SciELO - Scientific Electronic Library Online

vol.79 número5Tricoses compulsivasProfessor Doutor Luiz Marino Bechelli índice de autoresíndice de assuntospesquisa de artigos
Home Pagelista alfabética de periódicos  

Serviços Personalizados




Links relacionados


Anais Brasileiros de Dermatologia

versão impressa ISSN 0365-0596versão On-line ISSN 1806-4841

An. Bras. Dermatol. v.79 n.5 Rio de Janeiro set./out. 2004 



Verrucous carcinoma: a clinical-histopathologic variant of squamous cell carcinoma*



Maurício ZaniniI; Cláudio WulkanII; Francisco Macedo PaschoalIII; Marisa Homem de Mello MacielIII; Carlos D´Apparecida S. Machado FilhoIV

IDermatology specialist. Member of the Brazilian Society of Dermatology. Supervisor of Dermatological Surgery and Dermatocosmetology
IIDermatology Specialist
IIIAssistant Professor of Dermatology. Member of the Brazilian Society of Dermatology
IVInterim Head of the Dermatology Section. Ph.D. in Dermatology. Head of the Dermatological Surgery Department of the Brazilian Society of Dermatology





Verrucous carcinoma is a rare and indolent variant of the squamous cell carcinoma described by Ackerman in 1948. The oral cavity is a most common site. Clinically, it presents most often as a slow-growing verrucous lesion. The prognosis is good. Treatment of choice is surgery. Patients require frequent reevaluation because recurrences may occur.

Key words: Carcinoma, Squamous Cell; Carcinoma, Squamous Cell/diagnosis; Carcinoma, Squamous Cell/pathology




Squamous cell carcinoma (SCC) stems from keratinocytes.1 SCC presents as several clinical and histopathologic variants, including verrucous carcinoma (VC). Although malignant, this variant does present with characteristics of a benign tumor.2 The "benign" characteristics of VC are slow growth, a progression pattern that is more expansive than invasive, and good cellular differentiation.2,3

The expression verrucous carcinoma was defined by L.V. Ackerman4 in 1948 to characterize a well-differentiated verrucous neoplasia, with slow growth and without a tendency to metastasize.5 VC is a SCC with a low degree of dysplasia, and low incidence.6 Its biological aggressiveness is limited to the localization. As it is a tumor that has predominantly horizontal growth, it tends to erode more than infiltrate.7 It has a good prognosis, which rarely causes regional metastases. It does not present with remote metastasis.7,8

Depending on its localization, verrucous carcinoma or cutaneous papillary carcinoma tends to get various designations. Accordingly, at the genital area it is called Bushke-Loewenstein's tumor, at the plantar region epithelioma cuniculatum of the foot, and at the mouth oral florid papillomatosis, Ackerman tumor and/or oral VC.5 Hybrid VC is defined as a mixed tumor lesion. It consists predominantly of a VC and areas of SCC which acquire SCC prognostic factors.8

It may be localized on the skin and in the mucosas.7 The oral cavity is the VC site par excellence, being responsible for 70% of cases.5 Oral VC is responsible for a proportion of oral SCCs varying from 4.5-to-9.5%.5 It predominates in men over the age of 65 years.6 It is clinically characterized by papules or a notably verrucous, white-grey plaque, with slow growth. It most often affects the jugal, gingival and alveolar mucosas, even though any oral segment can be affected (Figure 1).6 Secondary infections are frequent, and may lead to an unpleasant odor and reactional adenopathy.1



Its etiopathogenesis is related to the following carcinogens: biologic (HPV), chemical (smoking) and physical (constant trauma). As for oral VC, smoking, a habit of chewing betel and snuff and human papilloma virus infection (HPV), they stand out as the main carcinogenic factors.2,5,6 A case has been described oral lichen planus in association with VC.6 OHPV is responsible for roughly 28% of cases, usually types 16 and 18, but also 2 and 11. Viral carcinogenesis is most likely caused by the suppression or mutation of gene p53, which is responsible for cellular tumor suppression activity. Nevertheless, the mere evidence of a viral infection is not enough to incur a malignant transformation, because most patients infected with HPV do not develop cancer. Co-factors are thus necessary.5

