Keloid scarring is the formation of dermal fibroproliferative cutaneous lesions caused by pathologic wound healing post skin injury, lacerations, abrasions, surgery, piercings, vaccinations, and minor skin trauma.  Keloid scars are characterized by excessive fibroblast proliferation and deposition of extracellular matrix and collagen fiber.  Morphologically, they appear as firm, mildly tender, pink to purple, bosselated tumors with a shiny surface and irregular outline.  Telangiectasia may also be seen.  Unlike hypertrophic scars, keloids typically project beyond the initial site of injury.  Keloids can develop at any age, but are observed more frequently between 10 and 30 years of age.  They may at times develop up to several years after minor injuries. 

Keloid scars are more common and prominent among females than males.  They also occur more frequently in darker-skinned individuals, suggesting that genetic factors play an important role in its pathogenesis. 

The presence of positive family history of keloid formation among patients suggested a genetic susceptibility for the condition.  Association studies conducted on the Japanese population found the following SNPs to be associated with keloid formation; rs873549 on chromosome 1q41, rs1511412 and rs940187 on 3q22.3-q23 and rs8032158 on 15q21.3.  In addition, several HLA-DRB1*15 seem to be associated with the risk of developing keloid scarring in white individuals.  Recently, −1997 G/T, +1245 G/T polymorphisms in the COL1A1were reported to be associated with Keloid scars formation in the Saudi population.