ETIOLOGICAL ASPECTS AND EPIDEMIOLOGICAL PATTERNS OF KERATOACANTHOMA: NARRATIVE REVIEW

Keratoacanthoma (KA) is a rapidly developing keratinizing epithelial neoplasm whose classification remains controversial because of its close relationship to cutaneous squamous cell carcinoma (cSCC). Despite its frequent occurrence in dermatological practice, the epidemiology and pathogenesis of KA remain incompletely understood. This narrative review summarizes current evidence regarding the etiological factors and epidemiological characteristics of KA. Available data indicate marked geographic variation in incidence, largely reflecting differences in ultraviolet (UV) exposure, environmental conditions, and population skin phototypes. The tumor occurs predominantly in fair-skinned individuals and is most commonly diagnosed in older adults with a history of chronic sun exposure. Current evidence supports a multifactorial origin of KA. Ultraviolet radiation is considered the principal environmental risk factor and is associated with characteristic molecular alterations, including mutations in TP53 and HRAS. Additional contributors include human papillomavirus infection, particularly cutaneous betapapillomavirus types; immunological dysregulation related to immunosuppressive therapy and immune-modulating drugs; chronic inflammatory stimuli following trauma, surgical procedures, or tattooing; exposure to chemical carcinogens such as arsenic and tar-derived compounds; and inherited cancer-predisposition syndromes, including Muir–Torre and Ferguson–Smith syndromes. Increasing evidence suggests that interactions between genetic susceptibility, environmental exposures, and local immune responses play a central role in tumor development. In conclusion, keratoacanthoma represents a multifactorial neoplastic process arising from the combined effects of environmental, genetic, viral, and immunological factors. Further epidemiological and molecular studies are needed to clarify disease mechanisms and improve risk stratification.