01OverviewDefinition, clinical context and the essential points that orientate the chapter.
The term keratoacanthoma describes a clinicopathological pattern whose biological boundary with SCC is contested. Record the growth timeline, exact size, site, immune state, medicines and previous tumours. Photograph with consent and palpate the base and nodes. A neat crater does not confer safety.
Pathologists need architecture: a central keratin crater, lipping epidermal shoulders and the deep interface. Complete excision provides both diagnosis and treatment. If size or anatomy prevents this, the skin-cancer team selects an incisional sample that includes an edge, crater and adequate depth rather than a central plug alone.
Although spontaneous involution is described, waiting can allow an SCC to grow and makes later reconstruction harder. Urgent suspected-cancer referral is the practical UK decision. Multiple lesions, unusual age or family clustering deserves assessment for medication effects and rare syndromes.
Key points
- A classic keratoacanthoma is a rapidly growing, symmetrical, dome-shaped nodule with a central keratin-filled crater on sun-exposed skin.
- Growth over two to eight weeks is typical, but speed does not prove benignity; SCC can show the same crateriform pattern.
- Manage a solitary suspected keratoacanthoma as SCC until complete architecture and depth have been assessed histologically.
- Urgent complete excision is preferred when feasible because partial punch or superficial shave may not show the diagnostic shoulders and deep interface.
- Do not observe for spontaneous regression when SCC cannot be excluded, especially in immune suppression or high-risk sites.
- Palpate regional nodes and ask about pain, numbness and weakness in a rapidly growing keratinising tumour.
- Multiple synchronous lesions should trigger medicine, immune and family-history review and specialist dermatology care.
- Destructive treatment such as curettage or cryotherapy without adequate histology risks erasing an SCC diagnosis.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Ultraviolet-associated follicular tumour
Most lesions arise from follicular epithelium on chronically sun-exposed skin in older adults after cumulative ultraviolet injury.
Trauma and treatment exposure
Some develop after injury, surgery, laser or radiotherapy, but temporal association does not establish benign behaviour.
Immune and medicine effects
Immune suppression and selected systemic targeted therapies can produce multiple, eruptive or unusually aggressive crateriform keratinocyte tumours.
Syndromic multiplicity
Rare inherited tumour syndromes cause numerous keratoacanthomas and require specialist dermatological, genetic and long-term cancer management.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Rapid epithelial proliferation
A symmetrical follicular tumour expands quickly over weeks, elevating a rim of keratinocytes around a central keratin-filled crater.
- 2Crater formation
Central keratin accumulates into a plug while lateral lips create a volcano-like architecture that pathologists need to see intact.
- 3Potential involution
Some lesions enter a regression phase over months and leave a scar, but predicting which will regress safely is impossible.
- 4SCC overlap
Cytological and architectural features overlap well-differentiated SCC, and destructive growth or metastasis can occur in lesions initially labelled keratoacanthoma.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
A smooth or telangiectatic dome surrounds a central firm keratin plug and grows visibly over weeks.
The lesion often has balanced epithelial shoulders, but symmetry cannot reliably distinguish it from SCC.
Increase from papule to centimetre-scale tumour within several weeks is characteristic and itself triggers urgent assessment.
Irregular infiltration, fixation, neurological symptoms, lip or ear location, recurrence or palpable nodes heightens SCC concern.
Numerous simultaneous or sequential crateriform tumours suggest immune, medicine-related or inherited susceptibility.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Complete excision histologyFirst step - Why
- Assess full crater architecture, invasive front, differentiation and margins while treating the lesion.
- Interpretation and limitations
- Histology may report SCC, keratoacanthoma-type SCC or keratoacanthoma; management integrates site and risk rather than label alone.
- 02
Deep architecture-preserving incisional biopsy - Why
- Sample a large or critical-site lesion that cannot be excised diagnostically in one step.
- Interpretation and limitations
- Include edge, shoulder, crater and deep interface; a central keratin plug alone is nondiagnostic.
- 03
Regional node and nerve assessment - Why
- Identify features of high-risk SCC spread.
