Deep incisions are repaired by stitching the wound edges together, resulting in a thin line of scar tissue on the surface of the skin. Deep excisional wounds require more extensive intervention to avoid major scarring. The gold standard treatment for a deep excisional skin wound of limited area is a full-thickness skin autograft (epidermis plus both layers of dermis). Full-thickness grafts give the best structural and cosmetic results because there is minimal contraction and scarring at the edges of graft and host skin. Furthermore, they take well because they contain a vascular plexus that can quickly establish connections with the vasculature at the wound site. The large area of harvested skin required to cover extensive excisional wounds, however, makes full-thickness skin grafts impractical because healing of the donor area is compromised.
To increase the area that can be covered by a skin autograft, surgeons use meshed split-thickness skin grafts (MSTSGs). A small area of partial-thickness donor skin consisting of epidermis and the papillary layer of the dermis is shaved off with a dermatome and the skin is meshed so it can be stretched out to cover a much wider wound area. The results obtained with MSTSGs, while saving lives, are often not satisfactory. Their vascular plexus is not as extensive as that of a full-thickness graft. Thus, in wounds where there has been extensive destruction of the reticular dermis, autografted MSTSGs can suffer weak attachment and epidermal blistering, reducing the percentage of grafts that take. Even in successful grafts, the healed skin is cosmetically unattractive due to excessive scar formation and contraction in the interstices of the mesh.
A major goal in treating normal and chronic skin wounds is to either accelerate their healing by fibrosis or to actually regenerate skin with the original architecture and function, using interventions based on what is known about the biology of skin repair. These interventions are the topical application of growth factors, cytokines, inhibitors of inflammation, and other compounds to accelerate fibrosis or regenerate skin, the use of keratinocyte transplants or bioartificial skin equivalents as living wound dressings until the host skin is repaired, or the use of acellular regeneration templates to induce skin repair from the sides and bottom of the wound.
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