Oral cancer remains a significant public health concern globally, with smoking identified as a primary risk factor. This abstract reviews the role of smoking in the etiology of oral cancer, emphasizing its contribution to carcinogenesis through the induction of genetic mutations, oxidative stress, and inflammation. Tobacco smoke contains carcinogenic compounds such as polycyclic aromatic hydrocarbons, nitrosamines, and heavy metals, which are implicated in the transformation of oral mucosal cells. Epidemiological studies consistently demonstrate a dose-response relationship between smoking intensity and oral cancer risk. Despite advances in prevention and treatment, smoking cessation remains a critical component in reducing oral cancer incidence. This review underscores the importance of public health initiatives and targeted interventions aimed at mitigating smoking-related oral cancer risk.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11888633 | PMC |
| http://dx.doi.org/10.4103/jpbs.jpbs_1305_24 | DOI Listing |
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