Biju Thomas, Sudhir Varma, Rajendra Prasad, Maher A.L Shayeb, Moutassem B M khair, Abed M. A Elkaseh, Emad S. Elsubeihi, Moyad Shahwan
Biju Thomas1, Sudhir Varma2,8*, Rajendra Prasad3, Maher A.L Shayeb4,8, Moutassem B M khair5,8, Abed M. A Elkaseh4,8, Emad S. Elsubeihi6,8, Moyad Shahwan7,8
1Department of Periodontics, A B Shetty Memorial Institute of Dental Sciences, Nitte,
(Deemed to be University), Mangalore–575018.
2,8Department of Clinical Sciences, College of Dentistry, Ajman University, Ajman, U.A.E.
3Department of Oral and Maxillofacial Surgery, A B Shetty Memorial Institute of Dental Sciences,
Nitte (Deemed to be University), Mangalore–575018.
4,8Department of Clinical Sciences, College of Dentistry, Ajman University, Ajman, U.A. E
5,8Department of Basic Sciences, College of Dentistry, Ajman University, Ajman, U.A. E
6,8Department of Clinical Sciences, College of Dentistry, Ajman University, Ajman, U.A. E
7,8Department of Clinical Sciences, College of Pharmacy and Health Sciences, Ajman University, Ajman, U.A.E.
8Centre of Medical and Bio-Allied Health Sciences Research, Ajman University, Aj
Volume - 14,
Issue - 2,
Year - 2021
Background: Periodontal disease and diabetes mellitus (DM) have a two-way relationship, the former being a major complication of the latter. However, while hyperglycemia has been identified as a factor activating oxidative stress, the role of antioxidants in periodontal disease is not fully understood. Objective: The purpose of this study was to determine the involvement of antioxidant enzymes in the systemic effects of chronic periodontitis and to assess their role as disease biomarkers. Method: Peripheral blood was collected from the antecubital vein. DTNB (5,5'-dithiobis (2-nitrobenzonic acid), Beauchamp and Fridovich, hydrogen peroxide reduction, and phosphomolybdenum assays were used to determine superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and total antioxidant (TAOC) levels; respectively; from the sera of chronic periodontitis patients with or without DM type II and from healthy controls. Results: Serum SOD levels were significantly higher (p < 0.001) in healthy controls (group III) than those in periodontitis patients with DM (group II), which in turn were significantly higher than those in periodontitis patients without DM (Group 1). GSH, CAT, and TAOC levels were significantly higher (p < 0.001) in group III than those in groups I and II, but CAT and TAOC levels were not significantly different between groups I and II. Conclusion: Antioxidant levels decrease in chronic disease conditions such as periodontitis with and without systemic diseases such as DM. Therefore, they are potentially effective biomarkers of chronic periodontitis. Moreover, periodontal disease might not be confined to the periodontium and could have systemic effects.
Cite this article:
Biju Thomas, Sudhir Varma, Rajendra Prasad, Maher A.L Shayeb, Moutassem B M khair, Abed M. A Elkaseh, Emad S. Elsubeihi, Moyad Shahwan. Assessment of the Antioxidant Levels in Sera of Periodontitis patients with or without Diabetes Mellitus. Research J. Pharm. and Tech. 2021; 14(2):1025-1032. doi: 10.5958/0974-360X.2021.00183.9
1. Kornman KS. Mapping the pathogenesis of periodontitis: a new look. J Periodontol. 2008; 79: 1560-1568.
2. Mathews JB, et al. Neutrophil hyper-responsiveness in periodontitis. J Dent Res. 2007; 86: 718-721.
3. Ali D, Abduelkarem AR, Shahwan M. Evaluation of factors associated with inadequate glycemic control and some other health care indicators among patients with type 2 diabetes in Ramallah. Res J Pharm Biol Chem Sci 2013;4(3):445e51.
4. Mealey BL, Oates TW. Diabetes mellitus and periodontal diseases. J Periodontol. 2006; 77: 1289-1303.
5. Al Amiry A, Shahwan M. Vitamin D deficiency and associated factors among Ajman University students, United Arab Emirates. Obesity Medicine. 2020 Mar 1;17:100176.
6. Halliwell B. Reactive oxygen species in living systems: source, biochemistry, and role in human disease. Am J Med. 1991; 91(3): 14-22.
7. Zhang T, et al. Total antioxidant capacity and total oxidant status in saliva of periodontitis patients in relation to bacterial load. Front Cell Infect Microbiol. 2016; 5: 97.
8. Shahwan MJ, galil Hassan NA, Shaheen RA. Assessment of kidney function and associated risk factors among type 2 diabetic patients. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 2019 Jul 1;13(4):2661-5.
