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Summary Table

Category	Details
Risk Factors	Children and young adults, immunocompromised patients (HIV, organ transplant recipients), occupational skin trauma (butchers, meat handlers), atopic dermatitis, nail biting (periungual warts)
Etiology	Human Papillomavirus (HPV), most commonly types 2 and 4; transmitted via direct skin contact or autoinoculation through microabrasions in the epidermis
Patient Presentation	Painless, rough, flesh-colored papule(s) on the hands, fingers, or periungual area; may also appear on knees and elbows; patient may note gradual enlargement or spread to adjacent sites
Classic Physical Exam	Firm, well-circumscribed, dome-shaped papule with a rough, hyperkeratotic surface; disruption of normal skin lines across the lesion; punctate black dots (thrombosed capillaries) visible on paring
Key Diagnostic Results	Clinical diagnosis; dermoscopy shows thrombosed capillary loops ("frog spawn" pattern); biopsy (if atypical) reveals koilocytes, papillomatosis, acanthosis, and hyperkeratosis
Management	First-line: topical salicylic acid (17%–40%); second-line: cryotherapy with liquid nitrogen; refractory cases: imiquimod, intralesional bleomycin, or surgical destruction
Keywords	"Rough, flesh-colored papule," "disruption of skin lines," "punctate black dots on paring," "thrombosed capillaries," "koilocytes on biopsy"

1. Pathophysiology

HPV is a non-enveloped, double-stranded DNA virus that belongs to the Papillomaviridae family. It has a strong tropism for squamous epithelium and gains entry into the basal keratinocytes through breaks or microabrasions in the skin surface. Once inside the basal layer, the virus integrates its early gene products (particularly E6 and E7 oncoproteins) into the host cell machinery. In low-risk HPV types (such as types 2 and 4, which cause verruca vulgaris), these oncoproteins primarily drive uncontrolled keratinocyte proliferation rather than malignant transformation.

The proliferative stimulus results in the three histological hallmarks seen in warts: papillomatosis (upward projection of dermal papillae creating the verrucous surface), acanthosis (thickening of the stratum spinosum), and hyperkeratosis (thickening of the stratum corneum creating the rough, scaly texture). This is why the wart feels hard and rough on palpation. The expanded dermal papillae contain dilated capillary loops that become thrombosed, producing the characteristic punctate black dots visible when the hyperkeratotic surface is pared down. This finding is a critical clinical discriminator because it confirms the presence of a wart and rules out a simple callus or corn, which lacks these vascular structures.

A key concept for understanding why warts spread and persist is that HPV remains strictly intraepithelial. It does not enter the bloodstream and does not trigger a strong systemic immune response. The virus exploits this immune evasion by downregulating MHC class I expression on infected keratinocytes, effectively hiding from cytotoxic T cells. This explains why warts are more numerous, larger, and more resistant to treatment in immunocompromised patients, particularly those with T-cell dysfunction (HIV/AIDS, post-transplant immunosuppression). When cell-mediated immunity eventually mounts an adequate response, the warts regress spontaneously, which is why up to 65% of common warts resolve within two years without any intervention in immunocompetent individuals.

The hallmark histological finding is the koilocyte, a virally infected keratinocyte in the upper stratum spinosum and granulosum characterized by a shrunken, hyperchromatic (raisin-like) nucleus surrounded by a perinuclear halo of cleared cytoplasm. The presence of koilocytes on biopsy is considered pathognomonic for HPV infection across all subtypes.

