Current Concepts In Treating Hypertrophic Scars And Keloids
Given that a keloid or hypertrophic scar may cause disfigurement, pruritus, pain and contractures that can result in deformity and disability, prevention is the first and most important step in the management of these scars. These authors discuss the pathophysiology of scar formation, risk factors, keys to prevention and available treatments for keloids or hypertrophic scars.
Normal wound healing involves reepithelialization, angiogenesis, fibroblast hyperplasia, fibrin deposition, and production of tissue components such as collagen. New tissue, in the form of a scar, has a different architecture from the normal skin. A balance usually occurs between new tissue biosynthesis and degradation so patients avoid excess scar formation. An imbalance in this process can lead to a keloid or a hypertrophic scar.1,2
Cutaneous scarring following skin trauma or a wound is a major cause of morbidity and disfigurement. Hypertrophic scars and keloids have very similar pathologic processes. By definition, hypertrophic scars do not extend beyond the initial site of injury while keloids typically project beyond the original wound margins. Hypertrophic scars may occur anywhere. However, keloids predominantly affect the ear lobe, neck and chest.1,2
The prevalence rate of hypertrophic scarring in patients treated in burn centers may be as high as 70 percent.3 Other insults to the deep dermis, including lacerations, abrasions, piercings and vaccinations, can also cause scarring. The resultant disfigurement, pruritus, pain and contractures can dramatically affect a patient’s quality of life.2
The occurrence of keloids and hypertrophic scars has the highest incidence in the second to third decade of life. African-American populations are more susceptible to keloid formation.2 Genetics and family history are strongly associated with the formation of keloid scars. More than 50 percent of all patients with keloids have a positive family history of keloid scarring.2
Understanding The Pathophysiology
We can categorize the process of wound healing into three overlapping phases. In the first inflammatory phase of wound healing (days one to three), macrophages enter the injury zone and phagocytize pathogens and tissue debris.
In the second proliferative phase (days four to 21), macrophages accumulate while endothelial cells and fibroblasts proliferate, and make new dermal tissue. Through the secretion of platelet-derived growth factor (PDGF) and transforming growth factor beta 1 (TGFb1), macrophages induce fibroblasts to proliferate and lay down type III collagen. An overactive second phase results in the formation of hypertrophic scars and keloids. Reepithelialization usually occurs in the first to second stage.
In the third remodeling phase (day 21 to year one), apoptosis occurs in a portion of the newly formed cells.1,4-7 As the wound matures, the composition of the extracellular matrix changes. The type III collagen deposited in the proliferative phase slowly degrades and type I collagen replaces it. Type I collagen is oriented as small parallel bundles that differ from the basket weave orientation of collagen present in normal dermis. Within this abnormal collagenous network, there is an absence of hair follicles, sebaceous glands and sweat glands. The extent to which these changes in skin structure occur after cutaneous injury depends on the severity and extent of inflammation, and the depth of injury. The deeper cutaneous injuries give rise to more scar tissue.1,4-6,8