• Keloids are benign hyperproliferative skin growths histologically characterized by overabundant deposition of extracellular matrix components, especially dermal collagen bundles, glycosaminoglycans, and fibroblasts.
  • Present as abnormal scar tissue 1 month to 1 year at the site of skin injury or spontaneously on the midchest without known injury
  • System(s) affected: skin/exocrine



  • Equal distribution between genders
  • Predominant age: 10 to 30 years; higher incidence during 2nd and 3rd decades and during pregnancy


  • 6–16% of the black and Hispanic populations
  • Higher incidence in Asian populations
  • Not seen in albino populations
  • High recurrence rates after excision

Etiology and Pathophysiology

  • Poorly understood pathogenesis
  • The mechanisms of keloid formation include alterations in growth factors, collagen turnover, skin tension alignment during aberrant wound healing after skin injury.
  • Genetic, hormonal, and immunologic contributions have also been implicated.
  • Trauma, foreign body reactions, infections, and endocrine dysfunction have all been proposed as risk factors for the development of keloids after surgery in genetically susceptible people.
  • Rarely occur in places on body lacking sebaceous glands; thus, sebaceous glands and the body’s reaction to this sebum are hypothesized to be an etiologic factor in keloid development. Moreover, humans are the only mammals with sebaceous glands and the only mammals affected by keloids.
  • Wounds: traumatic, surgical, body piercing (foreign body reaction)
  • Wound infection
  • Burn injury (thermal or chemical)
  • Other injuries:
    • Insect bite
    • Folliculitis
    • Acne
    • Chickenpox
  • Vaccination (especially bacillus Calmette-Guérin [BCG])
  • Increased dermal ratio of type I to type III collagen and glycosaminoglycan deposition in a disorganized fashion
  • Increased density and proliferation of fibroblasts due to failure of genetic downregulation


  • More common in blacks and Asians (~5 to 16 times) than in Caucasians; in all races, more darkly pigmented individuals are at higher risk.
  • Autosomal dominant with incomplete penetrance genetic pattern has been suggested.
  • Several genes have been implicated in the etiology of keloid disease, but no single gene mutation has thus far been implicated, which may reflect genetic heterogeneity.
  • High frequency of identical twins both developing keloids strongly supports a genetic role.
  • Two rare syndromes have been associated with keloid formation: Rubinstein-Taybi syndrome and Goeminne syndrome.

Risk Factors

  • Previous keloid
  • Prior keloid excision
  • Family history of keloids
  • Race
  • Darker skin pigmentation
  • Pregnancy
  • Puberty through early adulthood
  • Recurrent abnormal wound healing (e.g., earring sites)

General Prevention

  • Given the high recurrence rates and significant expense associated with treatment, primary prevention should take priority (1)[C]. Avoid elective surgery, body piercing, and tattooing in high-risk patients with either a personal or family history of keloids (2)[B].
  • When feasible, laparoscopic surgical approaches, as opposed to open surgery, are preferred in patients prone to keloid formation.
  • Occlusive pressure dressings, direct pressure application, and postoperative local steroid injection in high-risk patients may all be useful as prophylactic measures.
  • Physicians should be alert to delays in wound healing if erythema or pruritus persists as signs of impending keloid formation.

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