• Most commonly presents as a solitary, rapidly proliferating, dome-shaped, erythematous or flesh-colored papule or nodule with a central keratinous plug, typically reaching 1 to 2 cm in diameter
  • Clinically and microscopically resembles squamous cell carcinoma (SCC)
  • Other presentations include grouped, multiple, keratoacanthoma (KA) centrifugum marginatum, intraoral, subungual, regressing, nonregressing, and generally eruptive (1).
  • Majority are benign and resolve spontaneously, but lesions do have the potential for invasion and metastasis; therefore, treatment is required.
  • Three clinical stages of KAs (1):
    • Proliferative: rapid growth of the lesion over weeks to several months
    • Maturation/stabilization: Lesion stabilizes and growth subsides.
    • Involution: spontaneous resolution of the lesion, leaving a hypopigmented, depressed scar; most but not all lesions will enter this stage.
  • System(s) affected: integumentary


  • Greatest incidence age >50 years but may occur at any age
  • Presentation increases during summer and early fall seasons.
  • Most frequently on sun-exposed and hair-bearing skin but may occur anywhere
  • Predominant sex: male > female (2:1)
  • Most commonly in fair-skinned individuals; highest rates in Fitzpatrick skin type I to III
  • 104 cases per 100,000 individuals

Etiology and Pathophysiology

  • Derived from an abnormality causing hyperkeratosis within the follicular infundibulum
  • Squamous epithelial cells proliferate to extend upward around the keratin plug and proceed downward into the dermis. This process is followed by invasion of elastic and collagen fibers.
  • Cellular mechanism responsible for the hyperkeratosis is currently unknown. The role of human papillomavirus (HPV) has been discussed but has no established causality (2).
  • Regression may be due to immune cytotoxicity or terminal differentiation of keratinocytes.
  • Multiple etiologies have been suggested:
    • UV radiation
    • May be provoked by surgery, cryotherapy, chemical peels, or laser therapy
    • Viral infections: HPV or Merkel cell polyomavirus
    • Genetic predisposition: Muir-Torre syndrome, xeroderma pigmentosum, Ferguson-Smith syndrome
    • Immunosuppression
    • BRAF inhibitors (1)
    • Chemical carcinogen exposure


  • Mutation of p53 or H-ras
  • Ferguson-Smith syndrome (AD)
  • Witten-Zak (AD)
  • Muir-Torre syndrome (AD)
  • Xeroderma pigmentosum (AR)
  • Grzybowski (sporadic)
  • Incontinentia pigmenti (XLD)

Risk Factors

  • UV exposure/damage: outdoor and/or indoor tanning
  • Fitzpatrick skin type I to III
  • Trauma (typically appears within 1 month of injury): laser resurfacing, surgery, cryotherapy, tattoos
  • Chemical carcinogens: tar, pitch, and smoking
  • Immunocompromised state
  • Discoid lupus erythematosus
  • HPV infection

General Prevention

Sun protection measures

Commonly Associated Conditions

  • Frequently, the patient has concurrent sun-damaged skin: solar elastosis, solar lentigines, actinic keratosis, nonmelanoma skin cancers (basal cell carcinoma and SCC).
  • In Muir-Torre syndrome, KAs are found with coexisting sebaceous neoplasms and malignancy of the GI and GU tracts; may have sebaceous differentiation known as a seboacanthoma

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