! ! ! ! ! ! Wound healing is a complex and dynamic process of replacing devitalized and missing cellular structures and tissue layers.

The human adult wound healing process can be divided into 3 or 4 distinct phases. Earlier authors referred to 3 phases: inammatory, broblastic, and maturation,[1] which had been denoted in earlier versions as inammatory, proliferative, and remodeling and this is maintained by some authors.[2] In the 4-phases concept, there are the hemostasis phase, the inammatory phase, the proliferative phase, and the remodeling phase. In the 3-phases approach, the hemostasis phase is contained within the inammatory phase.! ! Not only do authors vary the number of phases, but authors also denote di"erences in the phase descriptors used as: hemostasis phase, inammatory phase, proliferative phase, and remodeling phase[3] or hemostasis phase, inammatory phase, proliferative phase, and maturation phase.[4] Therefore, certain phases have more than one name, such as remodeling or maturation and proliferation or granulation.[5]! ! A recent query for phases of wound healing in PubMed retrieved 1011 records. Under the search query, wound healing and repair, 1 article was identied in PubMed in 1899. In 1989, there were 101 articles and in 2011 there were 1600 related articles. As our understanding of wound! healing progresses, further phases and subphases may well be delineated.! ! Within these broad phases are a complex and coordinated series of events that includes chemotaxis, phagocytosis, neocollagenesis, collagen degradation, and collagen remodeling. In addition, angiogenesis, epithelization, and the production of new glycosaminoglycans (GAGs) and proteoglycans are vital to the wound healing milieu. The culmination of! ! ! these biological processes results in the replacement of normal skin

structures with broblastic mediated scar tissue. For more information on wound healing, visit Medscapes Wound Management Resource Center.! ! This process can go awry and produce an exuberance of broblastic proliferation with a resultant hypertrophic scar, which by denition is conned to the wound site. Further exuberance can result in keloid formation (see image below), in which scar production extends beyond the area of the original insult. The collagen is thicker, more irregularly arranged, and more often causes pain. In a hypertrophic scar, the collagen is thinner and arranged more parallel to the wound. Furthermore, hypertrophic scars occur in all races, although less so in young and elderly persons. Hormonal changes may have an impact. Keloid scarring is more often seen in nonwhite persons.[6]! ! ! A patient referred for keloid formation after excision of facial cancer and reconstruction.! Conversely, insu#cient healing can result in a hypotrophic or atrophic scar formation (see image below). All wounds in adult skin heal with a scar. The degree of inammation has a direct impact on the ultimate scar formation.[7]