[New views on the physiology of wound healing]

A great deal of progress has been made in the last few decades in understanding the cellular and biochemical interplay that comprises the normal wound healing response. This response is a complex process involving intricate interactions among a variety of different cell types, structural proteins, growth factors and proteinases.

Acute wounds maturate through phases of coagulation, inflammation, matrix synthesis and deposition, angiogenesis, fibroplasia, epithelialization, contraction and remodelling, but three classic phases of wound healing are inflammation, fibroplasia and maturation.

Two main forms of fibroproliferative disorders are hypertrophic scars and keloids. These disorders are characterized by an overabundance of wound collagen through overproduction of collagen or impaired degradation of collagen. Hypertrophic scars are raised, pruritic and edematous lesions that do not exceed the margins of the original wound (in contrast to keloids). Histologically, these lesions are indistinguishable and are characterized by thick, hyalinized collagen bundles arranged in nodules. The degree of hypertrophic scarring is believed to be related to the duration of time during which the wound is allowed to remain in inflammatory phase of healing. Wound closure tension may also play a role by altering the intracellular cytoskeletion of fibroblasts and increased secretion of TGF-beta and cytokines.

Healing of chronic cutaneous wounds is still a great problem of modern society--huge costs, impaired quality of life. In the last few decades a great progress was made in understanding the cellular and biochemical interplay.