Definition and epidemiology
A wart (verruca) is a benign, circumscribed proliferation of the epidermis caused by human papillomavirus (HPV) infection of keratinocytes. HPV is a non-enveloped double-stranded DNA virus with over 150 types; cutaneous (non-genital) warts are typically caused by HPV-1, -2, -4, -27, and -57.
- Common in children and adolescents; peak prevalence around ages 12-16
- Estimated point prevalence in school-age children is roughly 10-20%
- Transmission is via direct skin-to-skin contact or indirectly via fomites (locker rooms, swimming pools, shared towels)
- Microtrauma, maceration, and occlusion (e.g., wet communal floors) facilitate viral entry
- Immunosuppressed patients (organ transplant recipients, HIV) develop more numerous, persistent, and treatment-resistant warts
- Warts are caused by HPV infecting keratinocytes, most commonly types 1, 2, 4, and 27 for cutaneous warts
- Pinpoint bleeding on paring (thrombosed capillaries) distinguishes warts from calluses, which have preserved skin lines
- Most common warts resolve spontaneously within 1-2 years via cell-mediated immunity
- Immunosuppressed patients (transplant, HIV) get more numerous, larger, and treatment-resistant warts
- Salicylic acid and cryotherapy are the best-evidenced first-line treatments; no single therapy is clearly superior
- HPV 6 and 11 cause anogenital warts (condyloma acuminata), a distinct entity managed differently from skin warts
- Biopsy atypical, rapidly growing, or non-healing wart-like lesions to exclude SCC or amelanotic melanoma
- Epidermodysplasia verruciformis predisposes to widespread flat warts and skin cancer
Etiology and risk factors
Warts are caused exclusively by HPV; the specific type correlates loosely with clinical morphology and site.
| HPV type | Typical wart |
|---|---|
| 1, 2, 4, 63 | Common and plantar warts |
| 3, 10, 28 | Flat (plane) warts |
| 2, 7 | Filiform/digitate warts (face, neck) |
| 6, 11 | Anogenital warts (condyloma acuminata, separate clinical entity) |
Risk factors:
- Childhood and adolescence
- Barefoot activity on communal wet surfaces (pools, locker rooms)
- Occupational handling of meat/fish (butcher's warts, atypical HPV types)
- Nail biting, finger picking, eczema (breaks in skin barrier)
- Immunosuppression (transplant, HIV, chemotherapy) — increases number, size, and recalcitrance
- Epidermodysplasia verruciformis — rare genetic disorder with widespread flat warts and skin cancer risk
Pathophysiology
HPV enters keratinocytes through minor breaks in the epidermis and infects the basal layer. Viral early proteins (E6, E7) interfere with host cell cycle regulation (p53 and Rb pathways), promoting keratinocyte proliferation and delaying differentiation and apoptosis. This produces the thickened, hyperkeratotic epidermis characteristic of warts.
- Viral replication is confined to differentiating keratinocytes in the upper epidermis; mature virions are shed with desquamating cells, enabling further transmission
- Dilated, thrombosed capillaries in elongated dermal papillae account for the characteristic pinpoint black dots ("seeds") seen on paring
- Spontaneous regression occurs via cell-mediated (T-cell) immune response against HPV antigens, explaining why warts often resolve without treatment and why they are more persistent in immunosuppressed hosts
Clinical features
Morphology varies by subtype and location.
- Common wart (verruca vulgaris): dome-shaped, hyperkeratotic papule with a rough, papillomatous surface; found on hands, fingers, periungual skin
- Plantar wart (verruca plantaris): endophytic (inward-growing) due to pressure, often painful on walking, disrupts normal skin lines, shows pinpoint bleeding points when pared
- Flat/plane wart (verruca plana): small, smooth, flesh-colored to tan flat-topped papules, often numerous, on face or extremities; spread by shaving/scratching (Koebner phenomenon)
- Filiform wart: thin, finger-like projections, typically on face or neck
- Mosaic wart: coalescence of multiple plantar warts into a plaque
Key distinguishing clinical sign: interruption of normal skin lines (dermatoglyphics) over the lesion, which is absent in calluses or corns.
Diagnosis
Diagnosis is clinical in the vast majority of cases.
