ABSTRACT
Skin loss by burns, abrasions, surgical incisions, infection, or the termination of the local blood supply initiates the wound healing response. Irreversible cell death coupled with dermal disruption in burns usually requires replacement with a skin graft containing viable cells and a new connective tissue matrix. In the absence of skin grafting, the host’s response is to replace or repair lost tissues by either tissue regeneration or scar deposition. Skin repair by regeneration in mammals is limited to the epidermal layer. The restoration of lost dermis is by scarring, with the exception of fetal repair at specific gestational ages of specific species (1). Regenerative repair is the ideal modality for the restoration of lost skin, but cellular necrosis coupled with the disruption of the connective tissue matrix of dermis initiates the deposition of granulation tissue and its maturation of that transitional tissue into scar (2). Histological differences define scar from skin. Scar lacks both subepidermal appendages as well as re´te´ pegs at the epidermaldermal interface. The normal basketweave pattern of collagen fiber bundles from lost dermis is replaced with collagen fiber bundles arranged in arrays parallel to the skin surface. The basketweave pattern allow the flexibility of skin dermis associated with tissue strength. In scar, the parallel arrangement of the collagen fiber bundles accounts for the lack of tissue malleability and suppleness. Functionally, normal scar is less elastic.
