Proliferative verrucous leukoplakia of the gingiva

Citation
A. Fettig et al., Proliferative verrucous leukoplakia of the gingiva, ORAL SURG O, 90(6), 2000, pp. 723-730
Citations number
10
Categorie Soggetti
Dentistry/Oral Surgery & Medicine
Journal title
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS
ISSN journal
10792104 → ACNP
Volume
90
Issue
6
Year of publication
2000
Pages
723 - 730
Database
ISI
SICI code
1079-2104(200012)90:6<723:PVLOTG>2.0.ZU;2-6
Abstract
Objective. The purpose of this study was to describe the clinical-pathologi c features of what appears to be a gingival form of proliferative verrucous leukoplakia. Study design. Ten adult patients with recurrent and histologically progress ive gingival leukoplakias who were diagnosed and treated at the University of California, San Francisco between 1994 and 1999, comprised the subject g roup for this investigation. Clinical and microscopic features were reviewe d. Proliferation indices and p53 expression were evaluated immunohistochemi cally and the presence of human papillomavirus (HPV) DNA was determined by using polymerase chain reaction (PCR) amplification. Results, Lesions presented as solitary or regional flat/papillary/verrucal leukoplakias of the free and attached gingiva (tooth-bearing areas only). W ith time, flat lesions developed a papillary or verruciform profile. Althou gh lesions were recurrent, they were confined to the gingiva, and multiple lesions did not develop. Half the patients used tobacco, and HPV could not be detected by using PCR. Microscopically 6 cases began as hyperkeratotic l esions, and 3 initially exhibited a psoriasiform pattern with a marked infl ammatory component. With recurrences, the lesions became progressively atyp ical histologically. The proliferation indices for these lesions showed mod est increases over normal epithelium, and positive p53 staining was evident in 4 of 10 cases, indicating a disruption of the keratinocyte cell cycle i n these lesions. The mechanism associated with the positive p53 staining (p rotein binding to wild type p53 versus mutation of the p53 gene) was not de termined. Lesions recurred after conservative scalpel or laser excision, an d many developed into verrucous or squamous cell carcinoma. Conclusions, Proliferative verrucous leukoplakia of the gingiva (PVLC) appe ars to be a subset of oral proliferative verrucous leukoplakia. It can be c haracterized as a solitary, recurring, progressive white patch that develop s a verruciform architecture and may not be associated with HPV. PVLC has a n unpredictable course and is at risk for development into verrucous or squ amous cell carcinoma. Currently there is no way to determine or predict whi ch gingival white lesions will follow the clinical course described for thi s group of patients with PVLG.