Etiology
Most research on the etiology of this lesion has been performed on non-eyelid keratoacanthomas.
- In a study of 98 non-eyelid keratoacanthomas, using array comparative genomic hybridization, genetic instability was observed in both the growth and involutional phases of this self-limiting cutaneous neoplasm (Li 2012).
- Genomic instabilities differed between KA and squamous cell carcinoma (SCC) suggesting that they are distinct entities despite their histopathologic similarities.
- Deletion of the tumor suppressor gene p53 was observed in 27% of KAs, and 46% of SCC.
- Genetic aberrancy is most noticeable in chromosomes 7, 8, and10.
- In a study of 92 non-eyelid keratoacanthomas, more than 60 different types of HPV DNA were identified, suggesting that no specific HPV type plays an etiologic role in KA (Ekstrom 2011).
- Although previously considered a benign eyelid growth, keratoacanthomas are now felt to be more of a premalignant form of squamous cell carcinoma (in situ), and cells at the base of the lesion have been observed to progress to frank squamous cell carcinoma, in 5% of 3465 non-eyelid cases in one study, even higher in elderly patients (Weedon 2010).
Epidemiology
- In a study of 44 eyelid keratoacanthomas identified in the files of the Armed Forces Institute of Pathology, from military, civilian and Veterans Administration sources, the average age was 49 years (range 19–96 years) (Boniuk 1967).
- 27 were men and 17 were women (male predominance likely reflecting the military sources at that time).
- 13 were upper lid, 25 lower lid, and the rest canthal.
- 13 lesions occurred at the lid margin.
- Keratoacanthoma is generally more common in middle age and older patients
- There is some association with sun exposure, with some series documenting a higher incidence in Hawaii and Australia
- Although usually solitary, there are syndromes associated with multiple lesions:
- Muir-Torre syndrome: autosomal dominant, sebaceous tumors of the skin, associated with colon cancer
- Variant of Grzybowski syndrome: sporadic, large numbers of smaller keratoacanthoma-like lesions
- Ferguson Smith syndrome: autosomal dominant, keratoacanthomas appear in adolescence, spontaneously involute, then recur at older age
History
- Rapid growth (weeks to months) is the classic description.
- History of prior lesions
- Other types of cutaneous lesions
- Family history is also important
Clinical features
- Begins as a small flesh colored to slightly reddish mass
- Most often a solitary lesion with smooth, rolled, elevated edges surrounding a central core of keratin
- Often exhibits rapid growth, when it develops its more classic appearance
- Skin colored, often with signs of mild erythema
Testing
- Biopsy is the only way to establish the diagnosis.
- Must include cells from the base of the lesion to fully evaluate for possible malignancy
- The classic histopathologic description is a central keratin filled crater that papillary projections protrude into in a cup-shaped configuration.
- Beneath the crater there is acanthotic epithelium maturation as cells progress from deeper to more superficial.
- The base of the lesion is irregular and not a well-circumscribed mass, as seen in an inverted follicular keratosis.
Testing for staging, fundamental impairment
- No staging is needed for this benign tumor.
Figure 1. Keratoacanthoma. Courtesy Rona Z. Silkiss, MD, FACS.
Figure 2. Keratoacanthoma. Courtesy Evan H. Black, MD.
Figure 3. Keratoacanthoma. Courtesy Raymond Cho, MD.
(delete - irrelevant) Figure 4. Deep medial canthal basal-cell carcinoma. Courtesy Richard C. Allen, MD, PhD, FACS.
Figure 5. Keratoacanthoma. Courtesy Michael J. Hawes, MD, FACS.
Figure 6. Same Keratoacanthoma, 6 weeks later. Courtesy Michael J. Hawes, MD, FACS.