Defining wart types

Warts are usually defined by morphology, location and host immune response, which are not mutually exclusive [3, 19].

Definition by morphology (Tab. 1) Common warts (Fig. 1)

Common warts are rough, verrucous plaques of the skin that usually measure 3-10 mm in diameter. HPV type 2 is the most common immunotype; type 1 warts may be indistinguishable. These lesions are often located on the dorsal surface of the hands, but the knees and other areas of the body may also be affected. Common warts on the soles or heels, "plantar warts", often develop a thick overlying callus. Mosaic warts are agminated common warts, which take on the appearance of a single wart. Often these grouped warts are located on the soles and are covered by a single callus. The scalloped edge, which is seen due to the grouping of papules, may mimic cutaneous herpetic whitlow. The overlying thick callus may be painful, and paring may

Human papillomavirus infections in children


Table 1. Warts classification systems


Associated HPV viruses

1. Common warts

1-4, 7, 10

Mosaic warts

1-4, 7, 10

Callous-like warts

1-4, 7, 10

2. Filiform warts

1-4, 7, 10

3. Flat warts (tinea versicolor-like)

3, 5*, 8*, 10, 12, 14, 15, 17, 25-30, 41

4. Donut warts


5. Epidermal cyst, punctate type or pigmented warts


5. Sub-clinical infection



Associated HPV viruses

1. Common warts

2-4, 7, 10, 16, 29, 57

2. Palmoplantar warts

1, 2-4, 7, 10, 60, 63

3. Respiratory papillomatosis

6, 11, 16, 18

4. Periungual warts

1-4, 7, 10, 16*, 34*

5. Condyloma acuminatum

6, 11, 16*, 18*, 31*, 33*, 34*, 35, 39,

42-45, 51-53, 55, 56, 58, 59, 63, 66, 68

6. Oral papillomatosis (Heck's disease)

13, 24, 32*

7. Verrucous carcinoma

1-4, 6, 11, 18

*Types associated with malignant transformation +Associated with prior therapy of warts give a high degree of relief to the patient and reveal the true number of lesions [3, 19, 20].

Flat warts (verruca plana)

Flat warts are flesh- to tan-colored papules, which are smaller and smoother than common warts, usually 2-4 mm in size. These lesions are common on the face and neck. Flat warts may be spread by shaving (Koebner phenomenon) in adolescents, causing a linear appearance. Flat warts are also seen in the genetic immunodeficiency syndrome, epidermodysplasia verruciformis (EDV). In EDV, warts spread rapidly, and may progress to bowenoid papulosis or Bowen's disease (squamous cell carcinoma in situ). Such malignant conversion has been reported in children as young as toddler age both with and without immunodeficiency [21, 22].

Warzentypen Bilder
Figure 1. Common warts on the fingers in a teenage female.

Filiform warts/digitate warts

Filiform warts are long thin warts with a narrow base and verrucous tip. Digitate warts are a slightly larger version of filiform warts. These warts usually bleed excessively when cut, due to tortuous blood vessels in the stalk of the wart. Filiform warts often appear on the face in children, specifically around the nares and on the lips. Digitate warts are common on the scalp. These warts are an exophytic version of the common wart.

Tinea versicolor-like warts/extensive flat warts

When flat warts spread over a wide surface area and are either slightly hyper- or hypopigmented, they may mimic the appearance of tinea versicolor. This appearance is uncommon and is usually limited to patients with EDV, HIV infection, or other immune deficiency [23].

Doughnut or ring warts (many types)

Ring warts occur around the site of a wart that has been treated previously. These warts are seen after using destructive therapies, particularly liquid nitrogen or cantharidin [24].

Epidermal cyst-type warts (HPV 60, 63, 65)

Occasionally a wart virus can be associated with epidermal cyst formation, including keratinous contents. These generally occur on the sole of the foot [25].

Punctate warts (HPV 60, 63, 65)

Punctate warts are localized endophytic hyperkeratotic papules, seen on the palms. Clinically, these lesions mimic the palmar pits of basal cell carcinoma syndrome and punctate keratoderma. These types of warts are rare [19].

Pigmented warts (HPV 60)

Occasionally warts can present with a high degree of pigmentation, so as to mimic a primary melanocytic process.

Keratoacanthoma (HPV 37)

Keratoacanthomas have been associated with HPV 37, and can progress to squamous cell carcinoma, especially in patients with EDV or immunosup-pression [26].

Subclinical or latent infection

As the incidence of HPV 1 antibodies in select populations can be as high as 50%, clinically inapparent HPV infection is very likely the most common form of infection. Subclinical or latent infections are particularly common as well for genital warts caused by non-oncogenic HPV types.

Definition by location (Tab. 1)

Wart location is an important descriptor in defining and describing warts. Wart location may dictate appearance, biological behavior, therapeutic con cerns (e.g., scarring from treatment), and response to therapy. Warts may infect the normal skin or the mucosa.

Mucosal warts usually appear as finely verrucous papules and plaques, often grouped on a common base, taking on a grape-like appearance. Mucosal warts are often characterized by extensive subclinical infection in the surrounding mucosa. Thus, treatments are less a microscopic cure than a cure of clinical appearance. There are two benign types of significance, con-dyloma and Heck's disease, and two malignant types, verrucous carcinoma and bowenoid papillomatosis.

