IADR Abstract Archives
Assessment of human papilloma virus involvement in OSCC in Tunisia: a case control study
Objectives: To examine the association between human papilloma virus (HPV) especially high risk (HR) types with oral squamous cell carcinoma (OSCC) in Tunisia.
Methods: Formalin-fixed, paraffin-embedded cancer tissues of 83 OSCC patients were collected from pathology archive. 83 non-cancer controls’ tissues were obtained by incisional biopsies from consenting individuals. All samples were subject to histopathological evaluation, DNA quality control, and HPVDNA detection by chromogenic in situ hybridization (CISH) and polymerase chain reaction (PCR). Samples containing HPV-DNA were further subject to genotyping and to p16 and p53 immunohistochemistry. Final estimates of HPV positivity were based on HPV-DNA detection by both CISH and PCR and tumor biomarkers results. All statistical analyses were performed using IBM-SPSS statistics V.21. P values ≤ 0.05 were considered statistically significant. The association between OSCC and HPV, smoking, alcohol, Neffa, poor oral health and potentially malignant lesions (PML) was established using Chi-square test. Logistic regression was used to calculate adjusted odds ratios (OR) for the influence of mentioned risk factors.
Results: HPV assessments based on positivity for HPV-DNA and for biomarkers were 8.4% and 0% for OSCC and normal oral mucosa respectively (p= 0.007). HPV 16/18 were the most encountered HR types. High-risk HPV infection was not significantly associated with oral cancer(p=0.16). Participants with HPV infection were more likely to have poor oral health (p=0.05). The adjusted ORs for smoking, Neffa, alcohol, poor oral health and PML were 1.4 (95% CI: 0.6-3.3); 30.6 (95% CI: 3.7 -256.3); 3.3 (95% CI: 0.8 -14.8); 1 (95% CI: 0.4 -2.4) and 5.3 (95% CI: 1.4 -19.4). Neffa and PML were considered independent risk factors.
Conclusions: Our results could not establish a potential involvement of HPV in oral cancerogenesis. HPV might be a bystander infection, taking advantage of a tumor that was caused by other means. Smokeless tobacco and PML had possible combined effects.
Methods: Formalin-fixed, paraffin-embedded cancer tissues of 83 OSCC patients were collected from pathology archive. 83 non-cancer controls’ tissues were obtained by incisional biopsies from consenting individuals. All samples were subject to histopathological evaluation, DNA quality control, and HPVDNA detection by chromogenic in situ hybridization (CISH) and polymerase chain reaction (PCR). Samples containing HPV-DNA were further subject to genotyping and to p16 and p53 immunohistochemistry. Final estimates of HPV positivity were based on HPV-DNA detection by both CISH and PCR and tumor biomarkers results. All statistical analyses were performed using IBM-SPSS statistics V.21. P values ≤ 0.05 were considered statistically significant. The association between OSCC and HPV, smoking, alcohol, Neffa, poor oral health and potentially malignant lesions (PML) was established using Chi-square test. Logistic regression was used to calculate adjusted odds ratios (OR) for the influence of mentioned risk factors.
Results: HPV assessments based on positivity for HPV-DNA and for biomarkers were 8.4% and 0% for OSCC and normal oral mucosa respectively (p= 0.007). HPV 16/18 were the most encountered HR types. High-risk HPV infection was not significantly associated with oral cancer(p=0.16). Participants with HPV infection were more likely to have poor oral health (p=0.05). The adjusted ORs for smoking, Neffa, alcohol, poor oral health and PML were 1.4 (95% CI: 0.6-3.3); 30.6 (95% CI: 3.7 -256.3); 3.3 (95% CI: 0.8 -14.8); 1 (95% CI: 0.4 -2.4) and 5.3 (95% CI: 1.4 -19.4). Neffa and PML were considered independent risk factors.
Conclusions: Our results could not establish a potential involvement of HPV in oral cancerogenesis. HPV might be a bystander infection, taking advantage of a tumor that was caused by other means. Smokeless tobacco and PML had possible combined effects.