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 Table of Contents  
Year : 2014  |  Volume : 26  |  Issue : 3  |  Page : 274-278

Alterations in plasma lipid profile patterns in oral cancer

1 Departments of Oral Medicine and Radiology, KLR's Lenora Institute of Dental Sciences, Rajahmundry, Andhra Pradesh, India
2 Department of Oral Medicine and Radiology, SIBAR Institute of Dental Sciences, Guntur, Andhra Pradesh, India
3 Department of Oral Medicine and Radiology, Chettinad Dental College and Research Institute, Chennai, Tamilnadu, India
4 Departments of Oral and Maxillofacial Surgery, KLR's Lenora Institute of Dental Sciences, Rajahmundry, Andhra Pradesh, India

Date of Submission26-Jun-2014
Date of Acceptance10-Nov-2014
Date of Web Publication19-Nov-2014

Correspondence Address:
Mahesh Neerupakam
Reader, Department of Oral Medicine and Radiology, KLR's Lenora Institute of Dental Sciences, Rajahmundry, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-1363.145004

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Aims and Objectives: The aim of this study was to evaluate and compare the alterations in the plasma lipid profile patterns in oral cancer patients and controls. Materials and Methods: The study population comprised of 15 oral cancer patients and 15 controls. The lipid profile patterns, such as, total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), Very-low-density lipoprotein (VLDL) lipoprotein, and triglycerides were estimated in both the groups. Changes in the plasma lipid profiles of both groups were compared. Results: This study evaluated all the plasma lipid profile patterns in both the groups. A significant decrease in the total cholesterol and HDL was observed in oral cancer subjects when compared with the control groups. Conclusion: Lipids are the major cell membrane components, which are essential for various biological functions, such as, maintaining cell integrity, cell growth, and division of normal and malignant cells. The lower plasma lipid status may be a useful indicator for initial changes occurring in neoplastic cells.

Keywords: HDL, LDL, lipid profile, lipoproteins, oral cancer, triglycerides, VLDL

How to cite this article:
Neerupakam M, Alaparthi RK, Sathish S, Katta SA, Polisetty N, Damera S. Alterations in plasma lipid profile patterns in oral cancer . J Indian Acad Oral Med Radiol 2014;26:274-8

How to cite this URL:
Neerupakam M, Alaparthi RK, Sathish S, Katta SA, Polisetty N, Damera S. Alterations in plasma lipid profile patterns in oral cancer . J Indian Acad Oral Med Radiol [serial online] 2014 [cited 2022 Jun 29];26:274-8. Available from: https://www.jiaomr.in/text.asp?2014/26/3/274/145004

   Introduction Top

Despite various advances in the diagnosis and treatment modalities there is lack of identification of a definite cause and cure for cancer. [1] Cancer affects all communities worldwide. Approximately ten million people are diagnosed with cancer and more than six million die of the disease every year. [2] Tobacco is considered to be one of the major etiological factors in various cancers, such as, oral, oropharyngeal, respiratory tract, and esophageal cancers, worldwide. [3] Oral cancer is the eighth most common cancer in the world. Squamous cell carcinoma comprises about 90 to 95% of all oral malignancies, and hence, the term 'oral cancer' is used in a restricted sense to describe squamous cell carcinoma. [4],[5],[6] Oral cancer is also considered to be preceded by various mucosal lesions known as precancerous lesions and conditions. Although 2-12% of the precancers transform into cancers in different populations, 80% of the oral cancers progress from precancerous lesions. [7]

Lipids are major cell membrane components that are essential for various biological functions, such as, maintaining cell integrity, cell growth, and division of normal and malignant cells. Changes in the lipid profiles have been seen in various disease conditions, including oral cancer. Lipid metabolism of tumors may be different from that in the normal tissue, but the relationship between tumorigenesis and changes in the amounts of plasma lipids is unclear. Several studies have reported differences in total plasma lipid levels between untreated cancer patients (including head and neck cancers) and healthy subjects. [2] An inverse relationship between the plasma lipid profile has been seen in oral cancer and precancerous subjects. The lower plasma lipid status may be a useful indicator for the initial changes occurring in neoplastic cells. [2],[8] In the present study, we had compared the alterations of the plasma lipid profile patterns in oral cancer with the controls.

