Description

• Keloids are benign hyperproliferative growths of dermal fibroblasts characterized by the excessive deposition of extracellular matrix components, especially collagen, fibronectin, elastin, proteoglycans, and growth factors such as transforming growth factor (TGF) β (1)[B].
• System(s) affected: Skin/Exocrine

Epidemiology

• Predominant age: 10–30 years
• Higher incidence during puberty and pregnancy
• Predominant sex: Female > Male

• 4–16% of the black and Hispanic populations
• Higher incidence in the Asian population
• Data from the UK demonstrated that <1% of Caucasians had keloids.

Risk Factors

• Family history of keloids
• Dark skin pigment
• Location on the body (e.g., deltoids, chest, neck, earlobes)
• Pregnancy
• Adolescence

• More common in blacks and Asians (5–15×) than in whites; in all races, more darkly pigmented individuals are at higher risk.
• Both autosomal dominant and autosomal-recessive familial inheritance have been reported.
• Several genes have been implicated in the etiology of keloid disease, but no single gene mutation has thus far been found to be responsible.
• High frequency of identical twins both developing keloids strongly supports a role for genetics in keloid etiology.

General Prevention

• Primary prevention: Avoid elective surgery, body piercing, and tattooing in high-risk patients.
• Wounds should be kept clean to prevent infection.
• When feasible, laparoscopic approaches are preferred in keloid formers.
• Compressive pressure dressings may be useful in high-risk (e.g., burn) patients. Local steroid injection postoperatively in high-risk patients is also effective.
• Physicians should be alert to delays in wound healing, persistent erythema, or pruritus as impending symptoms of possible keloid formation and make all reasonable attempts to reduce inflammation and tension on the skin with appropriate methods.

Pathophysiology

• The mechanisms of keloid formation include alterations in growth factors, collagen turnover, and skin tension alignment, as well as genetic and immunological contributions.
• Trauma, foreign-body reactions, infections, and endocrine dysfunctions 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.

Etiology

• Wounds: Traumatic, surgical, body piercing (foreign-body reaction)
• Wound infection
• Burn injury
• Other injuries:
  • Insect bite
  • Folliculitis barbae and nuchae
  • Acne
  • Chickenpox
• Vaccination (especially bacille Calmette-Guérin [BCG])
• Increased ratio of type I to type III collagen
• Increased density and proliferation rate of fibroblasts