Oral Cancer Prevention And Control The Approach Essay
Oral Cancer Prevention And Control The Approach Essay
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The occurrence of oral cancer is one of the highest in the class of cancers in the world, especially among men in developing countries. Oral cancer is also another major world health problem causes by the use of tobacco. It is one of the most life threatening diseases caused by smoking. According to Regezi, Sciubba, & Jordan, (2016) 80 percent of oral cancer patients were tobacco smokers. World health organization reports have also concluded that tobacco smoking claims more lives that several other health hazards such as HIV/AIDS, homicides, car accidents, alcohol and other illegal drugs (Abro, & Pervez, 2017). This paper focuses on oral cancer caused as a result of smoking.
According to Morse, et al (2007) apart from causing oral cancer, smoking has been known to cause very many other cancers, dryness of the mouth, low birth weight and infant mortality, respiratory diseases such as asthma and bronchitis, discoloration of teeth and a precancerous condition oral epithelial dysplasia (OED) among other diseases. Oral Cancer Prevention And Control The Approach Essay. Overall, tobacco smoking has been said to cause about 4 million deaths and smoking populations reaching up to a billion people in the whole world. Worse still, the condition is expected to worsen in the near future. The effects of tobacco smoking has however affected even nonsmokers which has been concluded due to the presence of cotinine in their blood. However, the risk of oral cancer is not as high in non-smokers as compared to that of smokers.
According to Ram, et al (2011) oral cancer has been a known cause of death all over the world. This cancer largely affects the oral cavity, lip vermilion and the oropharynx. The prevalence rates are more in men as men have smoke more than women. In respect to age, oral cancer has been known to affect youths and young adults below the age of 40 years. However, the condition may fail to be diagnosed up to late adulthood. This has made oral cancer to be classified as a lifestyle disease. Cancer of the lip vermilion has however been attributed to exposure to sun but largely to cigar smoking. Similarly, oral cancer has also been attributed to other causes such as human papilloma virus (HPV), dietary deficiencies, syphilis and other oral dental diseases.
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The risk of oral cancer increases with increased smoking and decreases with cessation of smoking. In other words, people who smoke more cigarettes in a day are more likely to develop cancer as people who smoke less cigarettes and those who have also quitted smoking.Oral Cancer Prevention And Control The Approach Essay. Research has also proven that the risk of pre cancer is equally high as compared to that of oral cancer. As a matter of fact, tobacco has been largely associated with oral epithelial dysplasia than it has been associated with oral cancer as the OED does not have as many causes as oral cancer. Some of the risk factors of the disease include high alcohol consumption, chewing of khat and tobacco,
Cancer is one of the most common causes of morbidity and mortality today. It is estimated that around 43% of cancer deaths are due to tobacco use, unhealthy diets, alcohol consumption, inactive lifestyles and infection. Low-income and disadvantaged groups are generally more exposed to avoidable risk factors such as environmental carcinogens, alcohol, infectious agents, and tobacco use. These groups also have less access to the health services and health education that would empower them to make decisions to protect and improve their own health. Oro-pharyngeal cancer is significant component of the global burden of cancer. Tobacco and alcohol are regarded as the major risk factors for oral cancer. The population-attributable risks of smoking and alcohol consumption have been estimated to 80% for males, 61% for females, and 74% overall. The evidence that smokeless tobacco causes oral cancer was confirmed recently by the International Agency for Research on Cancer. Studies have shown that heavy intake of alcoholic beverages is associated with nutrient deficiency, which appears to contribute independently to oral carcinogenesis. Oral cancer is preventable through risk factors intervention. Prevention of HIV infection will also reduce the incidence of HIV/AIDS-related cancers such as Kaposi sarcoma and lymphoma.Oral Cancer Prevention And Control The Approach Essay. The WHO Global Oral Health Programme is committed to work for country capacity building in oral cancer prevention, inter-country exchange of information and experiences from integrated approaches in prevention and health promotion, and the development of global surveillance systems for oral cancer and risk factors. The WHO Global Oral Health Programme has established a global surveillance system of oral cavity cancer in order to assess risk factors and to help the planning of effective national intervention programmes. Epidemiological data on oral cancer (ICD-10: C00-C08) incidence and mortality are stored in the Global Oral Health Data Bank. In 2007, the World Health Assembly (WHA) passed a resolution on oral health for the first time in 25 years, which also considers oral cancer prevention. The resolution WHA60 A16 URGES Member states–To take steps to ensure that prevention of oral cancer is an integral part of national cancer-control programmes, and to involve oral-health professionals or primary health care personnel with relevant training in oral health in detection, early diagnosis and treatment;–The WHO Global Oral Health Programme will use this statement as the lead for its work for oral cancer control www.who.int/oral_health.
