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ScienceWeek
MEDICAL BIOLOGY: ON ORAL LEUKOPLAKIA
The following points are made by D. Greenspan and R.C. Jordan (New Engl. J. Med. 2004 350:1382):
1) Perhaps the earliest link between oral leukoplakia and cancer was made by James Paget (1814-1899), for whom Paget's disease was named; he also recognized the connection between oral leukoplakia and smoking. Leukoplakia is a clinical term that refers to an oral mucosal white patch that will not rub off and is not attributable to any other known disease. It is considered to be potentially malignant, with a transformation rate in various studies and locations ranging from 0.6 to 18 percent. Clinically, oral leukoplakia is in the same spectrum of disease as the more sinister red or speckled lesion erythroplakia, which has a much higher transformation rate and is more often found on biopsy to be squamous-cell carcinoma.
2) The leukoplakia discussed here should be distinguished from oral hairy leukoplakia, the lesion associated with Epstein Barr virus and seen in immunosuppressed persons, predominantly but not exclusively those with human immunodeficiency virus infection. White patches in the mouth may have other causes, including chronic trauma such as friction and mucocutaneous diseases such as white sponge nevus, lichen planus, or lupus erythematosus. However, the lesion discussed here is more commonly associated with tobacco-related habits -- notably, smoking and the use of some other forms of tobacco, including moist snuff (smokeless tobacco) and pan (betel nut). Another form of precancer, proliferative verrucous leukoplakia, is predominantly found in those who do not use tobacco, but it has a high rate of transformation to cancer.
3) On biopsy, most leukoplakias show histologic features of epithelial dysplasia, including basal-cell hyperplasia, bulbous rete ridges, loss of polarity of basal cells, abnormal keratinocyte stratification, an increased nuclear:cytoplasmic ratio, nuclear hyperchromatism and pleomorphism, abnormal keratinization, and abnormally increased numbers of mitoses and suprabasal mitoses. Unfortunately, the recognition of these features is subjective, and there is wide variation in the degree of interexaminer agreement and intraexaminer reproducibility in the diagnosis. Yet a microscopical diagnosis of oral epithelial dysplasia is still one of the few indicators of an increased risk of oral cancer that we have, despite the reality that most dysplasias do not progress to cancer.
4) Transformation rates, like those associated with a clinical diagnosis of leukoplakia, vary, ranging from 16 to 33 percent. Differences in the transformation rate may reflect differences in criteria for histologic grading, clinical follow-up, and populations of patients. Therefore, a search has long been under way for molecular markers that may indicate an increased likelihood of malignant transformation. The possibilities that have been explored include DNA aneuploidy, loss of heterozygosity as assessed on the basis of microsatellite markers, mutations in the p53 gene and aberrant expression of p53 protein, inappropriate expression of other oncogenes such as cyclin D1, and differentiation markers such as keratins, blood-group antigens, and other cell-surface carbohydrates. Some assays for these markers have shown promise in modeling the risk of cancer, but their use has been hampered by technical difficulties that make their wide-scale application challenging. Others have proved to be of limited predictive value for individual persons, thus necessitating a search for new markers of risk and methods of risk assessment.(1)
References:
1. Sudbo J, Ristimaki A, Sondresen JE, et al. Cyclooxygenase-2 (COX-2) expression in high-risk premalignant oral lesions. Oral Oncol 2003;39:497-505
New Engl. J. Med. http://www.nejm.org
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Related Material:
SMOKING PREVALENCE AMONG ADULTS IN THE US 1998
The US Centers for Disease Control and Prevention (CDC) presents the results of a 1998 survey administered to a nationally representative sample (n = 32,440) of the US non-institutionalized civilian population aged >= 18 years. The report (CDC Morbidity and Mortality Weekly Report 2000 49:881) makes the following points:
1) Participants were asked, "Have you smoked at least 100 cigarettes in your entire life? and "Do you now smoke cigarettes every day, some days, or not at al?" "Current smokers" were defined as persons who reported both having smoked greater than or equal to 100 cigarettes during their lifetime and having smoked every day or some days at the time of the interview. "Former smokers" were defined as those who had smoked >= 100 cigarettes during their lifetime but did not currently smoke.