   Materials and Methods Top

A case-control clinical study was conducted with a sample size of 30 patients, comprised of both cases and the controls, who consulted the Department of Oral Medicine and Radiology, SIBAR Institute of Dental Sciences, Guntur, Andhra Pradesh, India, during a six-month period. Of the 30 subjects, 15 subjects were diagnosed with oral cancer and 15 subjects without oral cancer served as the controls.

Selection of cases

Fifteen patients with oral cancer were included in the study. The bias in selection of the cases was avoided by considering only the untreated cases or the first-diagnosed and histopathologically proven cases. Recurrent cases, cases under treatment, and metastatic cases were excluded from the study. An age group of the fourth to seventh decade was considered in the sample where the incidence of oral cancer was more marked. Tumor-node-metastasis (TNM) staging was followed to grade the oral cancer after examination, followed by histological confirmation, before the procedure. Most of the patients included in the sample belonged to stage-III and stage-IV for better correlation of results.

Selection of controls

Fifteen healthy individuals without the habit of tobacco consumption were included in the study.

Exclusion criteria

Patients with cardiovascular diseases, uncontrolled diabetes mellitus, acute hepatitis, and renal disease were excluded from the sample in both the groups. Randomization of the sample was achieved by selecting cases and controls in different groups, ages, sexes, and in different areas.

Obese patients (evaluated on the basis of the standard World Health Organization (WHO) body mass index) were not included in the sample size. The socioeconomic status of the patients was also considered and the lower class and the higher class patients were not included in the sample. All the patients of the sample did not have a sedentary lifestyle and were from families with a pretty normal annual income. All the patients in both the groups were informed about the procedure to be conducted on them and patient-consent forms were obtained from all the subjects. Ethical clearance was obtained from the Institutional Ethical Committee.


Five milliliters of blood was collected from each subject in the early hours of the morning after eight hours of starvation. It was allowed to clot and the serum was separated by centrifugation. Following that, the lipid profile patterns such as total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), and triglycerides (TG) were estimated. A fully automated biochemistry auto-analyzer (EM-360) from Erba-Manheim [9] was used for the analysis. The LDL and VLDL values were calculated indirectly by using the Friedewald equation. [9]

Statistical methods

The lipid parameters were statistically analyzed by the paired-t test and Scheffe test, to evaluate the significant proportion of the lipid profile patterns between the two groups.

   Results Top

The TC level was slightly lower in the oral cancer subjects than in the controls, with a significant P-value of 0.049. The ranges of the TC were between 153 and 209 mg/dl in oral cancer. The range of HDL values in oral cancer was 32-54 mg/dl, which was slightly lower than that of the controls (37-59 mg/dl) with a significant P-value of 0.043. A significantly lower level of LDL was observed in our study in oral cancer patients compared to the controls, with a P-value of 0.044. The range of LDL in oral cancer was 83-133 mg/dl and in the controls it was 84-168 mg/dl. In our study, higher VLDL levels and decreased TG levels were observed in oral cancer patients on comparing with the control group. The respective mean and standard deviation of all the parameters are depicted in [Table 1].
Table 1: Mean and standard deviation values of group-I (oral cancer patients) and group-II (control group patients)

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   Discussion Top

The oral cavity is the site of the body where contact with exogenous material, microorganisms, and harmful agents like tobacco, alcohol, and areca nut are more intense. The oral mucosa functions as a mechanical as well as an immunological barrier. Protective mechanisms are noted in the form of increased capacity for epithelial regeneration and increased keratinization. These epithelial changes are reactive and reversible, but with progressive loss of normal control mechanisms, it leads to a precancerous state and oral cancer. [10]

The major risk factor for oral cancer includes tobacco, alcohol, and betel quid. Accordingly the geographic distribution of oral cancer is determined by these risk factors. Tobacco chewing and smoking have been identified as major risk factors for oral cancer in India. On account of a greater consumption of tobacco and betel quid in India, the incidence of oral cancer is high. [7],[11]

In the study group, 15 patients with oral cancer were in the age group of 35-80 years, with a mean age of 57.73 years and a standard deviation of 13.65. The male:female ratio was 1:1 in our study. All the oral cancer patients had deleterious oral habits, such as, smoking, alcohol, and tobacco chewing with betel nut. About 50% of the patients had a habit of both tobacco smoking, mostly in chutta (cigar) form, and alcohol. These are considered to be major etiological factors in oral cancer and precancerous lesions and conditions, in India.

