Abstract. Introduction. Inverted papilloma is the most common type of sinonasal papilloma. It refers to benign tumors, but its clinical course is often associated with post-surgical recurrences and malignancy. Although the morphological characteristics and clinical features of inverted papilloma are well known, its etiology and risk factors remain a matter of debate. Aim. The aim of the study was to analyze the contemporary literature and summarize the data available regarding the significance of viral infection, cell cycle regulator proteins, angiogenesis, chronic inflammation, environmental influences, and other factors for the risk of inverted papilloma. Materials and Methods. A search was made in databases, such as SCOPUS, PubMed, Google Scholar, and RSCI, using the following keywords: Sinonasal papilloma, inverted nasal papilloma, Schneiderian papilloma. Results and Discussion. Human papillomavirus is considered the main growth trigger of inverted papilloma. Potential role of human papillomavirus in initiating the tumor growth is related to the presence in its genome of genes encoding the E6 and E7 proteins. Certain cell cycle regulatory factors and angiogenic proteins contribute to the dysregulation of proliferation and apoptosis and facilitate cell migration and tumor invasion. However, despite the frequent detection of human papillomavirus DNA and associated transcription factors in inverted papilloma tissues, significance of the papillomavirus infection in the occurrence of inverted papilloma or its transformation into malignant forms has not been proven reliably yet. It should be noted that human papillomavirus stimulates not only apoptosis inhibition and the uncontrolled division of epithelial cells, but also angiogenesis, which is also a tumor growth trigger. Among other pathogenic factors, we also discussed the importance of chronic inflammation, smoking, occupational hazards, and industrial environmental pollution. Conclusions. Though etiology of sinonasal inverted papilloma remains controversial, the studies reviewed here indicate the importance of viral infection, cell cycle and angiogenic factors, environmental and occupational exposure, and chronic inflammation. Further studies on etiologic factors are required to ensure better clinical guidance and therapeutic targets.