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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 28  |  Issue : 4  |  Page : 375-380

Lipid profile in patients with oral submucous fibrosis, lichen planus, and leukoplakia


1 Department of Oral Medicine and Radiology, Panineeya Mahavidyalaya Institute of Dental Sciences and Research Center, Hyderabad, Telangana, India
2 Department of Oral Medicine and Radiology, People's Dental College, Bhopal, Madhya Pradesh, India
3 Department of Oral Medicine and Radiology, Dnyandeo Yashwantrao Patil Dental College and Hospital, Pune, Maharashtra, India

Date of Submission11-Jun-2015
Date of Acceptance02-Feb-2017
Date of Web Publication21-Feb-2017

Correspondence Address:
Dr. Mamatha Boringi
Department of Oral Medicine and Radiology, Panineeya Mahavidyalaya Institute of Dental Sciences and Research Center, Hyderabad, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiaomr.JIAOMR_127_15

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   Abstract 

Introduction: Lipids are essential for various biological functions, including cell growth and division of normal and malignant tissues. Changes in the lipid profile have long been associated with malignancies.
Aims: The aim of this study was to evaluate the alterations in lipid profile in patients with oral submucous fibrosis (OSMF), leukoplakia and lichen planus. Materials and Methods: This is a hospital-based study conducted among a total of 80 patients; 20 patients in the control group and 20 patients with histopathologically confirmed cases of OSMF, leukoplakia, and lichen planus group. Serum cholesterol, triglyceride, low density lipoprotein (LDL), very low density lipoprotein (VLDL), high density lipoprotein (HDL) and Apo A1were analyzed among the included patients. Statistical Analysis Used: Analysis of variance and post hoc tests were performed. Results: Serum total cholesterol, HDL and Apo A1levels were significantly decreased in OSMF patients, and HDL and Apo A1levels were also significantly decreased in leukoplakia patients. There was no difference in lipid profiles in lichen planus patients. Conclusions: The findings of the present study warrant in depth investigation of lipids and their mechanism of transportation through cell membranes as well as the role of receptors in maintaining cell integrity and their association with different precancerous lesions and conditions.

Keywords: Apo A1, cholesterol, HDL, LDL, lipid peroxidation, lipid profile, triglycerides


How to cite this article:
Boringi M, Bontha SC, Chavva S, Badam R, Waghray S, Milanjeeth. Lipid profile in patients with oral submucous fibrosis, lichen planus, and leukoplakia. J Indian Acad Oral Med Radiol 2016;28:375-80

How to cite this URL:
Boringi M, Bontha SC, Chavva S, Badam R, Waghray S, Milanjeeth. Lipid profile in patients with oral submucous fibrosis, lichen planus, and leukoplakia. J Indian Acad Oral Med Radiol [serial online] 2016 [cited 2021 Jan 28];28:375-80. Available from: https://www.jiaomr.in/text.asp?2016/28/4/375/200620


   Introduction Top


Lipids are major cell membrane components that are essential for various biological functions, including cell growth and division of normal as well as malignant tissues. Changes in the lipid profile associated with etiology of breast cancer and colorectal cancer has been reported.[1],[2] However, only a few reports are available regarding plasma lipid profile in head and neck cancer. Head and neck cancer is one of the leading causes of morbidity and mortality in Asian subcontinent compared to the West.[1],[3] The habit of tobacco and betel nut chewing is a known etiologic factor for the development of oral precancerous conditions and precancerous lesions leading to head and neck cancer.[4] One of the most prevalent oral precancerous conditions prevailing in India is oral submucous fibrosis (OSMF).[1],[4]

Many studies have reported the alterations in lipid profile level in OSMF, leukoplakia, and lichen planus. However, the present study compared the lipid profile in OSMF, leukoplakia, and lichen planus. The objective of the present study was to evaluate the serum lipid profile in patients with OSMF, lichen planus, leukoplakia, and healthy individuals. The study included the following parameters: total cholesterol, LDL cholesterol (LDLC), HDL cholesterol (HDLC), VLDL cholesterol (VLDLC), triglycerides (TGs), and Apo A1.


