Etiology

Precursor lesions are strongly associated with tobacco smoking and alcohol abuse, and especially a combination of these two {221,566,766,1607,1608, 1800,2564}. The risk of developing these lesions increases with duration of smoking, the type of tobacco and the practice of deep inhalation.

Additional etiological factors are: indus-

trial pollution, specific occupational exposures, nutritional deficiency, and hormonal disturbance {766,1253,1255, 1256,1608,1982}.

The role of human papillomavirus (HPV) infection in laryngeal carcinogenesis remains unsolved {2412}. The prevalence of HPV in laryngeal carcinoma varies significantly among various studies, ranging from 0% to 54.1% {2517}. Although the overall prevalence of HPV infection found in 9 studies of precursor lesions {97,276,793,853,927,928,1522, 2065,2172} was 12.4%, HPV DNA was detected in a clinically and histologically normal larynx in 12-25% of individuals {1912,2172}. Thus, definite evidence of an etiologic role of HPV in precursor lesions, at least at present, is lacking, and HPV infection in precursor lesions may represent an incidental HPV colonization rather than true infection of the laryngeal mucosa.

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