Multifactorial Pathogenesis of External Auditory Canal Cholesteatoma: A Literature Review on Epithelial Abnormalities and Infectious Factors

Abstract. External auditory canal cholesteatoma (EACC) is an uncommon but locally destructive disorder characterized by keratin accumulation and progressive erosion of the external auditory canal. Its pathogenesis remains incompletely understood, particularly regarding the interactions between epithelial abnormalities, infectious factors, and bone destruction. This structured narrative literature review synthesized evidence concerning epithelial migration, barrier dysfunction, microtrauma, anatomical and vascular susceptibility, microbial dysbiosis, and inflammatory pathways. Relevant publications from January 2016 to August 2026 were identified through targeted searches of PubMed/MEDLINE-indexed literature, publisher databases, and reference-list screening. Sources were selected according to their etiological and mechanistic relevance, prioritizing EACC-specific clinical studies, molecular investigations, systematic reviews, and meta-analyses. Evidence from middle ear cholesteatoma was considered indirect. Because a complete screening record and definitive number of included publications were not documented, the review cannot claim exhaustive or systematically reproducible coverage. The synthesis indicates that focal epithelial injury, impaired keratin clearance, anatomical obstruction, and microvascular vulnerability may contribute to disease initiation. Increased S100A8/S100A9 expression is associated with inflammatory and angiogenic pathways, while metagenomic findings identify microbial communities enriched in Staphylococcus and Corynebacterium. Infectious factors appear more likely to amplify persistent inflammation than represent universal initiating causes. Overall, EACC is conceptualized as a potentially self-perpetuating cycle involving epithelial injury, keratin retention, dysbiosis, inflammation, and bone erosion. Longitudinal studies are required to establish causal relationships and validate this proposed mechanism.