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Oral Cancer Abstracts



 Oral Cancer 


 

Abstracts:


 Warnakulasuriya S.
Guy's, Kings and St Thomas' Dental Institute, Kings College London, London, UK.
Bidi smokers at increased risk of oral cancer.
Evid Based Dent. 2005;6(1):19.

DATA SOURCES: Source articles were searched for using Medline, the Cochrane Library and within the references lists of identified articles. STUDY SELECTION: Articles were selected that included data enabling construction of 2 x 2 tables to estimate odds ratios (OR) and 95% confidence intervals (CI). DATA EXTRACTION AND SYNTHESIS: For each study, two-way contingency tables were constructed, based on exposure frequency distributions, for cases and controls. Unadjusted OR and 95% CI were recalculated based on the reported data using standard procedures. Separate contingency tables were made for bidi smoking, cigarette smoking and both types of smoking if the data were available in the same article. The overall OR combined across all studies, and its 95% CI, was calculated using a random-effects model for bidi and cigarette smoking. Tests for publication bias and heterogeneity were conducted. Confounding factors, for example, betel quid chewing or alcohol use, were not included in the meta-regression model. RESULTS: An increased risk of oral cancer was found for bidi smokers compared with people who had never smoked (OR, 3.1; 95% CI, 2.0-5.0) whereas no significant pattern of risk was found for cigarette smokers (OR, 1.1; 95% CI, 0.7-1.8). There was substantial heterogeneity in the pooled OR estimate. CONCLUSIONS: The results clearly indicate that bidi smokers are at increased risk of oral cancer. It is important that this information be incorporated into smoking prevention and cessation efforts, particularly in the urban poor and rural mass in south Asian countries where bidi smoking is widespread.















 Weinberg MA and Estefan DJ.
Assessing oral malignancies.
Am Fam Physician 2002 Apr 1; 65(7): 1379-84.
 

Oral cancers account for approximately 3 percent of all cases of cancer in the United States. An estimated 30,000 people will be diagnosed with oral cancer this year, and about one half of them will eventually die of the disease. The most common type of oral cancer is squamous cell carcinoma. Sixty percent of oral cancers are well advanced by the time they are detected, even though physicians and dentists frequently examine the oral cavity. The two most important risk factors for oral cancer are tobacco use and heavy alcohol consumption. The keys to reducing mortality are prevention and control. The earlier any intraoral or extraoral abnormalities or lesions are detected and biopsied, the more lives can be saved. Controversy exists whether screening programs effectively reduce the mortality rate. Specific step-by-step guidelines should be followed to perform an adequate examination of the head and neck.















 Balaram P, Sridhar H, Rajkumar T, Vaccarella S, Herrero R, Nandakumar A, Ravichandran K, Ramdas K, Sankaranarayanan R, Gajalakshmi V, Munoz N, Franceschi S.
Oral cancer in southern India: the influence of smoking, drinking, paan-chewing and oral hygiene.
Int J Cancer 2002 Mar 20; 98(3): 440-5.
 

Between 1996 and 1999 we carried out a case-control study in 3 areas in Southern India (Bangalore, Madras and Trivandrum) including 591 incident cases of cancer of the oral cavity (282 women) and 582 hospital controls (290 women), frequency-matched with cases by age and gender. Odds ratios (ORs) and 95% confidence intervals (CIs) were obtained from unconditional multiple logistic regressions and adjusted for age, gender, center, education, chewing habit and (men only) smoking and drinking habits. Low educational attainment, occupation as a farmer or manual worker and various indicators of poor oral hygiene were associated with significantly increased risk. An OR of 2.5 (95% CI 1.4-4.4) was found in men for smoking > or = 20 bidi or equivalents versus 0/day. The OR for alcohol drinking was 2.2 (95% CI 1.4-3.3). The OR for paan chewing was more elevated among women (OR 42; 95% CI 24-76) than among men (OR 5.1; 95% CI 3.4-7.8). A similar OR was found among chewers of paan with (OR 6.1 in men and 46 in women) and without tobacco (OR 4.2 in men and 16.4 in women). Among men, 35% of oral cancer is attributable to the combination of smoking and alcohol drinking and 49% to pan-tobacco chewing. Among women, chewing and poor oral hygiene explained 95% of oral cancer.















 Cox S.
Oral cancer in Australia--risk factors and disease distribution.
Ann R Australas Coll Dent Surg 2000 Oct; 15: 261-3.
 

There are approximately 2500 new cases of oral and pharyngeal cancer registered in Australia each year (Australian Institute of Health and Welfare). The life-time risk of developing oral cancer is approximately 1 in 90 for men and 1 in 200 for women (NHMRC 1996). In common with that of other developed countries, the incidence of oral and pharyngeal cancer in NSW showed a disturbing increase in recent decades although it has now levelled off, affecting primarily middle-aged men, (45-49 years). The highest incidence rates for males were in the western half of the State of New South Wales, sections of the Central Coast and in the inner and eastern suburbs of Sydney. Oral cancer accounts for up to 40% of all malignancies in parts of India and South East Asia. Recognized aetiological agents for oral cancer include tobacco, alcohol and use of the areca nut. The incidence of oral cancer amongst immigrant communities is examined. The easy availability of the areca nut and chewing tobacco in Australia suggests that there is a significant group at risk of developing oral cancer.