   Materials and Methods Top


This hospital-based study was conducted in the Department of Oral Medicine and Radiology. A total of 80 patients who were clinically diagnosed and histologically confirmed to suffer from OSMF, lichen planus, and leukoplakia were included in the study. Institutional ethical clearance was obtained, and the patients were subjected to extended serum lipid profile, which included total cholesterol, LDLC, HDLC, VLDLC, TGs, and Apo A1. Twenty healthy individuals, matched for age and sex, who had no complaint or any other major illness in the recent past, were included as controls. The inclusion criteria consisted of patients with precancerous lesions and conditions. The exclusion criteria included patients with hypertension, diabetic mellitus, genetic hyperlipidemia, triglyceridemia, liver, renal, and coronary heart disease, obese individuals, and patients with any systemic diseases. Approximately 5 ml 12-hour fasting blood samples were collected from the anticubital vein in a plain vial from the participants. Blood was allowed to clot and serum was separated from the blood samples by centrifuging at 3000 rpm for 10 min; the serum was stored at −20°C and analyzed. All the parameters were analyzed with a semi autoanalyzer (ERBA Company, Diamedics, USA). Cholesterol was estimated using the dynamic extended stability CHOD–PAP method.

TGs: Dynamic extended stability with lipid clearing agent GPO – Triender method, end point.

HDL: Cholesterol method: Phosphotungstic acid method, end point.

VLDL: Calculated from TGs. VLDL = TG/5.

LDL: Calculated from Friedewald equation: LDLC = Total cholesterol − HDLC − TGs/5.

Apo: Lipoprotein A1 method: Measurement of antig1ntibody reaction by the end-point method.


   Results Top


All the variables were statistically analyzed for the mean values, standard deviation (SD), standard error, range, and P value. Evaluation of results and statistical analysis was carried out using analysis of variance (ANOVA), post hoc test, and Mann–Whitney test. In all the above mentioned tests, P < 0.05 was considered to be statistically significant. The data was analyzed using Statistical Package for the Social Sciences (SPSS), IBM Inc., Chicago, IL. The confidence interval of the difference in the present study was 95%. The results obtained and the observations are as follows.

There was decrease in HDL and Apo A1 values among the groups according to ANOVA test, P value of 0.003 and 0.006, respectively which is statistically significant [Table 1] and [Table 2]. Cholesterol values were lower on the average by 37.15 units in the OSMF group compared to the control group according to the post hoc test, which was statistically significant (P = 0.019) [Table 3]. The HDL and Apo A1 levels were statistically significant (P = 0.007 and 0.004, respectively) in OSMF and leukoplakia (P = 0.005 and 0.003, respectively) patients when compared with controls according to the post hoc test [Table 4] and [Table 5]. The Apo A1 values were lower on the average in OSMF group by 24.900 units and in leukoplakia by 25.650 units compared to controls, which was statistically significant (P = 0.004 and 0.003, respectively) according to post hoc test.
Table 1: HDL significance according to ANOVA

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Table 2: Apo A1 significance according to ANOVA

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Table 3: Cholesterol significance in OSMF, lichen planus, and leukoplakia patients when compared with controls - post hoc test

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Table 4: HDL significance in OSMF, lichen planus, and leukoplakia patients when compared with controls - post hoc test

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Table 5: Apo A1 significance in OSMF, lichen planus, and leukoplakia patients when compared with controls - post hoc test

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Distribution of cholesterol, HDL, and Apo A1 levels in OSMF, leukoplakia, lichen planus, and control groups are graphically shown in [Figure 1],[Figure 2],[Figure 3],[Figure 4]. Cholesterol, TG, LDL, and VLDL values were not statistically significant in the leukoplakia group when compared with the control group according to the post hoc test. TG, LDL, and VLDL values were statistically not significant in the OSMF group when compared with the control group according to the post hoc test. There was no change in the total cholesterol, TGs, LDL, VLDL, HDL, and Apo A1 in lichen planus patients according to ANOVA and post hoc tests.
Figure 1: Cholesterol distribution in OSMF, leukoplakia, lichen planus and controls