2) In 1998 in the US, an estimated 47.2 million adults (24.1 percent of the adult population), comprising 24.8 million men (26.4 percent) and 22.4 million women (22.0 percent) were current smokers. Overall, 19.7 percent of adults were every day smokers, and 4.2 percent were some day smokers. Every day smokers constituted 82.4 percent of all smokers.
3) Prevalence of smoking was highest among persons aged 18 to 24 years (27.9 percent) and aged 25 to 44 years (27.5 percent), and lowest among persons aged >= 65 years (10.9 percent).
4) Among specific groups, prevalence of current smoking was as follows:
American Indians/Alaska Natives: 40 percent
Non-Hispanic whites: 25 percent
Non-Hispanic blacks: 24.7 percent
Hispanics: 19.1 percent
Asian/Pacific Islanders: 13.7 percent
5) Current smoking prevalence was lowest among persons with at least 16 years of education (11.3 percent) and highest among persons with 9 to 11 years of education (36.8 percent). Smoking prevalence was higher among persons living below the poverty level (32.3 percent) than among those living at or above the poverty level (23.5 percent).
6) In 1998, an estimated 44.8 million adults (22.9 percent of the adult population) were former smokers (25.7 million men and 19.1 million women). Former smokers constituted 48.7 percent of persons who had ever smoked >= 100 cigarettes. Among current daily smokers in 1998, an estimated 15.2 million (39.2 percent) had stopped smoking for at least 1 day during the preceding 12 months because they were trying to stop smoking.
7) The report concludes: "A comprehensive approach to tobacco control will require treatment for nicotine dependence and efforts at national, state, and local levels to reduce youth smoking, promote smoke-free environments, support countermarketing efforts, and eliminate disparities in tobacco use among population subgroups. Increased attention must be focused on groups that show no decline in smoking prevalence, including persons aged 18 to 24 years, adults with low education levels, and American Indians/Alaska Natives. Approaches with the widest scope (i.e., economic, regulatory, and comprehensive) are likely to have the greatest long-term population impact."
Centers for Disease Control and Prevention http://www.cdc.gov
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Related Background:
BIDI USE AMONG US URBAN YOUTH
Notes by ScienceWeek:
"Bidis" are small brown hand-rolled cigarettes primarily made in India and southeast Asian countries, and consisting of tobacco wrapped in a tendu or temburni leaf (Diospyros melanoxylon). In the US, bidis are purchased for $1.50 to $4.00 for one package of 20 and are available in different flavors (e.g., cherry, chocolate, and mango). Bidi use was first observed in the US during the mid-1990s and is apparently now widespread among various minority youth groups. Adolescents report a preference for the taste of bidis over cigarettes and a belief that bidis are less expensive, easier to buy, and safer than cigarettes. The US Centers for Disease Control and Prevention (CDC) recently presented a report on bidi use, the report (CDC Morbidity and Mortality Weekly Report 1999 48:796) making the following points:
1) Preliminary data collected from a sample of adolescents surveyed during March and early April 1999 in Massachusetts (US) on the prevalence of bidi use among urban youth indicate that of 642 youth surveyed, 40 percent had smoked bidis at least once during their lifetimes and 16 percent were current bidi smokers.
2) When tested on a standard smoking machine, bidis produced higher levels of carbon monoxide, nicotine, and tar than cigarettes, with one study reporting that bidis produced approximately 3 times the amount of carbon monoxide and nicotine and approximately five times the amount of tar as cigarettes. Because of low combustibility of the tendu leaf wrapper, bidi smokers inhale more often and more deeply, breathing in greater quantities of tar and other toxins than cigarette smokers. Like all tobacco products, bidis are mutagenic and carcinogenic. Bidi smokers risk coronary heart disease, cancers of the oral cavity, pharynx, larynx, lung, esophagus, stomach, and liver. Mortality of both the fetus and newborn infant is also associated with bidi use during pregnancy.
3) The report states that this investigation is the first in the US to estimate the prevalence of bidi smoking among students in grades 7 through 12, and that preliminary findings from this study support the need for additional research on bidis, particularly on smoking prevalence among youth from differing geographic, educational, and socioeconomic backgrounds.
Centers for Disease Control and Prevention http://www.cdc.gov
ScienceWeek http://scienceweek.com
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