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Oral Florid Papillomatosis Clinical Presentation

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

History

The patient may note a bulky tumor. Some patients experience localized pain and difficulty in mastication. Malignant conversion of florid oral and labial papillomatosis during topical immunotherapy with imiquimod was described in one patient.[32]

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Physical

The Ackerman tumor is evident as a confluence of whitish nonulcerated papillomas on the oral mucosa, often on a background of chronic irritation or leukoplakia. The surface may be pebbly or mamillated.[2] Leukoplakia may be the earliest sign.[25] The tumor may begin on the vermillion border of the lip or extend onto it. Of the 31 patients that Ackerman described, 18 had verrucous carcinoma on the buccal mucosa; 8, on the lower gingiva; 2, on the hard palate; and 1 each, on the upper gingiva, the tongue, and the tonsil.

The most common sites are the inner aspects of the cheek along the bite line and the gingiva. Verrucous carcinoma slowly extends into locally contiguous sites. It may expand into the mandible or to the cheek from the inner buccal surface.  It may be evident as a verrucous mass on the tongue.[33]

Concurrent infection is common, and the resultant enlarged and tender lymph nodes may be mistaken for malignant involvement of the regional lymph nodes. Concurrent infection can create the impression that the tumor is indurated rather than soft. Despite advancement near the lymph nodes, verrucous carcinoma invariably grows around them rather than metastasizing to them.

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Causes

The leading possible causes are infection with human papillomavirus (HPV) and tobacco use, especially for the Ackerman tumor. Perhaps, chemical and HPV viral co-carcinogens work together. Other factors may be important as well.

In 1967, Barnett and Hyman[34] first linked oral florid papillomatosis to HPV on the basis of ultrastructural findings. A number of HPV types are associated with squamous cell carcinoma, including HPV types 6 and 11. Oral verrucous carcinomas may be associated with or caused by HPVs, particularly in individuals who are predisposed. In one study, HPV types 6 and 11 were detected in 7 of 17 cases of oral verrucous carcinoma.[35] In an analysis of laryngeal verrucous carcinoma, HPV-16 DNA, HPV-18 DNA, or both were present in 13 of 29 cases.[24]

HPV may facilitate the development of verrucous carcinoma because of oncogenic expression.[36] The E6 oncoprotein encoded by HPV types 16 and 18 promotes the degradation of p53.[37] In addition, alterations of the amino acids in the HPV-6 E7 protein may result in HPV-16 oncoproteinlike transforming activity.[38]

Tobacco chewing may be an etiologic factor. The possibility of chemical carcinogenesis of verrucous carcinoma of the oral cavity from tobacco has long been suggested. Research has indicated that the use of chewing tobacco and snuff is strongly correlated with oral florid papillomatosis in many, but not all, patients. Why verrucous carcinomas develop in some patients and ordinary squamous cell carcinomas develop in other patients is unclear. Perhaps, some patients with oral verrucous carcinoma die from a highly aggressive second primary oral cancer due to the same carcinogenic stimuli rather than a transformation of the verrucous carcinoma.

In a study of 37 patients, 11 chewed tobacco and another 11 smoked tobacco.[25] Among Swedish men who had oral cancer and who used snuff, almost one half had verrucous carcinoma.[39] Betel nuts may be linked to verrucous carcinoma,[40] although the association may be due to the tobacco added to betel chew.

Other factors may contribute to the development of verrucous carcinoma. Chronic inflammatory processes may be involved, possibly by lowering the body's mutagenic resistance.[1] An important issue is whether the development of oral verrucous carcinomas is related to the patient's immune status. Another risk factor is chronic inflammation or irritation such as that caused by poorly fitted dentures.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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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