The oral cancers in the case group were distributed in various sites of the oral cavity. The buccal mucosa and alveolus showed the highest incidence of involvement accounting for about 52%, and the rest of the sites noted were the floor of the mouth, retro-molar area including the buccal mucosa, hard palate, and the commissural area of the lip and tongue [Figure 1]. In our study, 67% of the patients with oral cancer were in stage IV, 33.3% were in stage III, with a tumor size of T2 in 33.3%, T3 in 7%, and T4 in 60%. Nodal involvement was noted in all the cases, with no distant metastasis [Figure 2].
Figure 1: Distribution of patients by site of involvement in oral cancer

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Figure 2: Distribution by staging in oral cancer patients

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The low levels of cholesterol may be due to the process of carcinogenesis. Cholesterol is an essential constituent of lipoprotein fractions like LDL, HDL, and VLDL. Seventy-five percent of the plasma cholesterol is transported in the form of LDL. LDL receptors are necessary for metabolizing and circulating LDL and nearly 80% of the plasma LDLs are cleared through these receptors. This results in reducing the plasma cholesterol levels. The deficient or defective LDL receptors remove plasma LDL at a lower rate, and hence, elevated levels of LDL are seen in the plasma. [2]

The decrease in HDL may be related to the utilization of cholesterol for membrane biogenesis. Peroxidation of the lipids is caused by exposure to oxygen, which is responsible for the damage to the tissue, which may cause cancer, inflammatory disease, atherosclerosis, and aging. Lipid peroxidation is an essential biochemical process that involves the oxidation of polyunsaturated fatty acids, an important component of cell membranes. [2] The elevated lipid peroxidation makes the tobacco carcinogens generate reactive oxygen species and lipid peroxides, leading to tissue injury (by damaging the cellular structural blocks like lipids, proteins, DNA, etc.). Hence, lipid peroxidation may play a role in the endogenous formation of exocyclic DNA adducts. [7]

Hypocholesterolemia has been observed in patients with various forms of cancer. Several retrospective and prospective studies in the past have shown an inverse relationship between cholesterol and incidence, and disease stage and mortality, in various malignancies of the head and neck, blood, prostate, brain, gastrointestinal tract (GIT), colorectal cancer, and lung cancers. However, no causative relation has been established so far and some authors believe that hypocholesterolemia is the result rather than the cause of cancer. Irrespective of the various hypotheses, hypocholesterolemia and the associating lipoprotein disorder were found to be constant findings in untreated cancer patients. [12] Hence, the present study was conducted to observe the relationship between lipid profile and oral cancer [Figure 3]. [13]
Figure 3: Total cholesterol profi le of patients

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In the present study, the plasma lipid profiles were estimated by the enzymatic method. The parameters that were considered were TC, HDL cholesterol, LDL cholesterol, VLDL, and TG levels. The TC level was slightly lower in oral cancer patients as compared to those in the controls, similar to the results obtained in the studies done by Jacqueline et al. and Simo Campus et al., who reported that lower cholesterol levels occurred in subjects with widespread disease rather than with localized tumors. [12] An inverse relation between the TC, and disease stage and mortality was observed in various malignancies. A lower level of TC was suggested due to the increased utilization by tumor cells. [8] A lower level of cholesterol was also noted in the blood malignancies. [13] A slightly lower level was observed in the plasma HDL cholesterol in oral cancer subjects [Figure 4]. This finding was in accordance with the previous reports, where low HDL was an additional predictor of cancer. Patel et al. stated that the lower HDL level may be a consequence of the disease that is mediated by utilization of cholesterol for membrane biogenesis. [8] Oral cancer patients had lower LDL levels than the controls. This lower level was not observed by Patel et al. in head and neck malignancies. Dianne Budd et al. stated that the levels of LDL appeared to be related to the activity of the disease. [14] Significantly higher VLDL levels were observed in oral cancer patients in our study compared to the control group, similar to the results obtained in a study on breast cancer patients; [15],[16] however, there was no statistical difference between the two groups. Significantly decreased triglyceride levels were observed in oral cancer in our study compared to the control group, which was similar to the findings of Patel et al. [8]
Figure 4: High-density lipoprotein profile of patients