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Figure 2: HDL distribution in OSMF, leukoplakia and lichen planus and controls

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Figure 3: Apo A1 distribution in OSMF, lichen planus and leukoplakia

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Figure 4: Prevalence of age in OSMF, lichen planus and leukoplakia

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   Discussion Top


OSMF has always been a challenging disease with high prevalence in India.[5],[6] In this study, most of the OSMF cases were in the second and third decades of life [Figure 4], with a male preponderance [Figure 5] and addiction to areca nut [Figure 6].[7],[8] This is in accordance with previous reports. Because this is a disease with multifactorial etiology, various workers have proposed different theories of causation to establish the exact nature of the disease.[9],[10],[11],[12],[13] In some malignancies, serum cholesterol undergoes early and significant changes. Low levels of cholesterol in the proliferating tissues and blood compartments could be due to the rapidly dividing cells in malignancies.[14]
Figure 5: Gender prevalence in OSMF, lichen planus and leukoplakia

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Figure 6: Habits of OSMF subjects

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There are the three main competing hypotheses to explain the inverse association between cholesterol concentrations and incidence of cancer. (1)First, lower cholesterol values, even before the manifestation or detection of cancer, may be a result of the cancer process; (2) Second, lower cholesterol values may precede the development of the cancer, however, the association with cancer is secondary which indicates that cholesterol serves as a marker for other casual variables or set of variables. (3) Third, lower cholesterol values may precede the development of cancer and may be causally associated with the occurrence of some forms of cancer.[15],[16] Williams et al. reported one of the postulated mechanisms for the lower levels of serum cholesterol in cancer patients as an increased membrane permeability to carcinogens induced by transfatty acids.

It is has been demonstrated that oral cancer significantly interferes with food intake as well as lipid ingestion and absorption. Therefore, it can be expected that patients with oral cancer have low serum levels of lipids; however, other factors, such as genes and hormones, also interact to regulate the plasma cholesterol levels. These mechanisms can be understood through the lipoprotein transport system. Crucial components of this system are lipoprotein receptors in the liver and extrahepatic tissues that mediate the uptake and degradation of cholesterol-carrying lipoproteins. Lipoproteins are degraded because they deliver their cholesterol to tissues, whereas the cholesterol survives eventually to be excreted from the tissues bind to new lipoprotein carriers.

Removal of cholesterol from the body occurs only when the sterol is transported to the liver for extraction into the bile. Because of the continuous cycling of cholesterol into and out of the blood stream, the plasma cholesterol concentration is not a simple additive function of dietary cholesterol intake and endogenous cholesterol synthesis. Rather, it reflects the rate of synthesis of the cholesterol carrying lipoproteins and the efficiency of the receptor mechanisms that determine their catabolism. Thus, the cholesterol homeostasis in healthy individuals depends on the presence and function of specific receptors on the cell surface. These receptors normally control the degradation of LDL, which is the major cholesterol transport protein in human plasma. In neoplastic diseases, an increased LDL activity in tumor cells may produce hypocholestromia.[15],[16]

The habit of tobacco consumption is a known etiologic factor for the development of oral precancerous diseases and head and neck cancer. Patients with oral precancerous conditions have also been reported to show a significant tendency to develop cancer. It is believed that tobacco carcinogens induce generation of free radicals and reactive oxygen species, which are responsible for the high rate of oxidation/peroxidation of polyunsaturated fatty acids.[17] This peroxidation further releases peroxide radicals. This affects essential constituents of the cell membrane and might be involved in carcinogenesis/tumorigenesis. Because of the lipid peroxidation, there is a greater utilization of lipids including total cholesterol, lipoproteins, and TGs for new membrane biogenesis. Cells fulfil these requirements either from circulation, by synthesis through the metabolism, or from degradation of major lipoprotein fractions such as VLDL, LDL, or HDL. Earlier reports have shown that antioxidant vitamins have protective effects against lipid peroxidation.[18]

Several prospective and retrospective studies have shown an inverse association between blood lipid profiles and different cancers. Some scientists have observed an inverse trend between lower serum cholesterol and head and neck cancer as well as esophageal and colon cancers. Similar findings were reported by Patel et al. in 2004.[16] Schatzkin et al. and Chyou et al. observed an inverse trend between lower serum cholesterol and head neck as well as esophageal cancer.[16] In our study, there was significant decrease in the total cholesterol, HDL, and APO A1 in OSMF patients, as well as in HDL and APO A1 in leukoplakia patients. Similarly, there was a significant decrease in total cholesterol and HDL in oral leukoplakia compared with controls according to Lohe et al.[3]

Lipid peroxidation is an essential biochemical process that involves the oxidation of polyunsaturated fatty acids, which are important components of cell membranes. Tobacco carcinogens generate reactive oxygen species and lipid peroxides, leading to tissue injury due to elevated lipid peroxidation, further damaging the cellular structural blocks such as lipids, proteins, and DNA. Thus, lipid peroxidation may play a role in the endogenous formation of exocyclic DNA adducts.[6] Ninety-five percent of the OSMF and leukoplakia patients were tobacco consumers either in the form of gutkha, pan chewers, or cigarette and beedi smokers in the present study. Neufeld et al. have reported passive smoking to be a significant risk factor for decreased HDLC. Animal studies have shown that nicotine, a known tobacco carcinogen, affects the activity of enzymes responsible for lipid metabolism.[18]

Further, exposure to tobacco carcinogens hampers antioxidant defense, leading to accelerated lipid peroxidation. There is a strong relationship between vitamin E (a liposoluble antioxidant vitamin) and lipids, especially cholesterol. Vitamin E is cotransported with all forms of cholesterol and contributes to the first line of defense against lipid peroxidation. Further, TGs and cholesterol are positively correlated with vitamins.[6] The role of HDLC and TGs in explaining the overall pattern of total cholesterol change is less clear. HDL and Apo A1 levels may be a useful indicator reflecting initial changes occurring in pre-cancerous and neoplastic conditions.

A significant decrease in levels of HDL and Apo A1 was also observed in this study. This was in accordance with previous reports which reported that lower HDL is an additional predictor of oral potentially malignant disorders, as reported by Melhrotra et al.,[1] which might be a consequence of the disease that is mediated by utilization of cholesterol by membrane biogenesis. Schatzkin et al. also observed an inverse relationship between serum cholesterol and oral premalignant condition.[18]

There were no significant differences in TG levels in OSMF and leukoplakia patients in this study. This is in accordance with Alexopoulos et al. who have found no significance difference in serum TGs between controls and patients with leukoplakia. There were no changes in the lipid profile of the lichen planus patients. These values were not significant when compared with OSMF and leukoplakia patients, which may be because lichen planus is immunologically mediated disease, not associated with deleterious habits. The change in lipid levels may have a diagnostic or prognostic role in the early diagnosis or prognostication of oral potentially malignant disorder and malignant lesions.


   Conclusion Top


The lipid profile levels were decreased in OSMF and leukoplakia patients. These are habit associated diseases, with free radical release, causing decrease in the lipid profile. Because lichen planus is an immunologically mediated disease, there were no changes in the lipid profile. These findings warrant in depth study of lipids and their mechanism of transportation through cell membranes and role of receptors in maintaining cell integrity and their association with different precancerous lesions and conditions.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Chalko AF, Singh RS, Farooq R. A study on alterations in plasma lipid profile pattern in OSMF patients. J Indian Acad Oral Med Radiol 2011;23:36-8.  Back to cited text no. 1
    
2.
Dbrowa AB, Hannam S, Rysz J, Maciej Banach M. Malignancy-associated dyslipidemia. Open Cardiovasc Med J 2011;5:35-40.  Back to cited text no. 2
    
