Objectives Human papillomavirus (HPV) infects basal cells of the stratified squamous epithelium through micro epithelial trauma. However, laryngeal papillomatosis commonly appears in any site on the laryngeal mucosa not covered by stratified squamous epithelium. The purpose of this study is to clarify pathological mechanisms of laryngeal papillomatosis based on the characteristics of the laryngeal epithelium. Study Design Morphological and immunohistochemical study. Methods Larynges from one newborn and two adults were used. Morphological differences in the laryngeal squamo‐ciliary junction (lSCJ) were compared to those in the cervical squamo‐columnar junction (cSCJ) in a resected cervix uterus. Morphological characteristics of laryngeal epithelial distribution were also compared between the newborn and adult larynges. Immunohistochemical evaluations were performed using p63 (an epithelial stem‐cell marker) and integrin‐α6 (a cellular HPV receptor). Results Morphological differences were noted between the lSCJ and the cSCJ. The lSCJ was present in the adult, but not the newborn supraglottis. Goblet cells in the pseudostratified ciliated columnar epithelium were also found in the adult but not the newborn larynx. In addition, basal cells of the stratified squamous epithelium as well as the pseudostratified ciliated columnar epithelium expressed p63 and integrin‐α6 in both newborn and adult larynges. Conclusions HPV can infect any immature laryngeal epithelium with or without the lSCJ. Squamous metaplasia of pseudostratified ciliated columnar epithelium with a latent HPV infection can also cause tumorigenesis. Level of Evidence N/A

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These results suggest that the local laryngeal immune response is activated by infection or carcinogenesis due to human papilloma virus. The findings strongly suggest that secretory IgA has inhibitory activity against infection or carcinogenesis associated with human papilloma virus in the larynx.

Human papilloma virus (HPV) types 6 and 11 are thought to infect the basal cells of the squamous epithelium. These infections cause laryngeal papillomatosis and condyloma acuminatum in the uterine cervix, which manifest the same pathological phenotype. The site of predilection is the junction of the stratified squamous epithelium and simple columnar epithelium (SCJ) , however, the morphological characteristics of the epithelial junction in the larynx differ from that in the uterine cervix. Therefore, these observations suggest that the developmental mechanism of underlying the onset of laryngeal papilloma differs from that of condyloma acuminatum. The newborn larynx, which is infected by HPV in case of juvenile-onset laryngeal papillomatosis, has no SCJ in the supraglottic regions. This suggests that HPV infects the laryngeal epithelium with or without SCJ. Moreover, the immaturity of the epithelia in the newborn larynx allows HPV to easily infect the tissue. In investigations of adult larynges, the basal cells of the squamous epithelium and stratified ciliated epithelium in the larynx express p63, an epithelial stem cell marker. Integrin-α6 is, the receptor for HPV, is positive in the stratified ciliated epithelium and lower half of the squamous epithelium. These findings indicate that HPV is able to infect the squamous epithelium and stratified ciliated epithelium and that both infection with HPV in epithelial stem cells and stratification of epithelial cell layer are necessary for the development of laryngeal papilloma.