Assessing alpha-tocopherol levels in patients with keratocystic odontogenic tumor: A cross-sectional study
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-Toc...
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Published in | Indian journal of dental research : official publication of Indian Society for Dental Research Vol. 28; no. 2; p. 122 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
India
01.03.2017
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Subjects | |
Online Access | Get more information |
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Summary: | 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.
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.
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).
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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ISSN: | 1998-3603 |