to increase with the duration of smoking, the quality of tobacco, the practice of deep inhalation and the inability to stop smoking, and inversely with the age of the patient at the start of smoking.

Additional aetiological factors are: industrial pollution, chronic infections, voice abuse, obstruction of the upper respiratory tract, vitamin deficiency, and hormonal disturbance [115, 181, 184, 185, 228, 276]. The role of HPV infection in laryngeal carcinogenesis remains un-clarified [331]. The prevalence of HPV infection in laryn-geal carcinomas varies significantly among various studies, ranging from 0 to 54.1% [346]. The overall prevalence of HPV infection in nine studies of SILs [16, 54, 118, 128, 136, 137, 219, 281, 302] was found to be 12.4%. However, HPV DNA was also detected in a clinically and histologically normal larynx in 12-25% of individuals [267, 302]. Definite evidence of an aetiologic role of HPV in SIL, at least at present, is lacking, and HPV infection in SILs may represent an incidental HPV colonisation rather than true infection of the laryngeal mucosa.

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