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The major predisposing factors of developing oral cancer include smoking, alcohol drinking, and betel quid chewing. Betel quid chewing could cause the abrasion and damage of oral mucosa by crude fibers, chemical insults by additive slaked lime, and arecoline from areca nut. These would lead to the local consequence of oral submucosal fibrosis, which is regarded clinically as a precancer lesion and a major cause of trismus. In addition, the components and additives in betel quid contain chemical toxins and carcinogens, which would further affect the oral mucosa and gradually develop a malignancy. Following literature review, aside from having a greater total tumor burden and more local diseases in the oral cavity and digestive tract, patients with betel quid-related oral cancer also have more systemic diseases from metabolic syndrome, hypertension, cardiovascular disease, type II diabetes mellitus, and obesity than those without this habit. In conclusion, those patients who have the history of smoking, alcohol drinking, and betel quid chewing would present much more unique clinical characteristics than those who only have a history of smoking and alcohol drinking. More attention should therefore be paid to pretreatment evaluation, treatment strategy, and posttreatment follow-up among betel quid chewers. [ABSTRACT FROM AUTHOR]

Background: This retrospective cohort study was to assess the prognostic value of preoperative albumin-to-alkaline phosphatase ratio (AAPR) on survival outcome for patients with locally advanced oral squamous cell carcinoma (LAOSCC). Methods: A total of 250 patients with LAOSCC receiving upfront radical surgery at a single institute from January 2008 to December 2017 were enrolled. The primary endpoint was the survival predictability of preoperative AAPR on the 5-year overall survival (OS), cancer-specific survival (CSS), and disease-free survival (DFS). Cox proportional hazards model was used for survival analysis. The X-tile software was used to estimate the optimal cut-off value of preoperative AAPR on survival prediction. A predictive nomogram incorporating the clinicopathological factors on OS was further generated. Results: The 5-year OS, CSS, and DFS rates were 68.6%, 79.7%, and 61.7%, respectively. The optimal cut-off of preoperative AAPR to predict the 5-year OS was observed to be 0.51. For those with preoperative AAPR≧0.51, the 5-year OS, CSS, and DFS were statistically significantly superior to those with preoperative AAPR<0.51 (OS: 76.1% vs 48.5%, P <.001; CSS: 84.3% vs 66.4%, P =.005; DFS: 68.9% vs 42.6%, P <.001). In Cox model, we observed that preoperative AAPR<0.51 was a significantly negative prognosticator of OS (HR: 2.22, 95% CI: 1.466-3.361, P <.001), CSS (HR: 2.037, 95% CI: 1.16-3.578, P =.013), and DFS (HR: 1.756, 95% CI: 1.075-2.868, P =.025). After adding the variable of preoperative AAPR, the c-index of the predictive nomogram incorporating assorted clinicopathological factors increases from 0.663 to 0.692 for OS. Conclusion: Our results suggest that preoperative AAPR serves as an independent survival predictor for patients with LAOSCC. The nomogram incorporating preoperative AAPR and various clinicopathological features may be a convenient tool to estimate the mortality risk for patients with LAOSCC. [ABSTRACT FROM AUTHOR]