Oral Cancer And Its Causes In Non-Tobacco Users

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Oral cancer presents a significant health concern worldwide, predominantly associated with tobacco usage.

However, a subset of cases arises in non-tobacco users, shedding light on diverse etiological factors contributing to its development. While tobacco and alcohol remain primary culprits, emerging evidence underscores the role of other factors, including viral infections, dental issues, and genetic predispositions.

Alcohol consumption, often intertwined with tobacco use, independently elevates the risk of oral cancer. Chronic and excessive alcohol intake can instigate carcinogenesis within the oral cavity, accentuating the vulnerability of non-tobacco users.

Human Papillomavirus (HPV), notably strains 16 and 18, has emerged as a significant etiological agent in oropharyngeal cancers. These viruses, conventionally linked with cervical cancer, exhibit a tropism for oral tissues, particularly the tonsils and base of the tongue, contributing to a subset of oral cancers.

Poor oral hygiene and dental health, typified by chronic periodontitis or ill-fitting dentures, constitute another risk factor. Persistent inflammation and trauma from dental issues can evolve into malignant lesions over time, highlighting the importance of oral care in cancer prevention.

Inherent conditions such as oral lichen planus pose additional risks for oral cancer development. The chronic inflammatory nature of lichen planus can predispose affected individuals to malignant transformation, underscoring the multifaceted nature of oral carcinogenesis.

Furthermore, certain habits like betel nut or areca nut chewing, devoid of tobacco, can lead to premalignant conditions in the oral cavity like Oral Sub Mucus Fibrosis, Leukoplakia and erythroplakia which can convert into oral cancer over the years. These habits, prevalent in specific cultural contexts, exemplify the diverse risk factors contributing to oral malignancies.

Genetic predispositions, including mutations or downregulation of tumor suppressor genes like P53, confer susceptibility to oral cancer. Syndromes such as Li-Fraumeni syndrome underscore the intricate interplay between genetic factors and cancer development, emphasising the necessity for comprehensive risk assessment.

While tobacco remains a predominant risk factor, understanding the myriad contributors to oral cancer in non-tobacco users is imperative for effective prevention and management strategies. Incorporating these diverse etiological factors into clinical practice enables targeted interventions and enhances outcomes in oral cancer care.

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