Introduction
Oral cancer is the 11th most common cancer in the world, accounting for an estimated 300,000 new cases and 145,000 deaths in 2012 and 702,000 prevalent cases over a period of five years (old and new cases) (tables 5.1 and 5.2) (Bray and others 2013; Ferlay and others 2013). For this chapter, oral cancers include cancers of the mucosal lip, tongue, gum, floor of the mouth, palate, and mouth, corresponding to the International Classification of Diseases, 10th revision [ICD-10], codes C00, C02, C03, C04, C05, and C06, respectively. Two-thirds of the global incidence of oral cancer occurs in low- and middle-income countries (LMICs); half of those cases are in South aAsia. India alone accounts for one-fifth of all oral cancer cases and one-fourth of all oral cancer deaths (Ferlay and others 2013). Oral Cancer Prevention And Control The Approach Essay.
Table 5.1
Oral Cancer in Men (All Ages): Global Incidence, Mortality, and Prevalence, World Health Organization Geographic Classification, 2012.
Table 5.2
Oral Cancer in Women (All Ages): Global Incidence, Mortality, and Prevalence, World Health Organization Geographic Classification, 2012.
Tobacco use, in any form, and excessive alcohol use are the major risk factors for oral cancer. With dietary deficiencies, these factors cause more than 90 percent of oral cancers. Preventing tobacco and alcohol use and increasing the consumption of fruits and vegetables can potentially prevent the vast majority of oral cancers (Sankaranarayanan and others 2013). When primary prevention fails, early detection through screening and relatively inexpensive treatment can avert most deaths. Oral Cancer Prevention And Control The Approach Essay. However, oral cancer continues to be a major cancer in India, East Asia, Eastern Europe, and parts of South America (Forman and others 2013), where organized prevention and early detection efforts are lacking. This chapter discusses the epidemiology, prevention, early detection, and treatment of oral cancers, as well as the cost-effectiveness of interventions.
Oral Cancer: Incidence, Mortality, and Survival
Incidence and Mortality1
Oral cancer incidence and mortality are high in India; Papua New Guinea; and Taiwan, China, where chewing of betel quids with tobacco or without tobacco or areca nut chewing is common, as well as in Eastern Europe, France, and parts of South America (Brazil and Uruguay), where tobacco smoking and alcohol consumption are high. The age-standardized incidence rates for men are, on average, twice as high as those for women (tables 5.1 and 5.2). Incidence rates do not follow a particular pattern from low- to high-income countries (HICs), when countries are grouped into wealth strata (figure 5.1). In selected countries where some reliable cancer registries exist, India is highest and Belarus is lowest, with incidence rates varying by more than five times in men and women. The estimated age-standardized incidence rates of oral cancer also vary among countries in different regions (maps 5.1 and 5.2).
Figure 5.1
Age-Standardized Incidence and Mortality Rates of Oral Cancer, by World Bank Income Classification, 2012.
Map 5.1
Age-Standardized Incidence Rates of Oral Cancer in Men, 2012.
Map 5.2
Age-Standardized Incidence Rates of Oral Cancer in Women, 2012.
The buccal (cheek) mucosa is the most common site for oral cancer in South and Southeast Asia; in all other regions, the tongue is the most common site (Forman and others 2013). Regional variations in incidence and the site of occurrence relate to the major causes, which are alcohol and smoking in Western countries, and betel quid and tobacco chewing in South and Southeast Asia (Lambert and others 2011).Oral Cancer Prevention And Control The Approach Essay. Oral cancer mortality rates range between 1 and 15 per 100,000 persons in different regions; mortality rates exceed 10 per 100,000 in Eastern European countries, such as the Czech Republic, Hungary, and the Slovak Republic (Ferlay and others 2013). Oral cancer mortality rates are influenced by oral cancer incidence, access to treatment, and variations in site distribution.