2. Classification and Clinical Manifestation

Wart Type	HPV Types	Morphology	Typical Location
Verruca vulgaris (Common wart)	2, 4, 27, 57	Flesh-colored, dome-shaped, hyperkeratotic papule with rough surface; disrupted skin lines; black dots on paring	Dorsal hands, fingers, periungual region, knees, elbows
Verruca plana (Flat wart)	3, 10, 28	Flat-topped, smooth, skin-colored to light brown papule (1–5 mm); often numerous and grouped	Face, dorsal hands, shins; may appear in a linear pattern (Koebner phenomenon from scratching)
Verruca plantaris (Plantar wart)	1, 2, 4	Endophytic (growing inward due to weight-bearing pressure); thick callus-like plaque with central black dots; painful on lateral compression	Soles of feet, pressure points (heel, metatarsal heads)
Mosaic wart	2	Coalescing cluster of multiple plantar warts forming a large plaque	Soles of feet
Verruca filiformis (Filiform wart)	1, 2, 4	Finger-like, elongated projections on a narrow stalk	Face (around eyes, nose, mouth), neck, chin
Butcher's wart	7	Large, cauliflower-like, exophytic growths	Hands of meat and fish handlers (occupational exposure)
Condyloma acuminatum (Anogenital wart)	6, 11 (low-risk)	Soft, pink, pedunculated, cauliflower-like papillomatous growth	Anogenital mucosa, perianal skin
Epidermodysplasia verruciformis	5, 8 (high-risk for SCC)	Widespread, flat, reddish-brown plaques resembling pityriasis versicolor; lifelong susceptibility due to inherited T-cell defect	Trunk, extremities, face; onset in childhood

A clinical pearl worth noting: flat warts on the face often present after shaving, with lesions appearing in a linear distribution along the razor's path. This is an example of the Koebner phenomenon (isomorphic response), where trauma to the skin induces new lesion formation along the line of injury. This detail appears in exam vignettes as a clue pointing toward a viral etiology rather than simple folliculitis.

Plantar warts are commonly confused with corns or calluses. The distinguishing feature is that plantar warts disrupt normal dermatoglyphics (skin lines) and reveal black dots on paring, while a callus preserves normal skin lines and lacks vascular puncta. Additionally, plantar warts are painful with lateral compression (pinching), whereas calluses are painful with direct downward pressure.

3. Diagnostic Workup

Test	Role	Key Findings
Clinical examination	Best initial test (and usually sufficient)	Rough, hyperkeratotic papule with disrupted skin lines; punctate black dots on paring
Dermoscopy	Adjunct for equivocal lesions	Thrombosed capillary loops (red-black dots/globules in a "frog spawn" pattern); white-yellow papillomatous surface
Paring test	Confirmatory bedside test	Shaving the hyperkeratotic surface with a scalpel blade reveals punctate bleeding points from thrombosed capillaries; this distinguishes warts from calluses
Skin biopsy with histopathology	Gold standard (reserved for atypical or non-responsive cases)	Papillomatosis, acanthosis, hyperkeratosis, hypergranulosis; koilocytes (perinuclear halos with hyperchromatic nuclei) in the upper epidermis
HPV DNA typing (PCR)	Research and epidemiological use; not routine	Identifies HPV subtype; clinically relevant mainly for genital warts to assess oncogenic risk

Verruca vulgaris is overwhelmingly a clinical diagnosis. The combination of a rough, hyperkeratotic, flesh-colored papule in a characteristic location (hands, fingers) with disruption of skin lines is sufficient to make the diagnosis in most cases. The paring test is the most useful bedside maneuver: using a No. 15 scalpel blade to gently shave the surface of the lesion reveals the punctate thrombosed capillaries appearing as tiny black or red dots with pinpoint bleeding. This finding effectively rules out a callus (which shows a smooth, translucent keratin core without vascular puncta) and makes biopsy unnecessary.

Dermoscopy adds diagnostic confidence when the clinical picture is ambiguous. The classic dermoscopic pattern for verruca vulgaris is the "frog spawn" or "frog egg" appearance: multiple red-black dots and globules arranged in a clustered pattern, representing the loop-shaped dilated capillaries within each dermal papilla, surrounded by a whitish halo of hyperkeratotic epidermis.

Biopsy is indicated in the following situations: lesions that fail to respond to standard therapy after several months, rapidly growing or ulcerated lesions (raising concern for squamous cell carcinoma arising in a wart), lesions with atypical morphology, or lesions in immunocompromised patients where the differential includes malignancy. Histopathology serves as the gold standard and reveals the triad of papillomatosis, acanthosis, and hyperkeratosis alongside the pathognomonic koilocytes in the granular layer.

