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Oral cancer is caused by chewing and smoking of tobacco. To assess the feasibility of primary prevention of oral cancer, two cohorts were studied in base-line surveys and then followed up annually for 10-yr in Ernakulam district of Kerala state. The intervention cohort consisted of 12212 tobacco users aged 15 yr and over, who were exposed to a concentrated program of education against tobacco use. The control cohort was a non-concurrent cohort of 6075 tobacco users studied using similar methods but with a minimal amount of advice against tobacco use. The stoppage of tobacco use increased and the incidence rate of leukoplakia decreased significantly and substantially in the intervention cohort compared to the control cohort. The decrease in the incidence of leukoplakia was indicative of the decrease in the risk of oral cancer since the two were intimately related. This study demonstrated feasibility of primary prevention of oral cancer.

The melanin pigmentation in the palate of Indian reverse smokers was histologically studied in 80 biopsies, which were compared with corresponding tissue from 49 nontobacco users. The morphology of epithelium containing melanin in its basal part was normal in smokers and nonsmokers, in contrast to areas with a local melanin depigmentation of the epithelium found in some of the reverse smokers. Here an epithelial thinning, inflammation in the underlying connective tissue, and eventually a cancer was found. The histologic appearance was in accordance with the theory that as long as a smoker's melanosis or a genetic melanin pigmentation is present, melanin functions as a defence against toxic agents penetrating into the oral mucosa.

A case-control study to elucidate the etiology of oral submucous fibrosis was conducted in Bhavnagar, Gujarat. Sixty consecutively arriving oral submucous fibrosis patients at a dental clinic were selected as cases. An equal number of controls matched for age, sex, religion and socioeconomic status were selected from individuals who did not exhibit any oral mucosal lesion or condition. Among cases, 98% chewed areca nut regularly in one form or the other whereas among controls 35% chewed areca nut, giving an overall relative risk of 109.6. Areca nut chewing was practiced most commonly in the form of mawa: a mixture containing mainly areca nut (over 90% by weight), some tobacco, and a few drops of lime. Mawa chewers and those who chewed mawa along with other chewing habits showed very high relative risks. The relative risks increased with increase in the frequency as well as the duration of chewing habits. In a bivariate analysis the effect of frequency and duration of chewing appeared to be multiplicative. The present findings confirm areca nut as the most important etiologic factor in oral submucous fibrosis.

Incidence of oral submucous fibrosis was calculated from a 10-yr prospective intervention study of 12,212 individuals with a strong component of health education on tobacco and area nut chewing. Based on 11 new cases among 6341 chewers, the annual incidence was 8.0 per 100,000 among men and 29.0 for women. An earlier 10-yr follow-up study, with no intervention component, served as control. Based on 11 new cases among 3,809 chewers, the annual incidence was 21.3 per 100,000 for men and 45.7 for women controls. Although the decrease in the incidence in the intervention cohort was not statistically significant due to small number of cases, the results underscored the causal role of areca nut chewing and indicated the potential for primary prevention of oral submucous fibrosis.

The occurrence of central papillary atrophy of the tongue among tobacco users, its clinical characteristics and the long term behavior in relation to changes in tobacco use was studied in 182 individuals in Ernakulam district, Kerala, India. Almost all (98%) lesions occurred among bidi smokers. Clinically, about 31% occurred in combination with bidi smoking associated lesions such as palatal erythema (14%), leukoplakia (8%) or both (3%). Histologic evaluation in 12 biopsies using single PAS stained sections showed candidal hyphae in 67%. A 10-yr follow-up (mean: 6.7 yr) of the 182 lesions showed that the regression was highest (87%) among those who stopped their smoking habit and persistence among those who did not reduce or stop their smoking habits. The findings from this study confirm a strong link between bidi smoking and central papillary atrophy of the tongue in rural Indian populations.

The malignant potential of oral lichen planus was assessed on the basis of observations in 722 patients found among 27,599 individuals examined in various epidemiologic studies in Kerala, Ernakulam district, India. Seven hundred and two patients with oral lichen planus were re-examined annually over a 10-year period with a mean observation period of 5.1 years. Most of the lesions (93%) were observed among tobacco users. Carcinoma developed in 3 (0.4%) patients with oral lichen planus. Clinically, all 3 had atrophic components in their lesions, and all were tobacco users. The relative risk of a lichen planus developing oral cancer compared to a tobacco user was estimated as 3.3. However, this relative risk was not significant. Histologically, 74% of the 94 biopsies from oral lichen planus showed epithelial atrophy. Two of the 3 in whom cancer developed also showed epithelial atrophy. It is felt that epithelial atrophy probably renders the mucosa more vulnerable to the carcinogenic action of tobacco. Although this study could not confirm the precancerous nature of this disease with a high degree of certainty, the disease did not appear to be innocuous either.