for contraction to occur.
When the process of contraction occurs in vital areas where there is little or no redundant skin, the net effect may be detrimental. Examples include contraction of a lower eyelid defect that produces an ectropion or of a defect of the palmar surface of the hand to cause a flexion contracture. The best method for prevention of contraction is placement of a skin flap. Full-thickness grafts are nearly as effective as skin flaps, but split-thickness skin grafts provide only slight inhibition of contracture.
Open wounds heal more quickly when they are kept moist, and they should therefore not be left open to air. A scab (comprised of dried or denatured proteins and dead cells) may form and should be left intact, because wound healing will continue efficiently beneath it. When an eschar forms (representing necrotic tissue from burns or flap loss, for instance) it may inhibit healing and should be debrided gently.
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