Abstract
Objectives:A synergistic effect between smoking and alcohol intake is the major cause of premalignant and malignant lesions of the larynx, but the risk factors and pathogenesis of the neoplastic transformation in non‐smokers remain poorly‐defined. The aim of this retrospective study is to establish the relationship between smoking habits and HPV infection in laryngeal dysplasia.Methods:HPV DNA was amplified from 30 paraffin‐embedded laryngeal dysplasia tissue specimens by the polymerase chain reaction (PCR) using 2 groups of different consensus primers (MYO9/MY11 AND LCRF1, LCRF2, LCRF3, LCRF4, E7R1, E7R2, E7R3, E7R4). 15 samples were taken from smokers and 15 from non‐smokers. To select these tissue samples, we reviewed the medical charts of 164 patients who underwent suspension microlaryngoscopy between 1992 and 2012.Results:The present investigation failed to demonstrate HPV genome in all samples of laryngeal precancerous lesions, whereas HPV was detected in 4 laryngeal papilloma samples used as control to confirm the reliability of our method on paraffin‐embedded samples.Conclusions:The absence of viral genomes in laryngeal dysplasia specimens of smokers as well as non‐smokers suggests that other factors play a more important role than HPV infection in the carcinogenesis of these lesions.
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