- Inspection: rough, verrucous surface; loss of overlying skin lines
- Paring the surface with a blade reveals pinpoint bleeding points (thrombosed capillaries) — helps distinguish from calluses, which show no bleeding and preserved skin lines
- Dermoscopy can show papillomatous pattern with central red-brown dots
- Biopsy is reserved for atypical, non-resolving, pigmented, or rapidly growing lesions to exclude malignancy (e.g., squamous cell carcinoma, amelanotic melanoma), particularly in older adults or immunosuppressed patients
- No routine HPV typing or serology is used for cutaneous warts in clinical practice
Differential diagnosis
- Callus/corn: preserved skin lines, no bleeding points, pressure-related location
- Molluscum contagiosum: dome-shaped papule with central umbilication, caused by a poxvirus, not HPV
- Seborrheic keratosis: typically in older adults, "stuck-on" waxy appearance
- Squamous cell carcinoma / keratoacanthoma: rapidly growing, ulcerated, or non-healing lesion, especially in sun-exposed skin or immunosuppressed patients — biopsy if suspicious
- Acral melanoma: pigmented, irregular lesion on palms/soles — biopsy if any pigmentation or atypia
- Lichen planus: for flat warts, consider violaceous flat-topped papules with Wickham striae
Management
Many cutaneous warts resolve spontaneously within 1-2 years, especially in children, so observation is a reasonable first option, particularly for asymptomatic lesions. When treatment is desired (pain, cosmetic concern, spreading lesions), options include:
First-line (outpatient, self- or clinician-applied)
- Topical salicylic acid (keratolytic) — repeated application, mainstay of self-treatment
- Cryotherapy with liquid nitrogen — repeated clinic sessions every 2-3 weeks
Second-line / resistant warts
- Cantharidin (clinician-applied blistering agent)
- Topical immunotherapy: imiquimod, or contact sensitizers (e.g., diphenylcyclopropenone) to stimulate local immune response
- Intralesional immunotherapy (e.g., Candida antigen, intralesional bleomycin) for recalcitrant warts
- Duct tape occlusion — low-cost adjunct with modest evidence
- Laser therapy (pulsed dye laser) or surgical/electrocautery removal for refractory lesions, with risk of scarring
Guideline consensus (AAD, BAD, Cochrane reviews) agrees that no single therapy is clearly superior for all patients; salicylic acid and cryotherapy have the best evidence base and are generally tried first, with choice guided by site, number of warts, patient age, and tolerance of discomfort. Anogenital warts (HPV 6/11) are managed separately with agents such as imiquimod, podophyllotoxin, or ablative therapy, and are not covered by this cutaneous wart protocol.
Immunosuppressed patients often require more aggressive, combination, or prolonged therapy and have higher recurrence rates.
Complications and prognosis
- Most cutaneous warts in immunocompetent individuals, especially children, resolve spontaneously within 1-2 years without scarring
- Recurrence after treatment is common because HPV can persist in clinically normal adjacent skin
- Plantar warts may cause pain and altered gait due to pressure-related endophytic growth
- Autoinoculation (scratching, shaving) can spread warts to new sites
- Treatment-related scarring can occur with aggressive cryotherapy, cautery, or laser
- Rare but important: epidermodysplasia verruciformis and certain high-risk HPV types in immunosuppressed patients carry a risk of malignant transformation to squamous cell carcinoma, warranting biopsy of atypical or changing lesions
"WART" = Wait (many resolve spontaneously), Acid (salicylic acid), Refrigerate (cryotherapy), Trauma check (biopsy if atypical/non-healing)
Practice questions
1. A 10-year-old boy presents with a rough, 5-mm papule on the plantar surface of his right foot that is painful when walking. Paring the lesion's surface reveals multiple pinpoint black dots and bleeding. Which of the following best describes the underlying mechanism of this lesion?
2. A 45-year-old renal transplant recipient on tacrolimus develops numerous, rapidly increasing flat-topped papules on his face and dorsal hands over several months. He has had similar lesions treated previously with cryotherapy but they keep recurring and multiplying. What is the most appropriate next step in management given his immunosuppressed status and the changing lesion burden?
3. A 16-year-old girl has several small, smooth, slightly elevated, flesh-colored papules on her forehead that have spread in a linear pattern along scratch marks over the past month. Which historical detail would most support the diagnosis of flat warts over molluscum contagiosum?
Frequently asked questions
What causes warts?
Warts are caused by infection of skin keratinocytes with human papillomavirus (HPV), most commonly types 1, 2, 4, and 27 for common skin warts. The virus enters through tiny breaks in the skin and triggers excess keratinocyte growth, producing the thickened, rough papule. Spread occurs through direct skin contact or contaminated surfaces like pool decks and locker room floors.
What are the first symptoms of a wart?
The first sign is usually a small, rough, flesh-colored or gray bump that grows slowly over weeks. On the hands it feels rough and raised; on the soles of the feet it often grows inward and can be tender when walking or standing. Close inspection typically shows interrupted skin lines and tiny dark dots once the surface is pared down.
How are warts diagnosed?
Warts are diagnosed clinically by their rough surface, interruption of normal skin lines, and pinpoint bleeding points visible after gently paring the surface. No blood tests or imaging are routinely needed. Biopsy is reserved for lesions that look atypical, grow rapidly, bleed spontaneously, or fail to respond to treatment, to rule out skin cancer.
Are warts curable or do they come back?
Many warts clear on their own within 1 to 2 years as the immune system eliminates the virus, especially in children. Treatments like salicylic acid or cryotherapy speed clearance but recurrence is common because HPV can linger in nearby normal-looking skin. Immunosuppressed patients tend to have more persistent and recurrent warts.
Warts vs calluses — what is the difference?
Warts are caused by HPV and show interrupted skin lines with pinpoint bleeding points when pared, while calluses are caused by repeated friction or pressure and show preserved, unbroken skin lines without bleeding. Calluses typically occur over bony pressure points and resolve with reduced friction, whereas warts can appear anywhere and are contagious.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: B07
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.