The observed trends in incidence and mortality among men and women are closely correlated with the patterns and trends in tobacco and alcohol use. An increasing trend in incidence has been reported in Karachi, Pakistan (Bhurgri and others 2006), and in Taiwan, China (Tseng 2013), caused by increases in tobacco and areca nut chewing and alcohol drinking. Oral cancer incidence and mortality rates have been steadily declining over the past two decades because of declining smoking prevalence and alcohol consumption in the United States (Brown, Check, and Devesa 2011). However, a recent increase in cancers at the base of the tongue, possibly driven by the human papillomavirus (HPV), has been observed in white men in the United States (Saba and others 2011).
Oral cancer incidence and mortality rates have been declining steadily in most European countries over the past two decades; until recently, rates had been increasing in some Central European countries, including Hungary and the Slovak Republic, reflecting changes in alcohol and tobacco consumption (Bonifazi and others 2011). Oral Cancer Prevention And Control The Approach Essay. Oral cancer mortality has declined steadily in France since reaching a peak in the early 1990s, and the decline correlates with the reduction in per capita alcohol consumption. Incidence and mortality have been stable in the Nordic countries, the Russian Federation, and the United Kingdom. Mortality rates have been steadily declining in Australia and Hong Kong SAR, China, but increasing in Japan and the Republic of Korea (Yako-Suketomo and Matsuda 2010).
Survival
In the United States, five-year survival improved by more than 11 percentage points between 1992 and 2006 (Pulte and Brenner 2010) and is now approximately 65 percent (Howlader and others 2010; Ries and others 2008). In Europe, it is approximately 50 percent (Sant and others 2009). In India, five-year survival is less than 35 percent; in China, the Republic of Korea, Pakistan, Singapore, and Thailand, it ranges between 32 and 54 percent (Sankaranarayanan and others 2010; Sankaranarayanan and Swaminathan 2011). Overall, the five-year survival for early, localized cancers exceeds 80 percent and falls to less than 20 percent when regional lymph nodes are involved. Oral Cancer Prevention And Control The Approach Essay.
Oral Cancer: Risk Factors and Prevention
The major causes of oral cancer worldwide remain tobacco in its many different forms, heavy consumption of alcohol, and, increasingly, infection with certain types of HPV. Although the relative contribution of risk factors varies from population to population, oral cancer is predominantly a disease of poor people (Johnson and others 2011). Prevention of this devastating disease can come from fundamental changes in socioeconomic status, as well as from actions to reduce the demand, production, marketing, and use of tobacco products and alcohol (Johnson and others 2011). A healthy diet, good oral and sexual hygiene, and awareness of the signs and symptoms of disease are important. Success depends on political will, intersectoral action, and culturally sensitive public health messages disseminated through educational campaigns and mass media initiatives.
Smokeless and Smoking Tobacco Use
Smokeless tobacco in the form of betel quid, oral snuff, and betel quid substitutes (locally called guktha, nass, naswar, khaini, mawa, mishri, and gudakhu) increases the risk of oral precancerous lesions and oral cancer between 2-fold and 15-fold (Gupta and others 2011; Gupta, Ariyawardana, and Johnson 2013; IARC 2004b, 2007; Javed and others 2010; Johnson and others 2011; Somatunga and others 2012). In most areas, betel quid consists of tobacco, areca nut, slaked lime, catechu, and several condiments, wrapped in a betel leaf. Oral Cancer Prevention And Control The Approach Essay. In recent years, small, attractive, and inexpensive sachets of betel quid substitutes containing a flavored and sweetened dry mixture of areca nut, catechu, and slaked lime with tobacco (gutkha) or without tobacco (pan masala), often claiming to be safer products, have become widely available and are increasingly used by young people, particularly in India. These products have been strongly implicated in oral submucous fibrosis (OSMF), which places individuals at high risk for malignancy.
More than 50 percent of oral cancers in India, Sudan, and the Republic of South Sudan, and about 4 percent of oral cancers in the United States, are attributable to smokeless tobacco products. Smokeless tobacco use among young people is increasing in South Asia, with the marketing of conveniently packaged products made from areca nut and tobacco; as a consequence, oral precancerous conditions in young adults have increased significantly (Gupta and others 2011; Sinha and others 2011).
Consistent evidence from many studies indicates that tobacco smoking in any form increases the risk of oral cancer by twofold to tenfold in men and women (IARC 2004a). Risk increases substantially with duration and frequency of tobacco use; risk among former smokers is consistently lower than among current smokers, and there is a trend of decreasing risk with increasing number of years since quitting. Use of smokeless tobacco and alcohol in combination with tobacco smoking greatly increases the risk of oral cancer. The biological plausibility is provided by the identification of several carcinogens in tobacco, the most abundant and strongest being tobacco-specific N-nitrosamines, such as N-nitrosonornicotine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (IARC 2007). These are formed by N-nitrosation of nicotine, the major alkaloid responsible for addiction to tobacco. Oral Cancer Prevention And Control The Approach Essay.