Routine HPV DNA typing is not performed for common warts. It is reserved for anogenital lesions where distinguishing high-risk HPV types (16, 18) from low-risk types (6, 11) has prognostic and management implications.

4. Management and Treatment

Approach	Treatment	Details
Observation	Watchful waiting	Appropriate in immunocompetent patients (especially children) with few, painless warts; ~65% resolve spontaneously within 2 years
First-line (home-based)	Salicylic acid (topical, 17%–40%)	Applied daily after soaking in warm water for 5 minutes and filing dead skin with pumice stone; cover with occlusive tape; continue for 12 weeks
Second-line (office-based)	Cryotherapy (liquid nitrogen)	Applied to the wart for 10–30 seconds per freeze-thaw cycle, repeated every 2–3 weeks for 3–4 sessions; causes subepidermal blister formation
Refractory cases	Imiquimod 5% cream	Immune response modifier (TLR-7 agonist); applied 3 times per week for up to 16 weeks; induces local interferon and cytokine release
Refractory cases	Topical 5-Fluorouracil (5-FU) 5%	Antimetabolite; applied under occlusion daily for several weeks; particularly useful for flat warts
Refractory cases	Intralesional bleomycin	1 U/mL injected directly into the wart; causes vascular thrombosis and necrosis; painful; avoid in pregnancy and Raynaud disease
Surgical	Electrodesiccation and curettage	Reserved for isolated, refractory warts; higher recurrence rate and risk of scarring
Surgical	Pulsed dye laser (PDL)	Targets hemoglobin in capillary loops; useful for recalcitrant warts, especially plantar and periungual
Immunotherapy	Intralesional Candida antigen injection	Injected into the largest wart to stimulate delayed-type hypersensitivity response; may clear distant warts simultaneously

First-line therapy for most common warts is topical salicylic acid. The mechanism of action is keratolytic: salicylic acid softens and dissolves the intercellular cement substance in the stratum corneum, gradually destroying the virus-laden hyperkeratotic tissue. The recommended regimen involves soaking the affected area in warm water for approximately 5 minutes, then gently debriding the macerated surface with a pumice stone or emery board, applying the salicylic acid preparation directly to the wart (avoiding surrounding normal skin), and covering with an occlusive bandage. This cycle is repeated daily. Patients should be counseled that the treatment requires consistent daily application for at least 12 weeks before concluding that it has failed. Cure rates with salicylic acid approach 70%–80%.

Cryotherapy with liquid nitrogen is the most commonly used office-based treatment and serves as the second-line option. The mechanism involves rapid freezing that induces intracellular ice crystal formation, leading to cell membrane disruption, vascular damage, and local tissue necrosis. A subepidermal blister typically forms 24–48 hours after treatment, which is expected and should not be drained. Sessions are repeated every 2–3 weeks. Cryotherapy can be combined with salicylic acid between sessions to improve efficacy. Adverse effects include pain during the procedure, blistering, and hypopigmentation (particularly in darker-skinned patients, which is an important counseling point).

For refractory warts (persisting after 12 weeks of salicylic acid and multiple cryotherapy sessions), the options include imiquimod, 5-fluorouracil, intralesional bleomycin, and procedural approaches. Imiquimod is a toll-like receptor 7 agonist that stimulates local innate and adaptive immune responses against HPV-infected cells. It is applied three times weekly, and patients should expect erythema and irritation at the application site, which actually indicates an appropriate immune response.

Intralesional bleomycin deserves attention because it is a frequent exam topic: it is absolutely contraindicated in pregnancy (teratogenic) and in patients with Raynaud phenomenon or peripheral vascular disease (risk of digital ischemia and necrosis). The injection itself is painful, and patients should be warned about the possibility of nail dystrophy when treating periungual warts.