 Schildt EB, Eriksson M, Hardell L, Magnuson A.
Oral snuff, smoking habits and alcohol consumption in relation to oral cancer in a Swedish case-control study.
Int J Cancer 1998 Jul 29; 77(3): 341-6.
 

The use of oral snuff is a widespread habit in Sweden. We investigated whether the use of Swedish moist snuff leads to an increasing risk of oral cancer. Other risk factors such as smoking tobacco and alcoholic beverages were also investigated. Our study comprised 410 patients with oral cancer, from the period 1980-1989, and 410 matched controls. All subjects received a mailed questionnaire. The response rates were 96% and 91% for cases and controls, respectively. In the study, a total of 20% of all subjects, cases and controls, were active or ex-snuff users. The univariate analysis did not show any increased risk [odds ratio (OR) 0.7, 95% confidence interval (CI) 0.4-1.1] for active snuff users. We found an increased risk (OR 1.8, CI 1.1-2.7) for oral cancer among active smokers. Alcohol consumption showed the strongest risk for oral cancer. Among consumers of beer, an increased risk of 1.9 (CI 0.9-3.9) was found. Corresponding ORs for wine and liquor were 1.3 (CI 0.9-1.8) and 1.6 (CI 1.1-2.3), respectively. A dose-response effect was observed. Although not statistically significant, a multivariate analysis similarly suggested that the most important risk factors were beer and liquor consumption, followed by smoking.















 Rao DN, Ganesh B, Rao RS, Desai PB.
Risk assessment of tobacco, alcohol and diet in oral cancer--a case-control study.
Int J Cancer 1994 Aug 15; 58(4): 469-73.
 

A retrospective case-control study of 713 male oral-cancer patients seen at Tata Memorial Hospital, Bombay, during 1980-1984 was undertaken to assess the association between chewing, smoking and alcohol habits. Male controls were chosen among those persons who attended the hospital during the same period and were diagnosed as free from cancer, benign tumour and infectious disease. Statistical analysis was based on unconditional logistic regression and the confidence interval for RR was calculated using the standard error of the estimates. Established factors such as tobacco chewing and bidi smoking showed a significant association with oral cancer. For the alcohol habit, the relative risk was 1.42 and the dose-response relationship, in terms of frequency and duration of the habit, was also observed. The illiterate group showed an almost 2-fold significant excess risk compared to the literate group. After adjusting for confounding variables such as age, residence, illiteracy and known factors such as tobacco chewing and bidi smoking, the study has brought out the significance of a non-vegetarian diet as a high-risk factor for oral cancer compared to a vegetarian diet. Further studies are required to identify specific items in the non-vegetarian diet which may be associated with oral cancer.















 Mattson ME, Winn DM.
Smokeless tobacco: association with increased cancer risk.
NCI Monogr 1989; (8): 13-6.
 

Smokeless tobacco (chewing tobacco and snuff) contains known carcinogens shown to increase the risk for oral cancer. The effect of snuff has been more fully documented than other forms of smokeless tobacco, although the carcinogenic potential of all such products is acknowledged. Risk increases with increasing length of exposure, with risks greatest for anatomic sites where the product has been held in contact the longest time. In some studies, other organs, such as the esophagus, larynx, and stomach, have been shown to be at increased risk for cancer from the use of smokeless tobacco, although at present the data are insufficient to substantiate fully a causal association. Numerous reports have shown an association between snuff use and leukoplakia, with less evidence at present linking chewing tobacco use with leukoplakia. The documented early onset of the smokeless tobacco habit and reports of increases in certain oral cancers among young men raise serious concerns of an impending oral cancer epidemic in this population. In addition, synergistic interactions with other oral cancer risk factors, e.g., smoking and alcohol, and a high rate for second primaries observed for these cancers add to the concern. Unless the tide of its use is stemmed, long-term use can be expected to produce an increase in oral cancers, and perhaps cancers of other sites, as youthful users mature and accumulate exposure to this carcinogenic agent.















 Blot WJ, McLaughlin JK, Winn DM, Austin DF, Greenberg RS, Preston-Martin S, Bernstein L, Schoenberg JB, Stemhagen A, Fraumeni JF Jr.
Smoking and drinking in relation to oral and pharyngeal cancer.
Cancer Res 1988 Jun 1; 48(11): 3282-7.
 

A case-control study of oral and pharyngeal cancer conducted in four areas of the United States provided information on the tobacco and alcohol use of 1114 patients and 1268 population-based controls. Because of the large study size, it could be shown that the risks of these cancers among nondrinkers increased with amount smoked, and conversely that the risks among nonsmokers increased with the level of alcohol intake. Among consumers of both products, risks of oropharyngeal cancer tended to combine more in a multiplicative than additive fashion and were increased more than 35-fold among those who consumed two or more packs of cigarettes and more than four alcoholic drinks/day. Cigarette, cigar, and pipe smoking were separately implicated, although it was shown for the first time that risk was not as high among male lifelong filter cigarette smokers. Cessation of smoking was associated with a sharply reduced risk of this cancer, with no excess detected among those having quit for 10 or more years, suggesting that smoking affects primarily a late stage in the process of oropharyngeal carcinogenesis. The risks varied by type of alcoholic beverage, being higher among those consuming hard liquor or beer than wine. The relative risk patterns were generally similar among whites and blacks, and among males and females, and showed little difference when oral and pharyngeal cancers were analyzed separately. From calculations of attributable risk, we estimate that tobacco smoking and alcohol drinking combine to account for approximately three-fourths of all oral and pharyngeal cancers in the United States.














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