Palmoplantar warts, also known as myrmecia, are characterized as thick warts with a large overlying callus. These warts are often difficult to treat due to their thickness and the difficulty of eradicating wart at the base

Periungual warts (benign HPV 1-4, 7, 10/premalignant 16, 34)

Periungual warts are warts that involve the periungual skin, the cuticle, and/or the subungual skin. These warts present a treatment difficulty due to the physical blockade created by the nail itself. Furthermore, when treating a wart in this location, accidental injury to the nail matrix may occur. Induction of wart immunity is often best when risk of nail matrix injury exists, or for subungual warts.

Condyloma acuminatum/giant condyloma of Buschke and Ollendorf (HPV 6, 11, 16, 18, 31, 33, 34, etc.)

HPV infection of the mucosal surfaces is often asymptomatic, but may result in lesions, which are termed condylomata (condyloma singular) or papillomas. Condylomata are characterized as grouped papules that are usually smooth, unlike other wart subtypes. Condylomata may result from non-oncogenic types (HPV 6 and 11) and oncogenic types. When non-onco-genic lesions are very large, they are termed giant condyloma of Buschke and Ollendorf. Oncogenic virus types (HPV 16, 18, 31, 33, 34, etc.) may cause cutaneous, cervical, and penile dysplasia and/or neoplasia [1, 27]. Condylomata also develop when common wart HPV, such as HPV type 2, are transferred to the genitalia.

Condyloma with onset in children under the age of 4 years most commonly result from vertical transmission from a virally infected genital tract or caretakers with hand warts. When condylomata are observed in children, careful social and physical evaluation to search for the possibility of sexual abuse is required. It is estimated that nearly 10% of the adult population of the United States are infected with genital warts. Despite the probable high rate of perinatal exposure, pediatric condyloma is uncommon. Recently, a British study demonstrated HPV DNA in a cohort of girls with and without vulvar disease [28]. About a quarter of these girls carried HPV DNA in vulvar skin or urine samples, suggesting that vertical HPV transmission is more common than previously thought, but is usually subclinical or latent. This may relate to transplacental transfer of neutralizing antibodies for HPV [29].

Teenagers are at risk for condyloma through unprotected sexual contact, whether penetration is involved or not. The younger the age at first sexual contact and the greater the number of lifetime partners, the greater the risk of cervical intraepithelial neoplasia. Consequently, sex education and usage of condoms should be encouraged in teenagers. Of HPV genital infections, 82.9% can be diagnosed by dermatologists in the form of external genital disease. External genital disease does not imply cervical disease, which is seen in only 53.4% of patients [30]. Recently common warts have been found to be statistically linked to the development of cervical cancer later in life [31].

One study suggested that oral condyloma in young children is unlikely to be vertically transmitted. The patients examined in this study had mothers with condyloma of the genital area, but the mother's genital HPV infection and the child's oral infection were found to be of different HPV genotypes [32].

Juvenile onset-recurrent respiratory papillomatosis (HPV 6, 11, 16, 18)

A dreaded complication of vertical HPV transmission is JORRP, in which HPV infects the upper and occasionally lower respiratory tract including the tracheal and bronchial trees of children whose mothers were infected with HPV and transferred the virus via vertical transmission. The disease occurs in 7 offspring per 1000 women with genital warts and is 231 times higher in children of women with a condyloma history than in those without. This disease presents with hoarseness, stridor, cough and dyspnea and is often mistaken early on for asthma or laryngeal hemangiomas. Laryngoscopy and bronchoscopy may be required for proper diagnosis and sampling for pathological confirmation. The incidence is estimated at 1.7-2.6 per 100 000 children in the US, but the medical cost is $100 million per year!!! On average, 5.1 surgeries per year are required to ameliorate symptoms in young children [33, 34].

Because HPV types transmitted are primarily 6, 11, 16, and 18, HPV vaccination of women may ultimately help eliminate or reduce the morbidity, mortality and excessive cost of this illness [35]. Phase II study demonstrated a 93% increase in time between episodes of surgery with therapeutic vaccination with a hspE7 linked to E7 gene of HPV 16 [33].

Heck disease or oral papillomatosis is the appearance of many papules of the oral mucosa caused by viral infection. The lesions are mucosa colored and when stretched fade into the background mucosa. The disease is seen in many ethnic groups, but is most common in Native Americans and Eskimo girls. The lower lip, upper lip, buccal mucosa and tongue can be affected. Cryotherapy or carbon dioxide laser therapy has been shown helpful in these patients. Spontaneous regression follows a similar time schedule to standard wart resolution and aggressive therapy should be reserved for cases with a protracted course [36, 37].

Bowenoid papulosis (HPV1, 16, 18, 33, 34)/verrucous carcinoma (HPV 1-4, 6, 11, 16, 18)

Bowenoid papulosis is a form of squamous cell carcinoma in situ characterized by enlarging plaques of the genital region. It has been reported in immunocompetent and immunosuppressed children. Although sexual abuse need be suspected, acquisition of warts can occur through non-sexual manners and with viral types that are not considered oncogenic, e.g., HPV 1. This is particularly true for girls with human immunodeficiency virus. Verrucous carcinoma is usually seen on the external genitalia or digits, the latter representing the source of genital infection in some cases. Inoculation of hands through contact with genital lesions has been reported as a source of oncogenic virus types in the digits [38-42].

Definition by mode of regression

A recent article categorized warts via immune response. The details overlap with the categorizations above and are summarized in Table 2. Two subtypes add new information, HPV type 4 and intermediate warts. HPV type 4 is associated with a specific mode of regression, which produces, in addition to the usual koilocytes, signet-ring vacuolized keratinocytes on microscopy. Intermediate warts (HPV types 10, 27, 28, 29) are essentially common warts seen in patients with depressed cellular immunity, hence variable inflammatory cellular infiltrate and rates of regression can be seen [19].

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