The Incidence Of Oral Cancer Worldwide Biology Essay

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Tobacco is derived from the preparation of the leaves of the Nicotiana plant. As the plant name suggests, a composite of tobacco is nicotine. It is the nicotine that makes tobacco addictive and it acts by activating nicotinic acetylcholine receptors in the body, causing vasoconstriction, increased heart rate and alertness.(3). As blood nicotine levels fall, the detection by the brain causes a craving for more.

Tobacco is probably the most evident cause for oral cancer; about a quarter of all oral cancer cases are linked directly to cigarette smoking.(11). A pooled analysis of data from 15 case-control studies of head and neck cancer and cigarette smoking among never drinkers revealed that among never drinkers, smoking was associated with increased risk of oral cancer and there was a lucid dose-response relationships for the frequency, duration and number of cigarettes smoked. (11). The table below displays some of the results from this study; it shows that tobacco smoking was positively related to increased chance of oral cancer, amongst never drinkers. Having ever smoked a cigarette increased the odds ratio of getting head and neck cancer to 2.13 from 1. Odds ratio also increases with the number of cigarettes smoked and the duration that they are smoked for, thus supporting the dose-response relationship.

A Northern Italy study revealed that the single most potent factor for the cause of oral cancer was tobacco smoking. It accounted for 76% - 81% of all oral cancers. (5 pdf)

It is clearly evident that tobacco is a high risk factor of oral cancer

Table 3. Cigarette smoking among never drinkers and the risk of head and neck cancer*


 Never drinkers      

 Smoking variable      

 Case subjects      

 Control subjects      

 OR (95% CI)      

 Cigarette smoking      







 1.00 (referent)      




 2.13 (1.52 to 2.98)      

 Frequency, cigarettes/day      




     Never smokers      



 1.00 (referent)      




 1.82 (1.28 to 2.59)      




 2.36 (1.60 to 3.47)      




 3.58 (2.09 to 6.16)      




 4.46 (2.54 to 7.83)      

 Duration, y      




     Never smokers      



 1.00 (referent)      




 1.45 (1.04 to 2.03)      




 1.10 (0.75 to 1.61)      




 1.79 (1.20 to 2.67)      




 3.61 (2.26 to 5.75)      




 4.83 (3.18 to 7.33)    


Alcohol intake is also another factor that can cause oral cancer; such occurrence is dose- dependent. Many studies have shown that regular alcohol consumption increases the chances of oral cavity, pharynx and larynx cancers. (A Znaor, P Brennan and V Gajalakshmi et al., Independent and combined effects of tobacco smoking, chewing and alcohol drinking on the risk of oral, pharyngeal and esophageal cancers in Indian men, Int J Cancer 105 (2003), pp. 681-686_). For those who drink daily about 50g of alcohol increase their chance of these cancers by two to three fold compared to non-drinkers. (77). The recommended weekly limit is 168g. ( Oral cancer risks are greatly increased with combined effects of alcohol and other factors, such as tobacco and betel quid chewing. (18).

Alcohol dehydrogenase oxidises ethanol to acetylaldehyde, and aldehyde dehydrogenase detoxifies it to acetate. Acetaldehyde is the causative factor of the carcinogen effect of ethanol, due to its multiple mutagenic effects on DNA. In Asian populations, the variant allele ADH2, is more prevalent, deriving an inactive subunit in the aldehyde deyhdrogenase enzyme. The acetylaldeyde therefore remains in the oral mucosa with possibly causing an alteration in DNA. Apart from ethanol, other constituents of alcohol such as nitrosamines, acrylamide and polyphenols can also be classified as carcinogenic. Evidence for this is based on animal experiements. (80).

In the pooled analysis discussed before (11), data was also collected on drinkers whom are non-smokers, to investigate the relationship between alcohol consumption and head and neck cancers. The results didn't show a significant relationship between ever and never drinking and risk of cancer, ( OR for never drinking was 1.00 and for ever drinking was 1.18). However, there was a increased risk with the volume of alcohol consumed. Those who drink over five glasses a day had a much higher odds ratio of 2.81. (11)


Thirty to 40 percent of cancers worldwide are related to unhealthy diets, lack of physical activity and obesity. Incidence of oral cancer is also affected by the diet, with deficiencies in fruit, carotenoid foods and non-starchy vegetables. 10-15% of cases is accountable to low vegetable and fruit consumption. (86)

Vitamins A,C and E and caroteniods, flavenoids and folates (antioxidant and anti-carcinogenic foods) may play a vital role in counteracting the effects of tobacco intake, alcohol drinking and betel quid chewing.