The fact that more than 80 percent of oral cancers can be attributed to tobacco and/or alcohol consumption justifies regular oral examinations targeting tobacco and alcohol users, as well as prevention efforts focusing on tobacco and alcohol control (Radoi and others 2013). The World Health Organization Framework Convention on Tobacco Control, an evidence-based international treaty, aims to reduce the demand for tobacco globally by price, tax, and non-price measures. (See chapter 10 for a full discussion of tobacco control.)
Areca Nut Chewing
Areca nut or betel nut, because it is often wrapped in betel leaf, is now regarded as a type 1 carcinogen (IARC 2004b, 2007). It is chewed raw, dried, or roasted, or as part of betel quid, by millions of people in Asia; its use is spreading across the Pacific, as well as in emigrant Asian communities worldwide.Oral Cancer Prevention And Control The Approach Essay. Cheap, prepackaged areca nut products, such as pan masala, are of recent concern, especially among youth. The inclusion of tobacco in the betel quid adds considerably to the carcinogenicity (Amarasinghe and others 2010; Johnson and others 2011).
Alcohol Use
Epidemiological studies indicate that drinking alcoholic beverages increases the risk of oral cancer twofold to sixfold and is an independent risk factor (IARC 2010), with risk increasing with quantity consumed. The risk varies by population and individual and subsite within the oral cavity (Radoi and others 2013). The combined use of alcohol and tobacco has a multiplicative effect on oral cancer risk. The various pathways by which alcohol may exert carcinogenic influence include topical exposure leading to a direct effect on cell membranes, altered cell permeability, variation in enzymes that metabolize alcohol, and/or systemic effects, such as nutritional deficiency, immunological deficiency, and disturbed liver function. A recent review failed to identify an association between the use of mouthwash containing alcohol and oral cancer risk, or any significant trend in risk with increasing daily use of mouthwash (Gandini and others 2012). Oral Cancer Prevention And Control The Approach Essay.
Poor Nutrition
High consumption of fruits and vegetables is associated with a reduction of 40–50 percent in the risk of oral cancer (Lucenteforte and others 2009; Pavia and others 2006; World Cancer Research Fund/American Institute for Cancer Research 2007). In HICs, selected aspects of diet—such as lack of vegetables and fruits—may account for 15–20 percent of oral cancers; this proportion is likely to be higher in LMICs. Chemoprevention studies have not established a preventive effect of retinoid and carotenoid dietary supplements (Chainani-Wu, Epstein, and Touger-Decker 2011; Wrangle and Khuri 2007).
Other Risk Factors
Genetic Factors
Most carcinogens are metabolized through the cytochrome p450 system in the liver. If this system is defective by virtue of inheriting a particular form of the gene (a polymorphism), the risk of many cancers is enhanced. This risk is particularly important with oral and other head and neck cancers, although the relative risks are modest at 1.5 or lower (that is, less than a doubling of risk) (Lu, Yu, and Du 2011).
Polymorphisms in alcohol-metabolizing enzymes also contribute to the risk. Individuals with the fast-metabolizing version (allele) of alcohol dehydrogenase (ADH3[1-1]) have a greater risk of developing oral cancer in the presence of alcoholic beverage consumption than those with the slow-metabolizing forms; this higher risk re-enforces the role of acetaldehyde as the carcinogen involved (Harty and others 1997).
Mate Drinking
Mate, a leaf infusion that is commonly drunk many times a day in parts of South America—usually very hot—appears to enhance the risk of oral cancer by a small amount (Deneo-Pellegrini and others 2012).
Viruses
Recent evidence suggests that HPV infection may be an independent risk factor for cancer of the base of the tongue, tonsils, and elsewhere in the oropharynx. Oral Cancer Prevention And Control The Approach Essay. HPV may modulate the process of carcinogenesis in some tobacco- and alcohol-induced oral and oropharyngeal cancers, and it may act as the primary oncogenic agent for inducing carcinogenesis among nonsmokers (Johnson and others 2011; Prabhu and Wilson 2013). Growing evidence suggests that such oropharyngeal infections can be sexually transmitted (Heck and others 2010).
