The etiology of oral cancer is still unclear and is generally believed to be the result of a combination of factors. Notably, a large body of epidemiological evidence suggests that smoking, alcohol abuse, and betel nut chewing are the major risk factors for oral cancer, and that these factors can be avoided. Tobacco and oral cancer The health risks associated with tobacco use were well documented as early as the 1990s, when Professor Doll of Oxford’s 50-year prospective epidemiological study of 34,434 male physicians showed that mortality from 11 cancers among British male physicians was associated with smoking, including oral and oropharyngeal cancers. The incidence and location of oral cancer was directly related to the amount and mode of smoking, and the risk of oral cancer was positively correlated with smoking. Assuming that the risk of non-smokers is 1.00, the risk of oral cancer rises to 6.00 for those who smoke 10-19 cigarettes per day, 7.67 for those who smoke 20 or more cigarettes per day, and 12.4 for those who smoke 40 or more cigarettes per day. The amount and duration of smoking per day are risk factors for the development of oral cancer. In fact, people who have smoked for more than 20 years or smoked more than 20 cigarettes per day are at greater risk of developing head and neck tumors. Numerous studies have also shown that people who have quit smoking have a lower risk of developing oral cancer than current smokers, with the risk of developing the disease decreasing over time as they quit. Oral mucosal leukoplakia is an internationally recognized precancerous lesion, and oral mucosal leukoplakia is closely related to smoking, which is a direct causative factor of oral mucosal leukoplakia. The temperature of paper cigarette is about 200℃ when it is lit, and the burning temperature increases quickly to 500℃~700℃ when smoking, such high temperature can make the oral mucosa hyperkeratosis. Lips articulated tobacco can often see gray or gray-brown round or oval white plaques. Because tobacco contains phenols, aldehydes, organic acids and other substances, long-term smoking, the toxic substances in tobacco can stimulate the oral mucosa, from the clinical point of view, long-term smokers gums, cheek mucosa are reddened and with greenish purple, and white edema, which is the oral mucositis caused by smoking. In addition, the high temperature when smoking can cause burns on the contact part of the oral mucosa. Long-term stimulation of the oral mucosa by smoke can make the mucosal epithelium hyperkeratosis, this tobacco-induced abnormal mucosal hyperkeratosis, can contribute to the occurrence of oral mucosal white spots. The smoking-induced lesion of white mucosal keratinization and red palatal gland opening on the palate is known as nicotine palate. Most surveys show that there is a close relationship between smoking and leukoplakia: the incidence of leukoplakia is higher in smokers than in nonsmokers (23.93%: 0.21%); the incidence is significantly higher in those who have smoked for more than 20-30 years than in those whose smoking history is less than 20 years; if smoking is terminated, the leukoplakia of many patients can fade or improve on their own. Alcohol and oral cancer For a long time, alcohol has been considered as one of the risk factors leading to oral cancer. Epidemiological surveys show that alcohol can cause oral cancer and regular alcohol consumption can increase the risk of oral cancer, both of which are dose-dependent. The risk of oral cancer for those who drink alcohol 4-5 times a day is 2-3 times higher than that for non-drinkers, and 7%-19% of oral cancers are due to heavy drinking. The concept of one drink is 341ml of beer, 114ml of fruit wine or 43ml of spirits. Heavy drinking is defined as drinking more than the moderate drinking standard, such as: drinking more than three times a day, or drinking more than the standard amount of alcohol per time or per day, with at least 5 drinks per time and at least 1 time per week. The risk of oral cancer is higher for those who drink an average of ≥120 g/day, and the risk increases with the amount of alcohol consumed. The risk of oral, laryngeal, esophageal and hepatic cancers is increased in alcohol drinkers, and the incidence rate increases with the amount of alcohol consumed. For example, in Denmark, the incidence of oral cancer increases with the increase of alcohol consumption; in some Nordic countries, such as the United Kingdom, Finland and New Zealand, the incidence of oral cancer increases to a certain extent when the amount of smoking is maintained at a stable level or tends to decrease, but the amount of alcohol consumption increases. The risk of oral cancer increases with the frequency and duration of alcohol consumption. Abstinence from alcohol gradually decreases the risk, but the risk of oral cancer persists for several years after cessation of alcohol consumption. The risk of oral, esophageal, and laryngeal cancers is significantly lower in those who have abstained from alcohol for ≥10 years. Approximately 75% of oral cancer patients in the United States are due to alcohol and tobacco use, and mostly due to a synergistic effect of both. Almost all oral cancer patients drink alcohol, while non-oral cancer patients drink significantly less alcohol; almost all oral cancer patients who drink alcohol also smoke, while almost all smokers also drink alcohol. The risk of oral cancer among smokers increased with alcohol consumption, increasing to nearly 9-fold for those who drank ≥30 drinks/week after correcting for smoking, and to more than 4-fold for those who smoked 2 packs/day after correcting for alcohol consumption. The risk of oral cancer increased with alcohol consumption and smoking, and the risk of heavy alcohol consumption and heavy smoking was 37 times higher than that of non-drinkers and smokers, suggesting that alcohol may enhance the carcinogenic effect of tobacco. Alcohol consumption and smoking are closely related, and heavy drinkers are usually smokers, and heavy drinkers are often heavy smokers at the same time, and vice versa. Tobacco and alcohol are risk factors for oral cancer, and after strict control of exposure to one of them, a significant dose-related relationship can be observed between the other and the development of oral cancer, suggesting that each factor can induce cancer individually. However, smoking is not a necessary prerequisite for alcohol-induced cancer, and the risk of oral cancer in never-smokers or ex-smokers still increases with increasing alcohol consumption, suggesting that alcohol consumption alone can induce cancer and that alcohol can interact with other carcinogens to cause cancer in nonsmokers. However, the risk of alcohol consumption in combination with smoking is higher than the risk of each of these factors acting alone. Oral cancer is caused by the combination of many risk factors over a long period of time. In addition to smoking and alcohol consumption, diet and nutrition are also closely related to its development. Through a healthy lifestyle, such as avoiding the bad stimulation of smoking and alcohol, and maintaining adequate, reasonable and balanced nutrition, the occurrence of oral cancer can be effectively prevented. It is also recommended that regular oral examination should be conducted to detect oral cancer and precancerous lesions at an early stage and treat them in time to avoid or reduce disease troubles and improve life quality.