9. Öngöz Dede F, et al. Glutathione levels in plasma, saliva and gingival crevicular fluid after periodontal therapy in obese and normal weight individuals. J Periodontal Res. 2016; 51(6): 726-734.
10. Lee CY, et al. Associations between the phenotype and genotype of MnSOD and catalase in periodontal disease. BMC Oral Health. 2019; 19(1): 201.
11. Atabay VE, et al. Obesity and oxidative stress in patients with different periodontal status: a case-control study. J Periodontal Res. 2017; 52(1): 51-60.
12. Chapple IL, Milward MR, Dietrich T. The prevalence of inflammatory periodontitis is negatively associated with serum antioxidant concentrations. J Nutrition. 2007; 137(3): 657-664.
13. Eke PI, et al. Advances in surveillance of periodontitis: the Centers for Disease Control and Prevention periodontal disease surveillance project. J Periodontol. 2012; 83(11): 1337-1342.
14. Al-Qirim TM, Shahwan M, Zaidi KR, Uddin Q, Banu N. Effect of khat, its constituents and restraint stress on free radical metabolism of rats. Journal of ethnopharmacology. 2002 Dec 1;83(3):245-50.
15. Arana C, et al. Increased salivary oxidative stress parameters in patients with type 2 diabetes: relation with periodontal disease. Endocrinol Diabetes Nutr. 2017; 64(5): 258-264.
16. Gümüş P, et al. Oxidative stress markers in saliva and periodontal disease status: modulation during pregnancy and postpartum. BMC Infect Dis. 2015; 15(1): 261.
17. West IC. Radicals and oxidative stress in diabetes. Diabet Med. 2000; 17: 171-180.
18. Villa-Correa YA, Isaza-Guzmán DM, Tobón-Arroyave SI. Influence of periodontal clinical status on salivary levels of glutathione reductase. J Periodontol. 2016; 87(6): 716-724.
19. Sechi LA, et al. Renal antioxidant enzyme mRNA levels are increased in rats with experimental diabetes mellitus. Diabetologia. 1997; 40(1): 23-29.
20. Bansal N, et al. Impact of nonsurgical periodontal therapy on total antioxidant capacity in chronic periodontitis patients. J Indian Soc Periodontol. 2017; 21(4): 291-295.
21. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001; 414: 813-820.
22. Petelin M, et al. Local delivery of liposome-encapsulated superoxide dismutase and catalase suppress periodontal inflammation in beagles. J Clin Periodontol. 2000; 27(12): 918-925.
23. Akalin FA, Toklu E, Renda N. Analysis of superoxide dismutase activity levels in gingiva and gingival crevicular fluid in patients with chronic periodontitis and periodontally healthy controls. J Clin Periodontol. 2005; 32(3): 238-243.
24. Memisogullari R, et al. Effect of metformin or gliclazide on lipid peroxidation and antioxidant levels in patients with diabetes mellitus. Turk J Med Sci. 2008; 38(6): 545-548.
25. Cueno ME, Ochiai K. Gingival periodontal disease (PD) level-butyric acid affects the systemic blood and brain organ: insights into the systemic inflammation of periodontal disease. Front Immunol. 2018; 9: 1158.
26. Pavlović D, et al. Effect of four-week metformin treatment on plasma and erythrocyte antioxidative defense enzymes in newly diagnosed obese patients with type 2 diabetes. Diabetes Obes Metab. 2000; 2(4): 251-256.
27. Jacoby BH, Davis WL. The electron microscopic immunolocalization of copper-zinc superoxide dismutase in association with collagen fibers of periodontal soft tissues. J Periodontol. 1991; 62(7): 413-420.
28. Ellis SD, et al. Factors for progression of periodontal diseases. J Oral Path Med. 1998; 27(3): 101-105.
29. Misaki H, et al. The effect of superoxide dismutase on the inflammation induced by periodontal pathogenic bacteria and wound healing of gingival incisors. J Jpn Assoc Periodontol. 1990; 32(1): 93-110.
30. Evans JL, et al. Oxidative stress and stress-activated signaling pathways: A unifying hypothesis of type 2 diabetes. Endocr Rev. 2002; 23(5): 599-622.
31. Carmeli E, Coleman R, Berner YN. Activities of antioxidant scavenger enzymes (superoxide dismutase and glutathione peroxidase) in erythrocytes in adult women with and without type II diabetes. Exp Diabesity Res. 2004; 5(2): 171-175.
32. Engebretson SP, et al. Gingival crevicular fluid levels of interleukin-1beta and glycemic control in patients with chronic periodontitis and type 2 diabetes. J Periodontol. 2004; 75(9): 1203-208.