Abnormal Wound Healing: Keloids and Hypertrophic Scars
Keloids and hypertrophic scars
are characterized by an accumulation of excess collagen and are
distinguished from each other by their appearance. Keloids grow beyond
the borders of the original wound and do not tend to resolve
spontaneously. Hypertrophic scars stay within the limit of the original
wound and do tend to regress spontaneously. Hypertrophic scars are
generally seen soon after tissue injury, whereas keloids can form as
late as a year after injury. Hypertrophic scars tend to be associated
with a contracture across a joint surface.
Upon histological examination, keloids and hypertrophic scars differ from normal skin by a rich blood supply, high mesenchymal density, and a thick epidermal layer. The collagen fibers in hypertrophic scars are loosely arrayed in a wavy pattern. Keloids demonstrate a disorganized pattern of large, irregularly shaped collagen fibers with a lower content of collagen cross-links compared to normal skin. Keloids also contain a greater amount of type III collagen than a mature scar, which suggests a failure in scar maturation.
Little is known about the etiology of keloid and hypertrophic scar formation. Abnormalities in cell migration, proliferation, inflammation, and the synthesis and secretion of extracellular matrix proteins, cytokines, and remodeling have all been associated with keloid and hypertrophic scar formation. Increased activity of fibrogenic cytokines and exaggerated responses to cytokines have been described. Transforming growth factor-β (TGF-β) appears to play an integral role in aberrant healing. More recently, abnormal interactions between epidermal-mesenchymal cells and regulatory genes, such as TP53, have been proposed.
That certain patients and conditions may predispose to hypertrophic scar formation is well known. Both hypertrophic scars and keloids occur more commonly in dark-skinned individuals. Wounds that cross skin tension lines or wounds that are located on the ear lobes or presternal and deltoid areas are common sites for these forms of abnormal healing. The role of wound tension has been examined and found to be related to the exaggerated response to tension of keloid fibroblasts relative to normal fibroblasts with regard to production of pro-fibrotic growth factors.
A single, optimal treatment technique for hypertrophic scars and keloids has not been developed, and the recurrence rate of these abnormal scars is high. Surgical management is reserved for cases that are unresponsive to conservative management. Conservative management includes pharmacologic therapy, pressure, laser, and radiotherapy. Each method has varying degrees of reported success.
Recent work has demonstrated that treatment of fibroblasts with the combined CO2 and Er:YAG lasers alters the differential expression of mediators responsible for fibrosis and collagen formation and organization. Laser therapy may play a role in the prevention of keloid and hypertrophic scar formation.
Upon histological examination, keloids and hypertrophic scars differ from normal skin by a rich blood supply, high mesenchymal density, and a thick epidermal layer. The collagen fibers in hypertrophic scars are loosely arrayed in a wavy pattern. Keloids demonstrate a disorganized pattern of large, irregularly shaped collagen fibers with a lower content of collagen cross-links compared to normal skin. Keloids also contain a greater amount of type III collagen than a mature scar, which suggests a failure in scar maturation.
Little is known about the etiology of keloid and hypertrophic scar formation. Abnormalities in cell migration, proliferation, inflammation, and the synthesis and secretion of extracellular matrix proteins, cytokines, and remodeling have all been associated with keloid and hypertrophic scar formation. Increased activity of fibrogenic cytokines and exaggerated responses to cytokines have been described. Transforming growth factor-β (TGF-β) appears to play an integral role in aberrant healing. More recently, abnormal interactions between epidermal-mesenchymal cells and regulatory genes, such as TP53, have been proposed.
That certain patients and conditions may predispose to hypertrophic scar formation is well known. Both hypertrophic scars and keloids occur more commonly in dark-skinned individuals. Wounds that cross skin tension lines or wounds that are located on the ear lobes or presternal and deltoid areas are common sites for these forms of abnormal healing. The role of wound tension has been examined and found to be related to the exaggerated response to tension of keloid fibroblasts relative to normal fibroblasts with regard to production of pro-fibrotic growth factors.
A single, optimal treatment technique for hypertrophic scars and keloids has not been developed, and the recurrence rate of these abnormal scars is high. Surgical management is reserved for cases that are unresponsive to conservative management. Conservative management includes pharmacologic therapy, pressure, laser, and radiotherapy. Each method has varying degrees of reported success.
Recent work has demonstrated that treatment of fibroblasts with the combined CO2 and Er:YAG lasers alters the differential expression of mediators responsible for fibrosis and collagen formation and organization. Laser therapy may play a role in the prevention of keloid and hypertrophic scar formation.
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