- Interpretation and limitations
- Suspicious nodes need ultrasound-guided sampling and neurological symptoms may require MRI.
- 04
Medicine and immune review - Why
- Identify drivers of multiple or eruptive crateriform tumours.
- Interpretation and limitations
- Coordinate any essential medicine change with oncology, transplant or prescribing specialists rather than stopping independently.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Well-differentiated SCC
An indurated keratinising nodule can be indistinguishable and is the critical diagnosis that drives urgent excision.
Nodular basal-cell carcinoma
A pearly translucent border, arborising vessels and slower ulcerative growth support BCC rather than a symmetric keratin crater.
Amelanotic melanoma
A pink rapidly growing bleeding nodule may lack pigment and requires melanoma-preserving biopsy planning when dermoscopy is atypical.
Molluscum or viral wart
Small umbilicated molluscum and rough HPV warts usually lack rapid painful expansion and a large central keratin plug.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Solitary crateriform lesionTreat as SCC until proven otherwiseFirst stepA rapidly growing keratin-filled nodule is clinically compatible with keratoacanthoma.+
- 1Document growth, site, size, neurological symptoms, immune state and nodes and make an urgent suspected-cancer referral.
- 2Arrange complete excision with adequate depth when feasible, preserving the specimen and orientation for histopathology.
- 3DefinitiveReview the definitive report and manage margins and surveillance according to the SCC risk assessment.
02Critical site or large lesionPlan tissue-sparing diagnosisComplete simple excision could impair eyelid, lip, nose, ear, digit or another important structure.+
- 1Refer without destructive treatment and provide consented photographs and exact growth history.
- 2DefinitiveUse specialist incisional biopsy or Mohs planning that preserves architecture and allows definitive margin control.
- 3Coordinate reconstruction only after tumour extent and pathological risk are understood.
03Multiple eruptive lesionsInvestigate the systemic contextSeveral crateriform tumours arise together or recur unusually often.+
- 1Review immunosuppression, targeted medicines, age of onset, family history and other internal or skin malignancy clues.
- 2Biopsy representative lesions because not every nodule in a cluster has identical pathology.
- 3Establish dermatology, genetics or oncology surveillance and a prevention plan while coordinating medicine modification safely.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Missed invasive SCC
Observation of a presumed benign lesion can permit local invasion, perineural spread, nodal metastasis and more destructive surgery.
Local structural damage
Fast growth on eyelid, nose, lip, ear or digit can distort function before histology is obtained.
Scarring
Spontaneous involution, surgery and destructive treatment leave scars, with size and site shaping cosmetic and functional effect.
Multiple recurrent tumours
Syndromic or medicine-associated cases create repeated simultaneous lesions and substantial cumulative diagnostic, surgical, functional and psychological burden.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Track urgent referral and definitive pathology, ensuring a provisional label does not close the episode.
- Review margins, tumour depth, differentiation and perineural features when SCC is diagnosed.
- Examine scar and regional nodes and ask about pain, numbness or rapid local recurrence.
- For multiple disease, maintain a lesion map and biopsy changing outliers rather than assuming every lesion is identical.
- Provide ultraviolet protection and rapid self-referral advice for future fast-growing keratinising lesions.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Regression is retrospective
A lesion can only be known to have involuted after time that may be unsafe if the diagnosis was actually SCC.
Architecture makes diagnosis
Pathological interpretation depends on shoulders, crater and deep interface rather than cytology from a tiny centre sample.
Symmetry does not reassure
Well-differentiated SCC may form a beautifully regular crater and still behave malignantly.
The label varies
Reports may use keratoacanthoma-type SCC, reflecting genuine biological overlap and the need for risk-based care.
11Common pitfallsFrequent interpretation and management errors.
- 01
Waiting for spontaneous regression of a lesion that could be invasive SCC.
- 02
Punching only the central keratin plug and obtaining a nondiagnostic specimen.
- 03
Using cryotherapy before histology and destroying architecture.
- 04
Reassuring from symmetry despite rapid growth and a high-risk site.
- 05
Stopping an essential immunosuppressant without coordinating the treating team.