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   Conclusion Top

In our study TC, HDL, LDL, and TG levels were slightly lower and the VLDL levels were significantly high in oral cancer patients as compared to the controls. The alterations in lipid profile patterns were associated with cancer as they played a vital role in the maintenance of cell integrity. Evaluation of plasma lipid profile patterns in oral cancer patients may aid in the early detection of the dreadful disease. The results from this study warrant a further in-depth research in a larger sample.

   References Top

1.Kumar V, Abbas A, Fausto N, editors. Robins and Cotran Pathologic Basis of Disease. 7 th ed. Philadelphia: Saunders Publications; 2004. p. 270-88.  Back to cited text no. 1
2.Breckenridge WC, Patten RL. Principles of Biochemistry. New Delhi, India: CBS Publications; 1982. p. 103-4.  Back to cited text no. 2
3.Park K. Park's Text Book of Preventive and Social Medicine. 16 th ed. Jabalpur, MP: Banarsidar Bhanot Publishers; 2000. p. 283-8.  Back to cited text no. 3
4.Prabhu SR, Wilson DF, Daftary DK, Johnson NW. Text Book of Oral Diseases in Tropics. USA: Oxford Medical Publications; 1992. p. 429-46.  Back to cited text no. 4
5.Reddi SP, Shafer AT. Oral premalignant lesions: Management considerations. Oral Maxillofac Surg Clin North Am 2006;18:425-33.  Back to cited text no. 5
6.Gupta PC, Mehta FS, Daftary DK, Pindborg JJ, Bhonsle RB, Jalnawalla PN, et al. Incidence rates of oral cancer and natural history of oral precancerous lesions in a 10-year follow up study of Indian villagers. Community Dent Oral Epidemiol 1980;8:283-333.  Back to cited text no. 6
7.Proia NK, Paszkiewicz GM, Nasca MA, Franke GE, Pauly JL. Smoking and smokeless tobacco-associated human buccal cell mutations and their association with oral cancer - A review. Cancer Epidemiol Biomarkers Prev 2006;15:1061-77.  Back to cited text no. 7
8.Patel PS, Shah MH, Jha FP, Raval GN, Rawal RM, Patel MM, et al. Alteration 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. 8
[PUBMED]  Medknow Journal  
9.Dia-Sys. Lipid profile reagents bio-chemical manual.  Back to cited text no. 9
10.Damm DD, Bouquot JE, Neville BW, Allen C. Oral and Maxillofacial Pathology. 2 nd ed. New Delhi, India: Elsevier; 2002. p. 337-45.  Back to cited text no. 10
11.Greenberg M, Click M, Ship JA. Burkets Oral medicine, diagnosis and treatment. 10 th ed. New Delhi, India: Elsevier; 2003. p. 194-234.  Back to cited text no. 11
12.Halton JM, Nazir DJ, McQueen MJ, Barr RD. Blood lipid profiles in children with acute lymphoblastic Leukemia. Cancer 1998;83:379-84.  Back to cited text no. 12
13.Gerhardsson M, Rosenqvist U, Ahlbom A, Carlson LA. Serumcholesterol and cancer - A retrospective case-control study. Int J Epidemiol 1986;15:155-9.  Back to cited text no. 13
14.Budd D, Ginsberg H. Hypocholesterolemia and acute myelogenousleukemia. Association between disease activity and plasma low-density lipoprotein cholesterol concentrations. Cancer 1986;58:1361-5.  Back to cited text no. 14
15.Agurs-Collins T, Kim KS, Dunston GM, Adams-Campbell LL. Plasma lipid alterations in African-American women with breast cancer. J Cancer Res Clin Oncol 1998;124:186-90.  Back to cited text no. 15
16.Cowan LD, O'Connell DL, Criqui MH, Barrett-Connor E, Bush TL, Wallace RB. Cancer mortality and lipid and lipoprotein levels. Lipid research clinics program mortality follow-up study. Am J Epidemiol 1990;131:468-82.  Back to cited text no. 16


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1]

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