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VOLUME 21 , ISSUE 8 ( August, 2020 ) > List of Articles

ORIGINAL RESEARCH

Salivary, Plasma, and Gingival Levels of Melatonin and TNF-α in Nonsmokers and Current Smokers with and without Periodontal Disease

Suresh R Rao

Citation Information : Rao SR. Salivary, Plasma, and Gingival Levels of Melatonin and TNF-α in Nonsmokers and Current Smokers with and without Periodontal Disease. J Contemp Dent Pract 2020; 21 (8):897-904.

DOI: 10.5005/jp-journals-10024-2858

License: CC BY-NC 4.0

Published Online: 28-12-2020

Copyright Statement:  Copyright © 2020; The Author(s).


Abstract

Aim: The aim of this study was to quantify the levels of gingival, salivary, and plasma melatonin and tumor necrosis factor-α (TNF-α) in healthy individuals and chronic generalized periodontitis patients with and without cigarette smoking habit and to investigate whether a relationship exists between melatonin and TNF-α levels in the samples. Materials and methods: Blood of 5 mL, 5 mL of saliva, and gingival tissue samples were obtained from 30 periodontally healthy individuals without smoking habit (HP), 30 nonsmoking patients with chronic generalized periodontitis (CP), 30 periodontally healthy individuals with current smoking habit (SHP), and 30 current smoker patients with chronic generalized periodontitis (SCP). The levels of melatonin and TNF-α in the samples were measured using commercially available enzyme-linked immunosorbent assay (ELISA) kit. The results obtained were statistically analyzed using SPSS statistical software (23.0 version). Results: This study demonstrated the presence of melatonin and TNF-α in all the saliva, plasma, and gingival tissue samples. Gingival tissue melatonin levels were highest in the HP group and least in the SCP groups, while TNF-α levels were least in the HP group and highest in the SCP groups. No significant difference was observed between the groups with regard to salivary and plasma melatonin. An overall significant difference was also observed between the groups with regard to salivary TNF-α but not with regard to plasma TNF-α. Binary logistic regression analysis was carried out after dividing the study groups into current smokers and nonsmokers. Results revealed that a reduction in gingival melatonin and an increase in gingival TNF-α were associated with a transition from periodontal health to chronic generalized periodontitis in current smokers but not in nonsmokers. Conclusion: This study sheds light on the anti-inflammatory actions of melatonin in the gingival tissues in states of periodontal health and disease in current smokers. Clinical significance: Melatonin could be used as a supplement to boost anti-inflammatory mechanisms in periodontal therapy especially in cigarette smokers.

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  1. Page R, Offenbacher S, Schroeder H, et al. Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontol 2000 1997;14(5): 216–248. DOI: 10.1111/j.1600-0757.1997.tb00199.x.
  2. Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: findings from NHANES III. National Health And Nutrition Examination Survey. J Periodontol 2000;71(5):743–751. DOI: 10.1902/jop.2000.71.5.743.
  3. Tappia PS, Troughton KL, Langley-Evans SC, et al. Cigarette smoking influences cytokine production and antioxidant defences. Clin Sci (Lond) 1995;88(4):485–489. DOI: 10.1042/cs0880485.
  4. Wajant H, Pfizenmaier K, Scheurich P. Tumor necrosis factor signaling. Cell Death Differ 2003;10(1):45–65. DOI: 10.1038/sj.cdd.4401189.
  5. Stashenko P, Jandinski JJ, Fujiyoshi P, et al. Tissue levels of bone resorptive cytokines in periodontal disease. J Periodontol 1991;62(8):504–509. DOI: 10.1902/jop.1991.62.8.504.
  6. Boström L, Linder LE, Bergström J. Clinical expression of TNF-alpha in smoking-associated periodontal disease. J Clin Periodontol 1998;25(10):767–773. DOI: 10.1111/j.1600-051x.1998.tb02368.x.
  7. Türer ÇC, Durmuş D, Balli U, et al. Effect of non-surgical periodontal treatment on gingival crevicular fluid and serum endocan, vascular endothelial growth factor-A, and tumor necrosis factor-alpha levels. J Periodontol 2017;88(5):493–501. DOI: 10.1902/jop.2016.160279.
  8. Reiter RJ. Pineal melatonin: cell biology of its synthesis and of its physiological interactions. Endocr Rev 1991;12(2):151–180. DOI: 10.1210/edrv-12-2-151.
  9. Shimozuma M, Tokuyama R, Tatehara S, et al. Expression and cellular localizaion of melatonin-synthesizing enzymes in rat and human salivary glands. Histochem Cell Biol 2011;135(4):389–396. DOI: 10.1007/s00418-011-0800-8.
  10. Zmijewski MA, Sweatman TW, Slominski AT. The melatonin-producing system is fully functional in retinal pigment epithelium (ARPE-19). Mol Cell Endocrinol 2009;307(1-2):211–216. DOI: 10.1016/j.mce.2009.04.010.
  11. Itoh MT, Ishizuka B, Kuribayashi Y, et al. Melatonin, its precursors, and synthesizing enzyme activities in the human ovary. Mol Hum Reprod 1999;5(5):402–408. DOI: 10.1093/molehr/5.5.402.
  12. Chojnacki C, Popławski T, Blasiak J, et al. Expression of melatonin synthesizing enzymes in helicobacter pylori infected gastric mucosa. Biomed Res Int 2013;2013:845032. DOI: 10.1155/2013/845032.
  13. Carrillo-Vico A, Calvo JR, Abreu P, et al. Evidence of melatonin synthesis by human lymphocytes and its physiological significance; possible role as intracrine, autocrine and/or paracrine substance. FASEB J 2004;18(3):537–539. DOI: 10.1096/fj.03-0694fje.
  14. Arzt ES, Fernández-Castelo S, Finocchiaro LME, et al. Immunomodulation by indoleamines: serotonin and melatonin action on DNA and interferon-gamma synthesis by human peripheral blood mononuclear cells. J Clin Immunol 1988;8(6):513–520. DOI: 10.1007/bf00916958.
  15. Xia MZ, Liang YL, Wang H, et al. Melatonin modulates TLR4-mediated inflammatory genes through MyD88- and TRIF-dependent signaling pathways in lipopolysaccharide-stimulated RAW264.7 cells. J Pineal Res 2012;53(4):325–334. DOI: 10.1111/j.1600-079X.2012.01002.x.
  16. Almughrabi OM, Marzouk KM, Hasanato RM, et al. Melatonin levels in periodontal health and disease. J Periodontal Res 2013;48(3):315–321. DOI: 10.1111/jre.12010.
  17. Srinath R, Acharya AB, Thakur SL. Salivary and gingival crevicular fluid melatonin in periodontal health and disease. J Periodontol 2010;81(2):277–283. DOI: 10.1902/jop.2009.090327.
  18. Balaji TM, Vasanthi HR, Rao SR. Gingival, plasma and salivary levels of melatonin in periodontally healthy individuals and chronic periodontitis patients: a pilot study. J Clin Diagn Res 2015;9(3): ZC23–ZC25. DOI: 10.7860/JCDR/2015/11311.5652.
