Experiments were undertaken to find out whether administration of oral contraceptive (OC) per nasogastric tube could accelerate or inhibit early carcinogenesis of the rat palatal mucosa induced by painting 0.5% solution of 7,12-Dimethyl benz (a) anthracene (DMBA) in liquid paraffin. Forty female Sprague-Dawley rats were divided into 8 groups consisting of 5 animals per group. Group I--DMBA; Group II--DMBA + Oral Contraceptive I (13.0gm% Norethindrone + 8.7mg% ethyl estradiol); Group III--DMBA + Oral Contraceptive II (6.5mg% Norethindrone + 4.3% ethyl estradiol). Group IV--Oral Contraceptive I, Group V--Oral Contraceptive II, Group VI--liquid paraffin, Group VII--Corn oil and Group VIII--untreated control. Each animal was sacrificed at 18 weeks, the palatal mucosa degloved, fixed in 10% formal saline, sectioned in paraffin at 5u, stained with Hematoxylin and Eosin and evaluated histologically for features of epithelial dysplasia. Morphometric analysis was performed on epithelial and keratin thickness. Results indicate higher mean grade of epithelial dysplasia for group II when compared to group I (P less than 0.01) thereby suggesting a cocarcinogenic action for the Oral Contraceptive I. Lower dose Oral Contraceptive II was, however, unable to produce any significant mean grade of dysplasia in group III, suggesting further that the cocarcinogenic action of the Oral Contraceptive used was dose dependent. Morphometric analysis shows a decrease (P less than 0.01) in Keratin and palatal epithelium in DMBA treated animals and further decrease (P less than .001) in those two structures when Oral Contraceptive was used in combination with DMBA, suggesting that the cocarcinogenic action of Oral Contraceptive could result from the induced atrophy of keratin/epithelium and subsequent improved access of the DMBA to target cells in the basal layer of the epithelium. It is suggested that Oral Contraceptive accelerated the induction of early DMBA carcinogenesis of the rat palatal mucosa in this study.