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RESEARCH PRODUCT
HPV DNA in clinically different variants of oral leukoplakia and lichen planus
Chiara Di LibertoPietro AmmatunaGiuseppina CampisiMatteo D'angeloLucia GiovannelliAnna LamaPietro Aricosubject
AdultMalemedicine.medical_specialtyAlcohol DrinkingGenotypePolymerase Chain Reactionhpv leuokoplakia oral lichen planuslaw.inventionSex Factorsstomatognathic systemlawGenotypeHumansMedicineOral mucosaPapillomaviridaeGeneral DentistryPolymerase chain reactionAgedLeukoplakiaAged 80 and overbusiness.industryPapillomavirus InfectionsSmokingAge FactorsMouth MucosaHPV infectionSequence Analysis DNAOdds ratioMiddle Agedmedicine.diseaseDermatologystomatognathic diseasesmedicine.anatomical_structureOtorhinolaryngologyDNA ViralFemaleSurgeryOral lichen planusLeukoplakia OralOral SurgerybusinessNested polymerase chain reactionLichen Planus Oraldescription
Abstract Objectives Our objectives were to determine the prevalence of human papillomavirus (HPV) infection in oral leukoplakia (OL) and oral lichen planus (OLP) in comparison with that in healthy oral mucosa, also conditionally to age, gender, smoking, and drinking habits of patients, so as to investigate any possible association of HPV infection with a specific clinical variant of OL or OLP. Study design We did research on HPV DNA in 68 cases of OL (homogeneous form [H] in 45 cases and nonhomogeneous form [non-H] in 23 cases), and in 71 cases of OLP (nonatrophic/erosive form [non-AE] in 27 cases, atrophic/erosive form [AE] in 44 cases). HPV DNA was investigated in exfoliated oral mucosa cells by nested PCR ( n PCR: MY09-MY11/GP5-GP6) and the HPV genotype determined by direct DNA sequencing. Results HPV DNA was found in 17.6% of OL, in 19.7% of OLP, and in 5.6% of controls, with a statistically significant higher risk of HPV infection in both lesion groups (for OL: P = .01; Odds Ratio [OR] = 3.64; 95% CI: 1.21-10.80; for OLP: P = .005; OR = 4.17; 95% CI: 1.41-12.18). Demographic variables analysis showed that the only significant association was between HPV status and current smoking in OL patients (OR' = 3.40; 95% CI: 1.0-11.59). HPV DNA was found in 20% of H OL and 13% of non-H OL, without any association with the clinical variant ( P = .73; OR = 0.60; 95% CI: 0.14-2.48). HPV DNA was found in 18.5% of non-AE OLP and 20.4% of AE OLP, without any significant association with the clinical variant ( P = .84; OR = 1.13; 95% CI: 0.335-3.816). HPV-18 was the most frequently detected genotype (9/12 and 10/14 of HPV-positive OL and OLP, respectively), followed by HPV-16 (2/12 OL and 2/14 OLP), HPV-33 (1/12 OL), HPV-31 (1/14 OLP), and HPV-6 (1/14 OLP). Conclusions An increased risk of HPV infection was found in OL and OLP; however, no specific clinical variant of OL or OLP was noted to be associated with HPV infection. It is not possible to predict the likelihood of HPV infection from the clinical features of OL and OLP.
year | journal | country | edition | language |
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2004-12-08 | Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology |