Serum Lipid Profile In Patients With Oral Tobacco Habits and Oral Precancer Lesions and Conditions

Background & Objectives:. Tobacco carcinogens induce generation of free radicals and reactive oxygen species, which cause lipid peroxidation. Because of the lipid peroxidation, there is a greater utilization of lipids for new membrane biogenesis. Hence the present study was carried out to determine the variations, if any, in the serum lipid profile of subjects with tobacco habit and patients with oral precancers. Methodology: The study consisted of 30 healthy controls, 30 patients with oral tobacco habit and 30 oral precancer cases. After thorough clinical oral screening for all the subjects of the groups and histopathological confirmation for premalignancy, 5 ml of fasting blood was collected. Blood was allowed to clot and serum separated. The serum triglycerides were estimated by the GPO-PAP, End Point Assay method; Total cholesterol by CHOD-PAP and HDL-Cholesterol by PEG-CHOD-PAP, End Point Assay method with Lipid Clearing Factor (LCF). The LDL and VLDL levels were calculated using the Friedewald’s equation. One way ANOVA SPSS version 19.0 was used for statistical analysis. Results: In the present study there was no statistically significant change in values of serum lipid profile in either the oral tobacco habit group or the oral precancer group when compared with age and sex matched controls. There was no statistical significant change in the lipid profile parameters on comparing oral tobacco habit group with oral precancer group also. Conclusion: Therefore it was concluded that oral precancer, though it represents ‘potentially malignant lesions’, it is localized and hence might not cause a significant serum lipid profile change as frank cancers do. Hence the precancerous lesions might not have the required need for greater utilization of lipids for new membrane biogenesis, which are fulfilled by synthesis or degradation of the circulating lipids in the blood, which might cause a significant change in the serum lipid profile values. Introduction Lipids are major cell membrane components, essential for various biological functions including cell growth and division of normal and malignant tissues. Lipids are carried in body fluids with the help of lipoproteins; Chylomicrons transport triglycerides (TG) from intestine to all cells. Very low density lipoproteins (VLDL) are involved in the transportation of triglycerides from liver to other cells. Low density lipoproteins (LDL) are responsible for the transport of cholesterol from liver to the cells and high density lipoproteins (HDL) are involved for the transport of cholesterol from cells to the liver. Chylomicrons and VLDL are rapidly catabolized. Thus TG, Cholesterol, LDL–cholesterol and HDL–cholesterol constitute Plasma Lipid Profile. The recent decades have seen a massive global increase in tobacco use, the consumption of cigarettes alone having risen from 300 million per year in 1920 to 5.5 trillion in 2000. It has been pointed out that 82,000-99,000 young people worldwide are initiated into smoking each day. Smokeless tobacco users in India and Pakistan together have been estimated to number 100 million.The World Health Organization predicts that tobacco deaths in India may exceed 1.5 million annually by 2020. Epidemiological studies show that the risk of developing oral cancer is five to nine times greater for smokers than for nonsmokers. In one study of women in the southern United States, chronic users of snuff were estimated to have a four times greater risk of developing oral cancer. In addition, a significant number of oral cancers in smokeless tobacco users, develop at the site of tobacco placement. Tobacco usage leads to the uptake of many hazardous compounds and their metabolites extracted from burning tobacco. These substances may be electrophilic and react with biological molecules, and give rise to oxidative stress through the formation of reactive species, or the initiation of lipid peroxidation chain reactions in the membranes. Because of the lipid peroxidation, there is a greater utilization of lipids for new membrane biogenesis. Cells fulfill these requirements either from circulation, by synthesis through the metabolism or from degradation of major lipoprotein fractions like VLDL, LDL or HDL. Usage of only tobacco/ tobacco with other ingredients (areca nut) is responsible for WebmedCentral > Research articles Page 2 of 10 WMC004034 Downloaded from http://www.webmedcentral. com on 18-Feb-2013, 07:44:08 AM causing various oral precancers. Premalignancy / precancer can be defined as any lesion that displays the metabolic and histologic activity found in cancerous lesions and within whose boundaries it is possible, but not mandatory, for a carcinoma to develop. Oral cancer lesions are usually preceded by the occurrences of premalignant lesions and / or conditions. Malignant transformation of Oral Leukoplakia, a premalignant lesion is 1% to 2% over 5 years, while Oral Lichen planus (OLP) and Oral Sub Mucous Fibrosis (OSMF) , both being premalignant conditions have malignant transformation of 0.05% in 10 years and 5% to 8% respectively. Researchers have reported association of plasma/serum lipids and lipoproteins with different cancers, as cholesterol is essential for maintenance of structural & functional integrity of all biological membranes. As neoplastic disease is related to new growth, there is a greater utilization of lipids including total cholesterol, lipoproteins and triglycerides for new membrane biogenesis. Cells fulfill these requirements either from circulation, by synthesis through the metabolism or from degradation of major lipoprotein fractions like VLDL, LDL or HDL. The idea of screening and following patients by blood test is appealing from several points of view, which inc lude, i t ’s ease, economic advantage, non-invasiveness and possibility of repeated sampling. Hence the present study has been taken up to evaluate the variation in serum lipid profile (total cholesterol(TC), VLDL, LDL, HDL & total TG levels) if any, in patients with oral tobacco habits and in oral precancer lesions and conditions. Materials And Methods The study was conducted in the Department of Oral Medicine and Radiology, Sri Sai College of Dental Surgery, Vikarabad. A total sample size of 90 subjects was chosen, with study group consisting of a total of 30 patients each in Precancer group and Tobacco Habit group. The control group consisted of 30 age and sex matched individuals, without any systemic or oral condition. The controls and patients selected belonged to similar socio-economic background. Any subject with systemic disease (eg: diabetes mellitus, thyroid disorders and liver dysfunction) and taking any drugs (including steroids) for the same were excluded. Obese subjects weighing more than 20% above the ideal weight were excluded. The tobacco habit group subjects were selected on the basis of the study by Robson N. et al., who have defined a current smoker as someone who had smoked > 100 cigarettes in their lifetime and who at the time of the study reported that they were smoking. (U.S. Department of Health and Human Services 1996) and a current smokeless tobacco chewer as defined by Ernster VL. et al., (1990) in their study, as one who has used smokeless tobacco more frequently than once a month and who had used smokeless tobacco within the previous month. After obtaining informed consent, patients were tested for fasting blood glucose levels, and complete blood picture to rule out diabetes mellitus. An incisional biopsy was performed, if clinical evidence of oral precancer lesion and/or condition was present. After the confirmation of the precancerous state, 5 ml of fasting (12-14hrs) blood sample was collected in a sterile bottle and allowed to clot for about an hour at 37°C. The serum was then separated and stored at 4°C. The serum triglycerides were estimated by the GPO-PAP (Glycerol-3-phosphate Oxidase – Peoxidase), End Point Assay; Total cholesterol by CHOD-PAP (Cholesterol Oxidase – Peroxidase) and HDL-Cholesterol by PEG-CHOD-PAP(Polyethylene glycol 6000Cholesterol Oxidase – Peroxidase), End Point Assay with Lipid Clearing Factor (LCF). The LDL Cholesterol level was calculated by the Friedewald’s equation. VLDL= triglycerides/5 LDL=Total CholesterolHDL-VLDL. The data collected was tabulated based upon the LDL, VLDL, HDL, total cholesterol and serum triglyceride levels separately for each of the three groups and subjected to statistical analysis. One way ANOVA SPSS version 19.0 was used for multiple group comparison for statistical analysis. For all the tests p value of 0.05 or less was used for statistical significance.