A high-yield management pearl: in immunocompromised patients, warts tend to be numerous, recalcitrant, and carry a higher risk of progression to squamous cell carcinoma, particularly with high-risk HPV types. The treatment approach in these patients involves the same modalities but often requires combination therapy and closer surveillance with a lower threshold for biopsy.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Molluscum contagiosum	Small, flesh-colored papules on the skin of children; viral etiology (Poxvirus); may coexist with warts	Dome-shaped with central umbilication; smooth, pearly surface (not rough); biopsy shows Henderson-Patterson (molluscum) bodies, not koilocytes
Callus / Corn (Clavus)	Hyperkeratotic lesion on pressure-bearing skin; can mimic plantar warts	Preserves normal skin lines (dermatoglyphics run through the lesion); no punctate black dots on paring; painful with direct pressure (warts hurt with lateral squeeze)
Seborrheic keratosis	Hyperkeratotic, well-circumscribed, raised papule in adults	"Stuck-on" waxy appearance; horn pseudocysts on dermoscopy; occurs in older adults (not children); no disruption of skin lines
Squamous cell carcinoma (SCC)	Can arise within a longstanding wart (especially in immunocompromised); hyperkeratotic nodule	Progressive growth, ulceration, bleeding, induration; does not respond to standard wart therapy; biopsy shows invasion through the basement membrane with atypical keratinocytes
Acrochordon (Skin tag)	Flesh-colored papule on the neck or axillae	Soft, pedunculated, smooth surface; no hyperkeratosis or rough texture; no vascular puncta
Keratoacanthoma	Rapidly growing, dome-shaped, hyperkeratotic nodule	Central keratin-filled crater ("volcano-like"); rapid growth over weeks (warts grow slowly); may regress spontaneously; biopsy needed to rule out SCC
Condyloma latum (secondary syphilis)	Moist, raised, flat-topped papule that may appear wart-like	Found in intertriginous areas (perianal, genital folds); associated with secondary syphilis findings (diffuse rash, mucous patches, lymphadenopathy); positive RPR/VDRL and FTA-ABS

The most testable differential is callus versus plantar wart. Both present as hyperkeratotic lesions on the sole of the foot. The vignette will typically describe a patient who complains of pain while walking, and the stem will include a detail about what happens when you examine the lesion. If the lesion preserves skin lines and is painful with direct pressure, the answer is callus. If skin lines are interrupted, black dots are visible on paring, and pain worsens with lateral compression, the answer is plantar wart.

Another commonly tested distinction is verruca vulgaris versus molluscum contagiosum in a pediatric patient. Both are viral papules. The critical clue is surface texture: warts are rough and hyperkeratotic, while molluscum lesions are smooth and dome-shaped with a central dimple (umbilication).

6. Traps and High-Yield Pearls

The most common way students lose points on verruca vulgaris questions is by confusing warts with calluses on plantar lesion vignettes. The test-writer deliberately constructs a scenario of a painful foot lesion and expects you to apply two physical exam maneuvers mentally: check for disruption of skin lines and check for punctate black dots on paring. If you skip this reasoning step, you will default to the more "common" answer of callus and miss the diagnosis.

A second trap involves immunocompromised patients with non-resolving warts. The vignette may describe a transplant recipient with a longstanding wart that has begun to enlarge, ulcerate, or bleed. The expected answer is not "continue cryotherapy" but rather biopsy to rule out squamous cell carcinoma. HPV-driven malignant transformation is a real clinical concern in this population, and the exam tests whether you recognize the red flags that warrant tissue diagnosis over continued empiric treatment.

A third commonly tested concept is the Koebner phenomenon in the context of flat warts. A vignette describing a young woman with multiple tiny flat papules in a linear distribution along the jawline after shaving is pointing you toward verruca plana with isomorphic response, not acne, folliculitis, or contact dermatitis.

Finally, remember that salicylic acid is first-line, not cryotherapy. Many students reflexively choose cryotherapy because it sounds more "definitive," but guidelines consistently position topical salicylic acid as the initial treatment for uncomplicated common warts, with cryotherapy reserved for cases that fail conservative therapy or when a faster in-office result is desired. The core competency being tested across wart-related questions is pattern recognition of surface morphology (rough versus smooth, skin line disruption, vascular puncta) and appropriate stepwise management in both immunocompetent and immunocompromised hosts.

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