In the clinical differential diagnosis, the following were observed: SSC, viral verruca, amelanotic melanoma, histoplasmosis, secondary syphilis, Darier's disease, white spongy nevus and erythematous lupus.6 Due to its high degree of differentiation, the histopathologic diagnosis is quite difficult.5 The histopathologic alterations of VC include hyperkeratosis and parakeratosis, soft verrucous acanthosis with formation of enlarged key-shaped papillae and prominent perilesional inflammatory infiltrate. The hyperplasic epidermis presses against the basal membrane and dermis, but the basal membrane remains intact. Cellular atypia is not evident, and formation of keratin drops is not frequent.7 Mitosis and dyskeratotic cells might eventually be seen at the base of the lesion.8 For the histopathologic study to be reliable, the biopsy must be broad and deep in scope so as to demonstrate these histopathologic findings and allow adequate differentiation with SCC and other causes of pseudoepitheliomatous hyperplasia. Some authors define the histopathologic pattern of VC as intimidating, but not noxious.5

The management of oral VC must include general measures such as adequate oral hygiene, re-adaptation of eventual dental prostheses and regular patient reevaluation. VC may be considered a multifocal and recurrent disease, whether by genetic predisposition or by the duration of inductor factors. Accordingly, even as one focus is cured, the affection might recur at another localization.1

Mohs microsurgery is the treatment of choice for VC, with a 98% cure rate. Due to its association with HPV, therapy with imiquimod and cidofovir is raised as a possibility.10 Radiotherapy ought to be avoided as a result of the transformative potential of anaplasia.2,5,6 Cryosurgery, laser, photodynamic therapy, and intralesional bleomycin are therapeutic options.1,5



1. MacKie RM. Epidermal skin tumors. In: Rook A, Wilkinson DS, Ebling FJG. Textbook of dermatology. London: Blackwell Science; 1998. p.1687-92.         [ Links ]

2. Rinker MH, Fenske NA, Scalf LA, Glass F. Histologic Variants of Squamous Cell Carcinoma of the Skin. Cancer Control. 2001;8(4):354-63.         [ Links ]

3. Cotran RS, Kumar V, Robbins SL. Patologia estrutural e functional. 4a ed. Rio de Janeiro: Guanabara Koogan; 1991. p. 197-207.         [ Links ]

4. Ackerman LV. Verrucous carcinoma of the oral cavity. Surgery. 1948; 23: 670-8.         [ Links ]

5. Lübbe J, Kormann A, Adams V et al. HPV-11 and HPV-16 - Associated oral verrucous carcinoma. Dermatology. 1996;192:217-21.         [ Links ]

6. Warshaw EM, Templeton SF, Washington CV. Verrucous carcinoma occurring in a lesion of oral lichen planus. Cutis. 2000;65:219-22.         [ Links ]

7. Spiro RH. Verrucous carcinoma, them and now. Am J Surg. 1998;176:393-6.         [ Links ]

8. Batsakis JG, Suarez P, El-Naggar AK. Proliferative verrucous leukoplakia and its related lesions. Oral Oncology. 1999;35:354-9.         [ Links ]

9. Swanson NA, Taylor WB. Plantar verrucous carcinoma: literature review and treatment by the Mohs' chemosurgery technique. Arch Dermatol. 1980; 116(7):794-7.         [ Links ]

10. Schell BJ, Rosen T, Rady P et al. Verrucous Carcinoma of the Foot Associated With Human Papillomavirus Type 16. J Am Acad Dermatol. 2001;45:49-55.         [ Links ]



Correspondence to
Maurício Zanini
Rua Elsa Odebrecht, 538
89021-120 Blumenau SC
Tel.: (47) 326-4458

Received on June 05, 2002.
Approved by the Consultive Council and accepted for publication on Septembrt 10, 2003.



* Work done at the Prof. Dr. Luiz Henrique Camargo Paschoal Dermatology Sector, ABC Medical Faculty, Santo André, Sao Paulo State.

Creative Commons License Todo o conteúdo deste periódico, exceto onde está identificado, está licenciado sob uma Licença Creative Commons