title: The prevalence of human papillomavirus in oral premalignant lesions and squamous cell carcinoma in comparison to cervical lesions used as a positive control.
abstract: BACKGROUND
  Previous reports concerning the prevalence of human papillomavirus (HPV) in oral squamous cell carcinoma (OSCC) have observed varied results. The aim of this study was to evaluate the prevalence of HPV in oral premalignant lesions (OPL) and OSCC. For accurate HPV detection in oral lesions, comparative analysis was performed on cervical lesions as positive controls.
  
  
  METHODS
  Fifty-seven cases with OPL and 50 with OSCC were selected. Twenty-nine control cases were selected from cervical lesions. The HPV infection rate was analysed by consensus polymerase chain reaction (PCR) using the My09/My11 and Gp5+/Gp6+ primers, and genotyping detection was employed using a PCR-based micro-array. Immunohistochemical staining for p16(INK4a) was performed.
  
  
  RESULTS
  Twenty-eight (96.6%) cases of cervical lesions were positive for HPV by consensus PCR and 24 cases (82.8%) were positive by genotyping. The total HPV-positive rate in cervical lesions was 96.6%. HPV-DNA was detected in nine cases (15.8%) of OPL and six cases (12.0%) of OSCC by consensus PCR. Six cases (10.5%) of OPL and three cases (6.0%) of OSCC were positive by genotyping. The total HPV-positive rate in oral lesions was 22.4% (26.3% of OPL and 18.0% of OSCC). In cervical lesions, immunohistochemistry of p16(INK4a) identified 27 cases (93.1%) as positive. Fifteen cases (26.3%) of OPL and eight cases (16.0%) of OSCC were positive for p16(INK4a).
  
  
  CONCLUSIONS
  The HPV infection and p16(INK4a)-positive rates in oral lesions are lower than previously reported. This suggests that HPV may not play a major role in oral lesions although its involvement cannot completely be ruled out.
authors.affiliation: Department of Oral Pathology, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita, Osaka 565-0871, Japan.
authors.forename: Miki
authors.initials: M
authors.lastname: Ishibashi
authors.forename: Mitsunobu
authors.initials: M
authors.lastname: Kishino
authors.forename: Sunao
authors.initials: S
authors.lastname: Sato
authors.forename: Eiichi
authors.initials: E
authors.lastname: Morii
authors.forename: Yuzo
authors.initials: Y
authors.lastname: Ogawa
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Aozasa
authors.forename: Mikihiko
authors.initials: M
authors.lastname: Kogo
authors.forename: Satoru
authors.initials: S
authors.lastname: Toyosawa
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002294:Carcinoma, Squamous Cell / Q000473:pathology / Q000821:virology*; D002648:Child; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000032:analysis; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000473:pathology / Q000821:virology*; D009367:Neoplasm Staging; D027383:Papillomaviridae / Q000302:isolation & purification* / Q000472:pathogenicity; D030361:Papillomavirus Infections / Q000473:pathology / Q000821:virology*; D011230:Precancerous Conditions / Q000821:virology; D002583:Uterine Cervical Neoplasms / Q000473:pathology / Q000821:virology
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16; D004279:DNA, Viral