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