Chronic Trauma
It now seems clear that chronic trauma, from sharp teeth, restorations, or dentures, contributes to oral cancer risk, although this higher risk commonly occurs only in the presence of the other local risk factors (Piemonte, Lazos, and Brunotto 2010).
Oral Cancer: Natural History
Oral cancer has a long preclinical phase that consists of well-documented precancerous lesions. The precancerous lesions include homogeneous leukoplakia, nonhomogeneous leukoplakia, verrucous leukoplakia, erythroplakia, OSMF, lichen planus, and chronic traumatic ulcers.Oral Cancer Prevention And Control The Approach Essay. The estimated annual frequency of malignant transformation of oral precancerous lesions ranges from 0.13 percent to 2.2 percent (Amagasa, Yamashiro, and Uzawa 2011; Napier and Speight 2008).
Very early preclinical invasive cancers (early-stage cancers without symptoms) present as painless small ulcers, nodular lesions, or growths. These changes can be easily seen and are clinically detectable through careful visual inspection and palpation of the oral mucosa. Early, localized oral cancers—less than four centimeters—that have not spread to the regional lymph nodes can be effectively treated and cured with surgery or radiotherapy alone, with no functional or cosmetic defects, resulting in five-year survival rates exceeding 80 percent.
Leukoplakia is a white plaque that may be categorized clinically as homogeneous or nonhomogeneous. Homogeneous lesions are thin, flat, uniform, smooth, and white. Nonhomogeneous lesions may have a white and red appearance or tiny, white, pinhead-size raised nodules on a reddish background or a proliferative, warty appearance. Erythroplakia presents as a red patch with smooth or granular surface that cannot be characterized clinically or pathologically as any other definable disease (Warnakulasuriya, Johnson, and Van Der Waal 2007). Erythroplakia has a higher probability than leukoplakia to harbor occult invasive cancer and to undergo malignant transformation.
Oral lichen planus may present as interlacing white lines (known as Wickham’s striae) with a reddish border, or as a mix of reddish and ulcerated areas. Oral Cancer Prevention And Control The Approach Essay.
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OSMF, mostly restricted to people of Indian subcontinent origin and in certain Pacific islands such as Mariana Islands, presents with a burning sensation, blanching of the oral mucosa, and intolerance to spicy food. Stiffening and atrophy of the oral and pharyngeal mucosa occurs as the disease progresses, leading to reduced mouth opening and difficulty in swallowing and speaking.
Palatal lesions are seen in populations who smoke with the lighted end of the tobacco product inside the mouth, known as reverse smoking, resulting in white or mixed reddish-white lesions of the palate.
A higher risk of malignant transformation may be associated with the following factors: female gender, lesions of long duration, large precancerous lesions, precancerous lesions in nonusers of tobacco, tongue and floor of mouth lesions, nonhomogeneous lesions, and lesions showing epithelial dysplasia and aneuploidy (Hsue and others 2007; Napier and Speight 2008). However, it is impossible to predict with certainty which precancerous lesion will become malignant during follow-up in patients. The malignant transformation of precancerous lesions can be prevented by interventions, such as avoiding exposure to tobacco use and alcohol drinking, and in selected instances, by excision of the lesions.
Oral Cancer Screening: Accuracy, Efficacy, and Potential Harms
Although an affordable, acceptable, easy to use, accurate, and effective screening test for oral cancer is available in high-risk countries, a decision to introduce population-based screening should take into account the level of health service development and available resources to meet the increased treatment demand that screening generates. Oral Cancer Prevention And Control The Approach Essay. The target population for oral cancer screening consists of those age 30 years and older who use tobacco and/or alcohol.
Visual screening of the oral cavity has been widely evaluated for its feasibility, safety, acceptability, accuracy to detect oral precancerous lesions and cancer, and efficacy and cost-effectiveness in reducing oral cancer mortality (Johnson and others 2011; Sankaranarayanan and others 2005; Sankaranarayanan and others 2013). Visual screening involves systematic visual and physical examination of the intraoral mucosa under bright light for signs of oral potentially malignant disorders (OPMDs), as well as early oral cancer, followed by careful inspection and digital palpation of the neck for any enlarged lymph nodes. It is a provider-dependent, subjective test; accordingly, its performance in detecting lesions varies among providers. Comprehensive knowledge of the oral anatomy, the natural history of oral carcinogenesis, and the clinico-pathological features of the OPMDs and preclinical cancers are important prerequisites for efficient providers of oral visual screening. Oral Cancer Prevention And Control The Approach Essay.