A meta-analysis study has been conducted for fruit and vegetable consumption. From a possible of 71 potential studies, only 16 met the inclusion criteria, and so only these were included in the study. The data was accumulated from studies worldwide; though most were European, East Asia and America was also represented. A benefit of the study was that the age range was from 18 to 91, so many generations have been investigated into. The results were expressed in Odds ratio, with less than 1 being protective against oral cancer. The results were very supportive, backing the idea that both fruit and vegetables reduce risk of oral cancer. For example in Pakistan, the results showed that having 1 serving of fruit per week gave the Odds ratio as 0.34, whereas having 5 to 7 servings a week reduced the ratio even more to 0.09. Vegetable trends were similar as were the results for the other countries. (table 1)

Citrus fruits showed to be quite protective with an OR of 0.38. Studies with only women showed that fruit intake was very protective giving an Odds ratio of only 0.08. However, only two studies were included for women only, so this result may not be very reliable. In studies including both sexes, both fruit and vegetables reduced the OR to 0.53 and 0.51 respectively. That is about a 50% reduction in risk which is very significant. The main limitation of the meta-analysis was that not all the studies were adjusted for the same variables; though all were adjusted for age and sex, not all were adjusted for race, tobacco use and alcohol consumption. Thus these factors which could affect the outcome of the effect of fruit and vegetables on the risk of oral cancer were not taken into account at all times and so would affect the accuracy of the results. Nevertheless, the overall results do support the reduction in risk of oral cancer. (table 3)

Many studies provide convincing evidence of a rich diet in fruit and vegetables to be protective against oral cancer but it is likely that such activity may be overestimated. A study by ...... shows that heavy drinkers and smokers are least likely to consume fruit and vegetables, and so giving rise to suspicions that the relationship between low fruit and vegetables intake and increased cancer risk are bogus and it is all due to exposure to carcinogens simultaneously. [96]

Betel Quid

Betel Quid is used all around the world. Though it is commonly used in Asian countries such as Pakistan, India, Bangladesh, Nepal and China, its use is now also becoming more prevalent in migrant populated countries, such as North America, UK and Australia.

A recent study in ..... showed that betel quid acts on muscarinic M4 receptors, inducing cell migration and activation of Extracellular Signal-regulated Kinases (ERK 1/2). The receptors are directly involved in BQ-induced oral cancer cell migration. A recent case control study carried out in Sri Lanka looked into the causes of Oral Potentially Malignant Disorders (OPMDs); betel quid chewing is associated with this. (4). The study was conducted in two phases : firstly a cross-sectional community survey was carried out, involving house-to-house screening in Sabaragamuwa province and secondly, the subjects identified with OPMD were grouped into those with: leukoplakia, erthroplakia and lichen planus and those free of OPMD or with other oral abnormalities were kept as controls. Of the sampled province, 1029 subjects were chosen by a multistage, stratified, clustered sampling technique. Below is the table of results with regards to betel quid chewing and its risk on OPMD.

The results clearly express a dose- response relationship with regards to the frequency of chewing and risk of oral disease. Those most at risk are people whom began chewing before 18 years of age. Chewing more than 10 a day, (which includes 27% of the sample) increases the OR to 75.5, a very worrying and significant figure. What seems to be more perturbing is that 70% of the sample chewed 6 or more betel quid a day. Those who chewed for more than 20 years had a higher OR of 18.6 than if the chewed from 10 to 20 years (OR is 8.2). Clearly tobacco also has a great impact on the risk of disease, those chewing with tobacco have a 14.9 OR compared to only 5.5 for those without tobacco. Unfortunately, 81% of the sample was chewing with tobacco.

In this population, the prevalence of OPMD was 11.3%, higher than in previous studies for Sri Lanka. This could be because there could have been a more elderly population in this study, and as the results suggest, those chewing for more than 20 years have a higher risk. It could also be that the sample is not representative of the whole country, as the population is 21,324,791, much bigger than the sample

Human papillomavirus (HPV)

HPV is one of the commonest groups of virus to affect the skin and mucosal areas of the body; over eighty types have been discovered. Epithelial and mucosal areas such as the skin, mouth, throat, tongue vagina, penis and anus can be infected by it. Infection is caused when such areas come in contact with the virus.

A study by Dr. No-Hee Park revealed that at cellular level, the mouth was structurally similar to the vagina. Both organs have the same type of epithelial cells, which are targeted by HPV 16 and HPV 18. Smoking and drinking help to promote the invasion of the virus.