Warts

Benign epidermal proliferations caused by human papillomavirus (HPV) infection. Extremely common, particularly in children and young adults. Most resolve spontaneously within 2 years. Treatment includes topical salicylic acid, cryotherapy, and observation. Genital warts (condylomata acuminata) are sexually transmitted and managed differently.

Key Facts

Human papillomavirus (HPV): >100 types; common warts (HPV 2, 4), plantar warts (HPV 1), genital warts (HPV 6, 11) Extremely common: affect ~10% of population; up to 30% of school-aged children Spontaneous resolution: ~65% resolve within 2 years without treatment (immune-mediated clearance) Salicylic acid 15–26%: first-line topical treatment — apply daily after paring; ~75% clearance at 12 weeks Cryotherapy (liquid nitrogen): second-line — every 2–3 weeks; ~70% clearance after multiple treatments Gardasil 9 (HPV vaccine): protects against HPV 6, 11, 16, 18, 31, 33, 45, 52, 58 — offered to all 12–13 year-olds in UK Black dots: thrombosed capillaries within wart — distinguishing feature from callus Immunosuppressed patients: extensive, treatment-resistant warts; increased risk of HPV-related malignancy

Overview

Key Facts

Cutaneous warts are one of the most common presentations in primary care dermatology. They are benign but can be cosmetically distressing and painful (plantar). Understanding that most resolve spontaneously is important to avoid overtreatment.

Epidemiology

  • Prevalence: ~10% of general population; up to 30% of children
  • Peak age: 12–16 years
  • Equal sex distribution
  • More common and persistent in immunosuppressed patients
  • Genital warts: most common viral STI in UK

Aetiology

  • HPV: double-stranded DNA virus; >100 types identified
  • Common warts: HPV 2, 4, 27
  • Plantar warts (verrucae): HPV 1, 2, 4
  • Plane (flat) warts: HPV 3, 10
  • Genital warts (condylomata acuminata): HPV 6, 11 (low-risk); HPV 16, 18 (high-risk — oncogenic)
  • Transmission: direct skin contact, autoinoculation, fomites (swimming pools for plantar warts)

Pathophysiology

  • HPV infects basal keratinocytes through micro-abrasions → viral DNA integrates or remains episomal → stimulates keratinocyte proliferation → epidermal hyperplasia (acanthosis, papillomatosis)
  • Immune evasion: HPV downregulates MHC class I, interferon signalling → persistent infection
  • Immune clearance: cell-mediated immunity eventually clears virus → spontaneous resolution in most cases

Clinical Presentation

Common Warts (Verruca Vulgaris)

  • Firm, rough, dome-shaped papules with verrucous (cauliflower-like) surface
  • Most common on hands, fingers, knees
  • Black dots (thrombosed capillaries) visible on surface
  • May be single or multiple; may coalesce

Plantar Warts (Verrucae)

  • On soles of feet; pushed inward by weight-bearing → flat/endophytic
  • Painful on lateral compression (callus is painful on direct pressure)
  • Black dots visible after paring surface
  • Mosaic warts: coalescent plantar warts

Plane (Flat) Warts

  • Small (2–4 mm), flat-topped, skin-coloured or pink papules
  • Often on face and dorsum of hands
  • May be very numerous; Koebner phenomenon common

Genital Warts (Condylomata Acuminata)

  • Flesh-coloured, soft, filiform or pedunculated papules
  • Genital, perianal skin
  • HPV 6, 11 (benign); screen for HPV 16, 18 co-infection

Red Flags

  • Immunosuppressed patient with extensive/refractory warts — monitor for malignant transformation
  • Rapidly growing, atypical, or pigmented lesion — consider SCC, amelanotic melanoma
  • Genital warts in children — safeguarding assessment (may also be non-sexual transmission)

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Seborrhoeic keratosisStuck-on, waxy, well-demarcated; elderly patientsDermoscopy
Squamous cell carcinomaIndurated, ulcerated, rapidly growingBiopsy
Molluscum contagiosumPearly papules with central umbilicationClinical
Callus/cornNo black dots, painful on direct pressure (not lateral)Pare surface — no punctate bleeding
Amelanotic melanomaFlesh-coloured nodule, irregularExcision biopsy
KeratoacanthomaRapid growth, crateriform, central keratin plugExcision biopsy

Diagnosis / Investigation

Bedside

  • Clinical diagnosis: usually straightforward; pare surface to reveal black dots
  • Dermoscopy: frog-spawn pattern (black dots = thrombosed capillaries), absence of dermatoglyphics

Biopsy

  • Not routinely required for typical warts
  • Indicated if: atypical appearance, rapid growth, pigmented, immunosuppressed with treatment-resistant lesion

Bloods

  • Not required for cutaneous warts
  • HIV test: if extensive/refractory warts in at-risk patient

Special Tests

  • HPV typing: not routine for cutaneous warts; relevant for genital warts and cervical screening
  • STI screen: if genital warts — screen for co-existing STIs

Management

Non-Pharmacological

  • Observation: first-line for children — majority resolve spontaneously within 2 years
  • Patient education: benign condition, avoid picking/biting (autoinoculation)
  • Occlusion with duct tape: anecdotal evidence; limited trial support

Pharmacological

  • Salicylic acid 15–26% (Bazuka, Occlusal): first-line topical
    • Pare wart, apply daily, cover; continue for up to 12 weeks
    • Cure rate ~75% at 12 weeks
  • Cryotherapy (liquid nitrogen): second-line — applied every 2–3 weeks; 2–3 freeze-thaw cycles per session
    • Cure rate ~70% after 3–4 treatments
    • Painful — less suitable for young children
  • Topical formaldehyde 3% or glutaraldehyde 10%: for plantar warts

Genital warts (GUM clinic):

  • Podophyllotoxin 0.5% cream/solution: patient-applied; BD for 3 days, repeat weekly for up to 4 cycles
  • Imiquimod 5% cream: 3 nights/week for up to 16 weeks
  • Cryotherapy or electrosurgery: clinic-based

Refractory/specialist:

  • Intralesional bleomycin: specialist use for resistant warts
  • Photodynamic therapy: limited evidence
  • Cidofovir topical: specialist use in immunosuppressed

Referral Criteria

  • Dermatology: diagnostic uncertainty, treatment-resistant, immunosuppressed
  • GUM clinic: genital warts
  • Safeguarding: genital warts in children

Prognosis

  • ~65% of cutaneous warts resolve spontaneously within 2 years
  • Treatment accelerates resolution but no treatment is 100% effective
  • Recurrence common (~20–30%) even after successful treatment
  • Immunosuppressed: persistent, extensive, treatment-resistant; increased malignant transformation risk
  • Genital warts: 70–80% resolve with treatment; recurrence ~20–30%
  • HPV vaccination: expected to dramatically reduce genital wart incidence (already seen in vaccinated populations)

Other Relevant Information

HPV Types and Associated Lesions

HPV TypeLesionRisk
1, 2, 4Common/plantar wartsBenign
3, 10Plane wartsBenign
6, 11Genital warts, laryngeal papillomatosisLow-risk
16, 18Cervical, anal, oropharyngeal cancerHigh-risk (oncogenic)
31, 33, 45, 52, 58Cervical cancerHigh-risk

Treatment Comparison

TreatmentEfficacyAdvantagesDisadvantages
Salicylic acid~75%Home-based, painlessSlow (12 weeks)
Cryotherapy~70%Clinic-based, fasterPainful, scarring risk
Observation~65% at 2 yearsNo side effectsSlow
Imiquimod (genital)~50–75%Immune-mediatedLocal irritation