title: Human papillomavirus as a risk factor in oral carcinogenesis: a study using in situ hybridization with signal amplification.
abstract: BACKGROUND
  It is still controversial whether human papillomavirus (HPV) can be considered a risk factor in oral carcinogenesis. The aim of this study was to detect HPV DNA in 50 cases diagnosed as oral leukoplakias, with different degrees of epithelial dysplasia, and as oral squamous cell carcinomas, using in situ hybridization with signal amplification (CSA-ISH).
  
  
  METHODS
  HPV DNA was assessed in paraffin sections using CSA-ISH with a wide-spectrum biotinylated DNA probe. In HPV-positive cases, genotyping with specific probes to HPV types 6/11, 16/18 and 31/33 was performed.
  
  
  RESULTS
  The overall prevalence of HPV infection was 24%, markedly higher than that found in the control group. Results showed a discrete proportional relationship in the indices found in leukoplakia with no dysplasia, leukoplakia with dysplasia, and squamous cell carcinoma, but this was not statistically significant. When separating the group of leukoplakia by degrees of dysplasia, this relation of proportion was not observed. In genotyping, HPV types 16/18 were the most prevalent, and types 6/11 were only found in groups of mild or no dysplasia.
  
  
  CONCLUSIONS
  The results suggest that HPV is not likely to play a role in the progression of malignant transformation in oral lesions. Nevertheless, the increased prevalence of HPV infection compared to normal oral mucosa and the fact that high-risk HPV types were the most frequently identified do not allow the exclusion of HPV as a risk factor in oral carcinogenesis.
authors.affiliation: Oral Pathology Department, School of Dentistry, University of São Paulo, São Paulo, Brazil. acay@usp.br
authors.forename: R
authors.initials: R
authors.lastname: Acay
authors.forename: N
authors.initials: N
authors.lastname: Rezende
authors.forename: A
authors.initials: A
authors.lastname: Fontes
authors.forename: A
authors.initials: A
authors.lastname: Aburad
authors.forename: F
authors.initials: F
authors.lastname: Nunes
authors.forename: S
authors.initials: S
authors.lastname: Sousa
mesh_terms: D052685:Alphapapillomavirus / Q000235:genetics / Q000302:isolation & purification*; D002294:Carcinoma, Squamous Cell / Q000473:pathology / Q000821:virology; D015344:DNA Probes, HPV; D004279:DNA, Viral / Q000235:genetics; D004848:Epithelium / Q000473:pathology / Q000821:virology; D005838:Genotype; D052140:Human papillomavirus 11 / Q000235:genetics / Q000302:isolation & purification; D052162:Human papillomavirus 16 / Q000235:genetics / Q000302:isolation & purification; D052161:Human papillomavirus 18 / Q000235:genetics / Q000302:isolation & purification; D052163:Human papillomavirus 6 / Q000235:genetics / Q000302:isolation & purification; D006801:Humans; D017403:In Situ Hybridization; D007972:Leukoplakia, Oral / Q000473:pathology / Q000821:virology; D009061:Mouth Mucosa / Q000473:pathology / Q000821:virology; D009062:Mouth Neoplasms / Q000473:pathology / Q000821:virology*; D030361:Papillomavirus Infections / Q000473:pathology / Q000821:virology*; D011230:Precancerous Conditions / Q000473:pathology / Q000821:virology; D012307:Risk Factors
chemical_list: D015344:DNA Probes, HPV; D004279:DNA, Viral