Keloids are disfiguring scars that proliferate beyond the boundaries of the original site of cutaneous injury . Keloids can continue to grow indefinitely and no satisfactory treatment has been identified. Etiological evidence has pointed to a possible genetic predisposition in humans. However, it is unclear what the inheritance patterns of this disease are. Various studies have provided conflicting evidence, supporting an autosomal recessive pattern, an autosomal dominant pattern, or an autosomal dominant with incomplete penetrance. The greatest occurrence of keloid formation is among the female population, although the statistical evidence is obscured due to the number of females forming keloids following ear-piercing.
In vitro studies of keloid fibroblasts have implicated several cytokines in the pathogenesis of keloid formation, including transforming growth factor beta (TGF-b), epidermal growth factor (EGF), fibroblast growth factor (FGF), and platelet derived growth factor (PDGF). TGF-b has received the most attention of all the cytokines due to its ability to promote the synthesis of collagen, which is the principal constituent of the keloid mass. Three different isoforms of TGF-b have been identified (b1, b2 and b3), with each isoform performing a different biological role in the wound healing process. According to western blot studies, keloid fibroblasts have increased amounts of the TGF-b1 and TGF-b2 cytokine present compared to normal dermal fibroblasts. Our research will use a procedure known as gene screening to determine whether any of the cytokines mentioned above result in a pattern of expression that could lead to keloid formation and to determine if there is a simple method of intervention that could prevent this from occurring.
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