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Keloids and hypertrophic scars

Beth G Goldstein, MD
Adam O Goldstein, MD, MPH
Section Editors
Robert P Dellavalle, MD, PhD, MSPH
Moise L Levy, MD
Deputy Editor
Rosamaria Corona, MD, DSc


Keloids and hypertrophic scars represent an excessive tissue response to dermal injury characterized by local fibroblast proliferation and overproduction of collagen [1,2]. Keloids (from a Greek word meaning "crab's claw") are fibrous growths that extend beyond the original area of injury to involve the adjacent normal skin. Hypertrophic scars may have a similar clinical appearance, but in contrast with keloids, remain confined within the boundaries of the wound area and tend to regress spontaneously over time [3].

Keloids and hypertrophic scars may cause functional impairment and cosmetic disfigurement and are often associated with low self-reported patient quality of life [4].

This topic will review the pathogenesis, diagnosis, and treatment of keloids and hypertrophic scars. The management of keloid and hypertrophic scars following burn injuries is discussed separately. (See "Hypertrophic scarring and keloids following burn injuries".)


The precise incidence and prevalence of keloids and hypertrophic scars are unknown. Keloids have been reported in 5 to 16 percent of individuals of Hispanic and African ancestry [5]. An annual incidence of 15 per 10,000 has been reported in Taiwan [6]. Keloids affect men and women equally and are more common in younger individuals. There is a familial tendency to develop keloids; family studies suggest an autosomal dominant inheritance with incomplete penetrance [7].


The pathogenesis of hypertrophic scars and keloids is incompletely understood. It involves alterations in the sequential process of wound healing and may be influenced by multiple local and genetic factors [8-10]. In normal wound healing there is an initial marked local inflammatory reaction, followed by the formation of new blood vessels, activation of keratinocytes and fibroblasts at the edge of the wound, and synthesis of extracellular matrix components [11]. After the reepithelialization is completed, the dermal granulation tissue is remodeled into a scar and the replacement tissue adapts to biomechanical requirements. (See "Basic principles of wound healing".)

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Literature review current through: Nov 2017. | This topic last updated: Nov 02, 2016.
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