Keratoacanthoma – KA
Keratoacanthoma (KA) is a tumor of epidermal keratinocytes known for three things: very rapid growth, a volcano-like shape with a central keratin plug, and a tendency to regress on its own over a few months. It was once classed as benign or as a "pseudocancer," but current medical thinking, including the World Health Organization (WHO) classification, treats KA as a well-differentiated form of cutaneous squamous cell carcinoma (cSCC). The real clinical difficulty is that KA cannot be reliably told apart from invasive cSCC by eye or on a superficial biopsy. For that reason, the accepted standard of care is to treat and follow KA definitively, just as one would a cSCC.
At Haute-Derma, we follow a standardized pathway for keratoacanthoma: high-resolution dermoscopy, an excisional biopsy that captures the full depth of the lesion, careful histopathologic review, and complete removal, so that an invasive, progressing cSCC is not missed.
Clinical Features and Histopathology
Natural Course and Clinical Stages
A typical KA passes through three distinct stages:
- Proliferative phase: The lesion grows explosively (over just 2–8 weeks) into a firm, raised, pinkish-red nodule 1–2 cm across.
- Mature (stable) phase: The tumor reaches its maximum size and takes on the classic "volcano" shape, with a central crater filled by a dense keratin plug. It then stays stable for 2–8 weeks.
- Regressive phase: The tumor sheds its keratin and gradually flattens over 2–6 months, leaving a depressed atrophic scar.
Causes and Special Variants
- Predisposing factors: ultraviolet (UV) radiation, local trauma, exposure to harmful chemicals (tar, mineral oils), a weakened immune system, HPV infection (types 9, 11, 16, 33), and side effects of targeted or immune-based drugs (such as the BRAF inhibitors vemurafenib and dabrafenib).
- Special clinical variants:
- Giant KA: larger than 2 cm and capable of extensive local tissue destruction, especially on the nose and ears.
- Ferguson-Smith syndrome: repeated crops of self-healing KAs, inherited in an autosomal dominant pattern.
- Grzybowski syndrome: thousands of small papular KAs scattered over the whole body and the mucous membranes.
- Muir-Torre syndrome: multiple KAs together with internal cancers (particularly colorectal cancer), caused by mutations in DNA repair genes (MSH2, MLH1).
Histopathologic Features
An accurate microscopic diagnosis of KA requires a specimen that spans the full depth of the tumor, including both lateral edges and the dermal base:
- Crateriform architecture: a cup-shaped tumor with a central crater packed with keratin, flanked on both sides by raised epidermal "lips" (buttresses) that hug the lesion.
- Eosinophilic keratinocytes: squamous cells with abundant, deeply pink, "glassy" cytoplasm.
- Neutrophilic microabscesses: often seen within keratin pearls or the hyperplastic epidermis.
- Base of the lesion: shallow, pushing the dermal border downward without invading deeper than the level of normal hair follicles; there is no marked nuclear atypia and no dense cluster of abnormal mitoses at the base.
Differential Diagnosis and Immunohistochemistry (IHC)
| Condition | Distinguishing Histologic Features | Immunohistochemical (IHC) Markers |
|---|---|---|
| Keratoacanthoma (KA) | Crateriform architecture, glassy pink cytoplasm, flat and shallow base, intact basement membrane. | p53 (+) confined to the outer rim of tumor lobules; Ki-67 (< 10–20%) raised only in the peripheral basal layer; cytokeratin 17 (+). |
| Invasive squamous cell carcinoma (cSCC) | Atypical keratinocytes invading haphazardly into the deep dermis/subcutis, numerous abnormal mitoses, loss of polarity. | p53 diffusely positive or completely lost; Ki-67 (> 40–50%) markedly raised in the center and throughout the tumor. |
| Seborrheic keratosis (KA-like variant) | Benign proliferation of basaloid cells, pseudo-horn cysts, no glassy cytoplasm or large keratin crater. | Very low Ki-67 (< 2–5%); normal p53 expression. |
Haute-Derma's Approach to Keratoacanthoma
Although KA can in theory regress on its own, Haute-Derma consistently takes a proactive approach grounded in patient-safety standards:
- No waiting for spontaneous regression: Waiting for the lesion to resolve risks missing a genuinely invasive cSCC. Natural regression also usually takes months and leaves a worse depressed scar than planned surgery.
- Histologic assessment of the entire base: We do not rely on superficial shave biopsies, because they cannot show the architecture at the base of the tumor that is needed to distinguish KA from cSCC.
- Standardized surgical removal: The whole tumor is excised with an appropriate safety margin and closed with cosmetic reconstruction, so patients heal quickly with the best possible appearance.
- Screening for inherited syndromes: When KAs are multiple or appear in younger patients, Haute-Derma takes a detailed family history and arranges screening for Muir-Torre or Ferguson-Smith syndrome.
How We Diagnose Keratoacanthoma at Haute-Derma
To reach an accurate diagnosis and rule out a progressing cSCC, Haute-Derma follows a four-step process:
- Clinical Examination and High-Resolution Dermoscopy: We look for the hallmark signs of KA, such as a central gray-yellow keratin mass, branching vessels, and hairpin vessels arranged in an arc around the keratin core.
- Excisional or Deep Incisional Biopsy: The entire tumor is removed, or an elliptical wedge is cut through its center that includes both lateral edges and the deep dermal base.
- Immunohistochemistry (IHC): p53, Ki-67, and CK17 staining helps separate well-differentiated KA from invasive cSCC when the slides are equivocal.
- Internal and Genetic Screening (when indicated): Patients with multiple KAs or a family history of colorectal cancer are referred for gastrointestinal endoscopy and genetic testing of the DNA mismatch repair (MMR) genes.
Specialist Treatment at Haute-Derma
Haute-Derma's treatment plan for keratoacanthoma puts complete cure and a good cosmetic result first:
- Complete Surgical Excision:
- First-line option: excision of the entire lesion with a safety margin of 4–5 mm.
- This delivers the whole tumor to the pathologist to confirm clear (R0) margins and leaves a neat suture line, far better than the depressed scar left when a KA regresses naturally.
- Mohs Micrographic Surgery (MMS):
- Used for giant KAs, recurrent KAs, or KAs in cosmetically important sites (the H-zone: eyes, nose, lips, ears).
- The entire surgical margin is checked under the microscope, so the lesion can be removed completely while sparing as much healthy tissue as possible.
- Nonsurgical Local Treatments (when surgery is not an option):
- Intralesional therapy: methotrexate (MTX) or 5-fluorouracil (5-FU) injected directly into the base of the tumor shrinks it quickly when the lesion is very large or when an older patient is not fit for surgery.
- Prescription topical therapy: imiquimod 5% cream can help clear early-stage lesions.
- Cosmetic Restoration and Aftercare: fine suturing techniques that hide the scar, LED light therapy to reduce swelling, and dedicated post-operative scar management.
