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ORIGINAL RESEARCH Table of Contents   
Year : 2017  |  Volume : 28  |  Issue : 2  |  Page : 122-125
Assessing alpha-tocopherol levels in patients with keratocystic odontogenic tumor: Across-sectional study


Department of Oral and Maxillofacial Pathology, Panineeya Mahavidyalaya Institute of Dental Sciences, Hyderabad, Telangana, India

Correspondence Address:
Bhargavi Krishna Ayinampudi
Department of Oral and Maxillofacial Pathology, Panineeya Mahavidyalaya Institute of Dental Sciences, Hyderabad, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijdr.IJDR_714_16

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Aims and Objectives: A keratocystic odontogenic tumour (KCOT) is a benign uni- or multicystic, intraosseous tumour of odontogenic origin, with a characteristic lining of parakeratinized stratified squamous epithelium and potential for aggressive, infiltrative behaviour. Various studies in hamsters showed that, alpha-Tocopherol, which is an active biological form of Vitamin E, is a potent antioxidant known to inhibit tumour formation and also regression of established tumours. So, the aim of the present pilot study was to assess the levels of Alpha-Tocopherol(Vitamin E) in Patients with KCOT and compare them with Vitamin E levels in normal healthy individuals. Materials and Methods: A sample of 20 individuals were taken and Alpha Tocopherol levels in serum were assessed. Independent sample t test was used to analyse the data. Serum Vitamin-E levels were found to be decreased in KCOT cases. Results: Mean Vitamin-E level was found to be decreased (mean + S.D. = 10,549.34 +/- 2494.21 ng/mL) as compared to healthy controls (mean + S.D. = 13,982.42 +/- 2178.02 ng/mL). The reduction in serum vitamin E level was statistically significant (P < 0.05). Conclusion: The reduction in Vitamin E levels in KCOT patients might be suggestive of the possible interrelation between Vitamin E and KCOT invivo. Also, increase in intake of Vitamin E might help in reducing the risk of recurrence in KCOT by reducing the dysregulation of Cyclin D1 and Down-Regulation of mutant p53.


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