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Chronic Periodontitis–Human Papillomavirus Synergy in Base of Tongue Cancers
Mine Tezal, DDS, PhD;
Maureen Sullivan Nasca, DDS;
Daniel L. Stoler, PhD;
Thomas Melendy, PhD;
Andrew Hyland, PhD;
Philip J. Smaldino, BS;
Nestor R. Rigual, MD;
Thom R. Loree, MD
Arch Otolaryngol Head Neck Surg. 2009;135(4):391-396.
Objective To assess whether chronic periodontitis history predicts human papillomavirus (HPV) status in patients with base of tongue cancers.
Design Case-control study using existing patient data.
Setting Roswell Park Cancer Institute.
Patients Thirty patients newly diagnosed with base of tongue squamous cell carcinoma between 1999 and 2005 for whom both tumor samples and periodontal records were available. Patients younger than 21 years, edentulous, immunocompromised, and those with a history of cancer were excluded. Periodontitis history was assessed on the basis of alveolar bone loss (in millimeters) from panoramic radiographs by one examiner who was blinded to cancer status.
Main Outcome Measure HPV-16 and HPV-18 DNA were identified on paraffin-embedded tumor samples by polymerase chain reaction. Multiple logistic regression was used to estimate odds ratios and 95% confidence intervals.
Results The prevalence of tumors positive for HPV-16 DNA was 21 of 30 (70%). None of the samples were positive for HPV-18 DNA. Compared with participants with HPV-negative tumors, patients with HPV-positive tumors had significantly higher mean alveolar bone loss (3.90 mm vs 2.85 mm, P = .01). After adjustment for age at diagnosis, sex, race/ethnicity, alcohol use, smoking status, and number of missing teeth, every millimeter of alveolar bone loss was associated with an approximately 4-fold (odds ratio, 3.96; 95% confidence interval, 1.18-13.36) increased risk of HPV-positive tumor status. Number of missing teeth was not associated with tumor HPV status (odds ratio, 0.95; 95% confidence interval, 0.74-1.21).
Conclusions Chronic periodontitis may be a significant factor in the natural history of HPV infection in patients with base of tongue cancers. Additional confirmation in larger studies is required.
Author Affiliations: Departments of Oral Diagnostic Sciences (Dr Tezal), Oral Biology (Dr Tezal), Restorative Dentistry (Dr Sullivan Nasca), Social and Preventive Medicine (Drs Tezal and Hyland), Microbiology and Immunology (Dr Melendy), and Surgery (Dr Loree), State University of New York at Buffalo; and Departments of Dentistry and Maxillofacial Prosthetics (Drs Tezal and Sullivan Nasca), Head and Neck Surgery (Drs Stoler, Rigual, and Loree), Cancer Pathology and Prevention (Dr Stoler and Mr Smaldino), and Cancer Prevention and Population Sciences (Dr Hyland), Roswell Park Cancer Institute, Buffalo, New York.
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