Keloid scarring: bench and bedside

Abstract

Wound healing is a fundamental complex-tissue reaction leading to skin reconstitution and thereby ensuring survival. While, fetal wounds heal without scarring, a normal "fine line" scar is the clinical outcome of an undisturbed wound healing in adults. Alterations in the orchestrated wound healing process result in hypertrophic or keloid scarring. Research in the past decades attempted to identify genetic, cellular, and molecular factors responsible for these alterations. These attempts lead to several new developments in treatments for keloids, such as, imiquimod, inhibition of transforming growth factor beta, and recombinant interleukin-10. The urgent need for better therapeutics is underlined by recent data substantiating an impaired quality of life in keloid and hypertrophic scar patients. Despite the increasing knowledge about the molecular regulation of scar formation no unifying theory explaining keloid development has been put forward until today. This review aims to give an overview about the genetic and molecular background of keloids and focus of the current research on keloid scarring with special emphasis on new forthcoming treatments. Clinical aspects and the spectrum of scarring are summarized.

Scar Management in the Pediatric and Adolescent Populations

“…Keloid formation typically affects dark-skinned individuals (Fitzpatrick IV-VI skin type) to a greater extent than those with lighter skin (Fitzpatrick I-III skin type), with the majority of keloids manifesting in persons 10 to 30 years of age. 2,6,7 Younger children are still susceptible, however, as bilateral earlobe keloids have been documented in a 9-month-old African American girl 6 months after piercing. 8 In addition to differences in clinical appearance, keloids often differ histopathologically from hypertrophic scars in a variety of ways, with the most distinguishing feature being the presence of thickened hyalinized collagen (keloidal collagen).…”

“…Any scar can be symptomatic, and even clinically benign-appearing scars may cause a patient physical, psychological, and social comorbidities leading to severe impairment of quality of life. 2 To label 1 type of scar "pathologic" and another "normal" by virtue of morphology or histopathology alone misses this point.…”

Genetic association of the COL1A1 gene promoter –1997 G/T (rs1107946) andSp1 +1245 G/T (rs1800012) polymorphisms and keloid scars in a Jeddah population

“…They are unique in humans, and especially in genetically susceptible individuals from nonwhite populations (1)(2)(3). It has been estimated that about 15%-20% of Blacks, Hispanics, and Orientals suffer from keloids and there appears to be a genetic predisposition to keloid formation (4).…”

“…It has been estimated that about 15%-20% of Blacks, Hispanics, and Orientals suffer from keloids and there appears to be a genetic predisposition to keloid formation (4). Keloids can develop at every age, but they have a higher incidence between 10 and 30 years (1,3). A slight female predominance is also noted, but this could be related to the higher rate of earlobe piercing in females (3,5).…”

Onion extract and quercetin induce matrix metalloproteinase-1 in vitro and in vivo

“…The abnormal growth of fibroblasts and excessive accumulation of extracellular matrix (ECM) proteins are prominent features of hypertrophic scar and keloid (7,8). Type I collagen is a prototype of ECM and MMP-1 is a prototype of collagenase, which plays a key role in the dynamic remodeling of extracellular matrix in cells.…”