3.
Lohe VK, Degwekar SS, Bhowate RR, Kadu RP, Suwarna B, Dangore SB. Evaluation of correlation of serum lipid profile in patients with oral cancer and precancer and its association with tobacco abuse. J Oral Pathol Med 2010;39:141-8.  Back to cited text no. 3
    
4.
Renuka JB, Sameena P, Krishna B. The role of gutkha chewing in oral submucous fibrosis: A case-control study. Quintessence Int 2009;40:19-25.  Back to cited text no. 4
    
5.
Ganapathy KS, Gurudath S, Balikai B, Sushmini B, Sujatha D. Role of iron deficiency in oral submucous fibrosis: An initiating or accelerating factor. J Indian Acad Oral Med Radiol 2011;23:25-8.  Back to cited text no. 5
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6.
Tilakaratne WM, Klinikowski MF, Takashi S, Peters TJ, Warnakulssuriya S. Oral submucous fibrosis: Review on aetiology and pathogenesis. Oral Oncol 2006;42:561-8.  Back to cited text no. 6
    
7.
Murti PR, Bhonsle RB, Gupta PC, Daftary DK, Pindborg JJ, Mehta FS. Etiology of oral submucous fibrosis with special reference to the role of areca nut chewing. J Oral Pathol Med 1995;24:145-52.  Back to cited text no. 7
    
8.
Yusuf H, Yong SL. Oral submucous fibrosis in a 12-year-old Bangladeshi boy: A case report and review of literature. Int J Paediatr Dent 2002;12:271-6.  Back to cited text no. 8
    
9.
Chang YC, Hu CC, Tseng TH, Tai KW, Lii CK, Chou MY. Synergistic effects of nicotine on arecoline–induced cytotoxicity in human buccal mucosal fibroblasts. J Oral Pathol Med 2001;30:458-64.  Back to cited text no. 9
    
10.
Shah N, Sharma PP. Role of chewing and smoking habits in the etiology of oral submucous fibrosis. Case–control study. J Oral Pathol Med 1998;27:475-9.  Back to cited text no. 10
    
11.
Trivedy C, Meghji S, Warnakulasuriya KA, Johnson NW, Harris M. Copper stimulates human oral fibroblasts in vitro: A role in the pathogenesis of oral submucous fibrosis. J Oral Pathol Med 2001;30:465-70.  Back to cited text no. 11
    
12.
Meghy S, Warnakulasuria S. Oral submucous fibrosis: An expert symposium. Oral Dis 1997;3:276-91.  Back to cited text no. 12
    
13.
Axell T, Pindborg JJ, Smith I, van der Waal CJ. An international collaborative group on oral white lesions oral white lesions with special reference to precancerous and tobacco-related lesions: Conclusions of an international symposium held in Uppsala, Sweden, May 18. J Oral Pathol Med 1996;23:49-54.  Back to cited text no. 13
    
14.
Halton JM, Nazir DJ, Mc Queen MJ, Barr RD. Blood lipid profiles in children with acute lymphoblastic leukemia. Cancer 2000;83:379-84.  Back to cited text no. 14
    
15.
Manoharan S, Baskar AA, Manivasagam P, Subramanian P. Circadian rhythmicity of plasma lipid peroxidation and anti-oxidants in oral squamous cell carcinoma. Singapore Med J 2005;46:184-6.  Back to cited text no. 15
    
16.
Mehrotra R, Shruti P, Chaudhary AK, Singh HP, Jaiswal RK, Singh M. Lipid profile in oral submucous fibrosis. Lipids in Health and Disease 2009;8:29.  Back to cited text no. 16
    
17.
Gupta A, Bhatt MLB, Misra MK. Lipid peroxidation and antioxidant status in head and neck squamous cell carcinoma patients. Oxid Med Cell Longev 2009;2:68-72.  Back to cited text no. 17
    
18.
Patel PS, Shah MH, Jha FP, Raval GN, Rawal RM, Patel MM, et al. Alterations in plasma lipid profile patterns in head and neck cancer and oral precancerous conditions. Indian J Cancer 2004;41:25-31.  Back to cited text no. 18
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