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Oral Florid Papillomatosis Workup

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
Updated: Jun 21, 2016

Laboratory Studies

Ultrastructural studies may be considered. Findings suggest a well-differentiated squamous cell carcinoma[48] and are similar to those of conventional squamous cell carcinomas. The findings include prominent microvilli, decreased tonofilaments, and underdeveloped desmosomes.

With oral verrucous carcinoma (VC), tissue typing for HPV may be beneficial, assuming it proves clinically useful to divide verrucous carcinomas on the basis of HPV infection.[49] In one series, HPV was identified with the polymerase chain reaction in 13 of 29 cases of laryngeal verrucous carcinoma.[24]


Imaging Studies

The latest radiographic techniques, such as magnetic resonance imaging, should be used to define the extent of the tumor and to determine whether underlying bone or other structures are involved.

Computed tomography (CT) can be used to demonstrate the exact location and the extent of the tumor for preoperative staging and surgical planning. Dual-energy CT may be used to enhance assessment of tumor margins.[50]


Histologic Findings

The typical microscopic section shows a well-differentiated typical squamous cell carcinoma with verrucous clinical morphology.[1]

Histologically, oral verrucous carcinoma shows exophytic and endophytic growth patterns.[1] Its massively hyperplastic and exophytic epidermis has marked hyperkeratosis, sometimes with parakeratosis. Its prominent granular layer has tumor cells that may be vacuolated, resembling and indistinguishable from the koilocytes of condylomata acuminata.

Verrucous carcinoma is characterized by blunt projections of well-differentiated epithelium supported by an edematous stroma, with chronic inflammatory cells of lymphohistiocytic origin at its infiltrating margins. These blunt tumor masses extend into the dermis and deeper structures, forming sinuses and keratin-filled cysts. Bulbous islands of benign-appearing epithelium may infiltrate the subcutaneous tissue. This deceptively benign quality is associated with a basement membrane adjacent to its basal epithelial layer despite the composition of infiltrating tumor islands.[25]

Rare areas of focal disruption of the basement membrane are noted in oral verrucous carcinomas. Thus, neither the presence nor the absence of a basement membrane is a reliable indicator of tumor behavior. Atypical mitotic figures, individual cell necrosis, dyskeratosis, and multinucleated keratinocytes are rarely, if ever, evident. Centripetal keratinization of individual keratinocyte islands may be seen, but horn pearls are not. Individual cell cytologic features are relatively benign, with minimal dysplasia. Individual cells may be large and have big nuclei and prominent nucleoli. Occasionally, giant nuclei and enlarged malpighian keratinocytes may be evident. Intracytoplasmic glycogen is scant in verrucous carcinoma, as compared with keratoacanthoma and pseudoepitheliomatous hyperplasia.

Some oral mucosal verrucous carcinomas may be associated with small foci of floridly malignant squamous cell carcinomas,[35, 51, 52] adjacent ordinary squamous cell carcinomas,[53] or regional node metastases.[53, 54] In one study,[51] 21 (20%) of 104 oral verrucous carcinomas had similar foci with less differentiation than that of the verrucous carcinoma. Such foci of dysplasia are associated with a doubled recurrence rate and a 10% incidence of lymph node metastases.[52] Therefore, careful sectioning to remove as much tumor as possible is indicated.

Radiation therapy has been implicated in the anaplastic transformation of some verrucous carcinomas,[54] although anaplastic transformation may represent a possible terminal event in the natural progression of verrucous carcinoma.[55] This phenomenon may be an example of a verrucous carcinoma undergoing programmed dedifferentiation to become a classic squamous cell carcinoma. The hybrid verrucous carcinoma–squamous cell carcinoma deserves careful scrutiny.

The extraoral expansion of a local tumor into the underlying cartilage and bone results in moderate dyskeratosis and numerous mitotic features as the bone is replaced by tumor. Acute and chronic inflammation and a granulation tissue reaction are also present. Tumor cells are usually not found in the blood vessels or the lymphatics; this finding is presumably correlated with the general absence of metastases in patients with mucosal verrucous carcinoma.

An ordinary squamous cell carcinoma may be a clinically silent verrucous carcinoma with histologic patterns reflecting its warty and exophytic surface. If clusters of poorly differentiated cells are present, the tumor is a conventional squamous cell carcinoma with a high malignant potential and a tendency to metastasize. However, typical verrucous carcinomas with foci of conventional squamous cell carcinoma, that is, the hybrid verrucous carcinoma–squamous cell carcinoma, may be troubling.

The distinction between verrucous carcinoma and a large and persistent verruca vulgaris may be difficult at both clinical examination and histologic examination. Verrucous carcinoma and verruca vulgaris both have the keratinocytic vacuolization that is said to be characteristic of viral warts.[56] Avoid obtaining only a small superficial skin biopsy specimen; larger specimens facilitate the correct diagnosis. Verrucous hyperplasia of the oral mucosa must also be considered; it is best evaluated in biopsy specimens obtained from the lesional margins.[57]

Contributor Information and Disclosures

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.


Channing R Barnett, MD Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey

Channing R Barnett, MD is a member of the following medical societies: Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Julie C Harper, MD Assistant Program Director, Assistant Professor, Department of Dermatology, University of Alabama at Birmingham

Julie C Harper, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Received honoraria from Stiefel for speaking and teaching; Received honoraria from Allergan for speaking and teaching; Received honoraria from Intendis for speaking and teaching; Received honoraria from Coria for speaking and teaching; Received honoraria from Sanofi-Aventis for speaking and teaching.

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