HUMAN PAPILLOMAVIRUS IN ORAL PREMALIGNANT LESIONS

Citation
H. Nielsen et al., HUMAN PAPILLOMAVIRUS IN ORAL PREMALIGNANT LESIONS, European journal of cancer. Part B, Oral oncology, 32B(4), 1996, pp. 264-270
Citations number
47
Categorie Soggetti
Oncology,"Dentistry,Oral Surgery & Medicine
ISSN journal
09641955
Volume
32B
Issue
4
Year of publication
1996
Pages
264 - 270
Database
ISI
SICI code
0964-1955(1996)32B:4<264:HPIOPL>2.0.ZU;2-W
Abstract
The aetiology of oral premalignant lesions is generally accepted to be multifactorial. Tobacco and alcohol are established as important cofa ctors in malignant development in the oral cavity, but in addition mic roorganisms, such as human papillomavirus (HPV), have gained much inte rest over the past decade. For many years, HPV has been accepted as an important cofactor in the development of cervical cancer, originating from a mucous membrane with similarities to the oral mucosa. 49 patie nts with oral prernalignant lesions and 20 control patients with norma l oral mucosa and no history of HPV infection were examined for the pr esence of HPV by immune histochemical staining using the peroxidase an ti-peroxidase technique (PAP), DNA-DNA in situ hybridisation (ISH), an d polymerase chain reaction (PCR) analysed by Southern blot hybridisat ion with an HPV 16 specific probe. The investigations revealed that HP V was found in 62.5% of the verrucous leucoplakias, 50.0% of the eryth roplakias, 45.5% of the homogeneous leucoplakias, 33.3% of erythroleuc oplakias and in 12.5% of the nodular leucoplakias. An overall HPV dete ction rate in the examined premalignant lesions was 40.8% and no patie nts in the control sample were positive. Concerning oral cancer develo pment, it seems likely that HPV may be a cofactor, as 100% of patients who developed oral cancers within 4-12 years were all positive for HP V, one being positive for HPV 16. Copyright (C) 1996 Elsevier Science Ltd