  19. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4(1):1–6. DOI: 10.1902/annals.1999.4.1.1.
  20. Centers for Disease Control and Prevention. Health topic data guide: alcohol use in past 30 days, smoking status [Internet] Atlanta: Centers for Disease Control and Prevention; [cited 2015 Feb 12].
  21. Löe H. The gingival index, the plaque index and the retention index systems. J Periodontol 1967;38(6):610–616. DOI: 10.1902/jop.1967.38.6.610.
  22. Lenox JA, Kopczyk RA. A clinical system for scoring a patient's oral hygiene performance. J Am Dent Assoc 1973;86(4):849–852. DOI: 10.14219/jada.archive.1973.0178.
  23. Abdolsamadi H, Goodarzi MT, Ahmadi Motemayel F, et al. Reduction of melatonin level in patients with type II diabetes and periodontal diseases. J Dent Res Dent Clin Dent Prospects 2014;8(3):160–165. DOI: 10.5681/joddd.2014.029.
  24. Ismail AI, Burt BA, Eklund SA. Epidemiologic patterns of smoking and periodontal disease in the United States. J Am Dent Assoc 1983;106(5):617–621. DOI: 10.14219/jada.archive.1983.0137.
  25. Grossi SG, Genco RJ, Machtet EE, et al. Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol 1995;66(1):23–29. DOI: 10.1902/jop.1995.66.1.23.
  26. Kraal JH, Kenney EB. The response of polymorphonuclear leukocytes to chemotactic stimulation for smokers and non-smokers. J Periodontal Res 1979;14(5):383–389. DOI: 10.1111/j.1600-0765.1979.tb00235.x.
  27. Pabst MJ, Pabst KM, Collier JA, et al. Inhibition of neutrophil and monocyte defensive functions by nicotine. J Periodontol 1995;66(12):1047–1055. DOI: 10.1902/jop.1995.66.12.1047.
  28. Sharma S, Haldar C. Melatonin prevents X-ray irradiation induced oxidative damage in peripheral blood and spleen of the seasonally breeding rodent, Funambulus pennant during reproductively active phase. Int J Radiat Biol 2006;82(6):411–419. DOI: 10.1080/09553000600774105.
  29. Moller DE. Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. Trends Endocrinol Metab 2000;11(6):212–217. DOI: 10.1016/s1043-2760(00)00272-1.
  30. Sack M. Tumor necrosis factor-alpha in cardiovascular biology and the potential role for anti-tumor necrosis factor-alpha therapy in heart disease. Pharmacol Ther 2002;94(1-2):123–135. DOI: 10.1016/s0163-7258(02)00176-6.
  31. Alijotas-Reig J, Esteve-Valverde E, Ferrer-Oliveras R, et al. Tumor necrosis factor-alpha and pregnancy: focus on biologics. An updated and comprehensive review. Clin Rev Allergy Immunol 2017;53(1): 40–53. DOI: 10.1007/s12016-016-8596-x.
  32. Battino M, Bompadre S, Politi A, et al. Antioxidant status (CoQ10 and Vit. E levels) and immunohistochemical analysis of soft tissues in periodontal diseases. Biofactors 2008;25(1-4):213–217. DOI: https://doi.org/10.1002/biof.5520250126.
  33. Baltacıoğlu E, Yuva P, Aydın G, et al. Lipid peroxidation levels and total oxidant/antioxidant status in serum and saliva from patients with chronic and aggressive periodontitis. Oxidative stress index: a new biomarker for periodontal disease? J Periodontol 2014;85(10): 1432–1441. DOI: 10.1902/jop.2014.130654.
  34. Tüter G, Kurtiş B, Serdar M. Interleukin-1beta and thiobarbituric acid reactive substance (TBARS) levels after phase I periodontal therapy in patients with chronic periodontitis. J Periodontol 2001;72(7):883–888. DOI: 10.1902/jop.2001.72.7.883.
  35. Tsai CC, Chen HS, Chen SL, et al. Lipid peroxidation: a possible role in the induction and progression of chronic periodontitis. J Periodontal Res 2005;40(5):378–384. DOI: 10.1111/j.1600-0765.2005.00818.x.
  36. Tan DX, Manchester LC, Reiter RJ, et al. A novel melatonin metabolite, cyclic 3-hydroxymelatonin: a biomarker of in vivo hydroxyl radical generation. Biochem Biophys Res Commun 1998;253(3):614–620. DOI: 10.1006/bbrc.1998.9826.
  37. Fernandes PA, Cecon E, Markus RP, et al. Effect of TNF-alpha on the melatonin synthetic pathway in the rat pineal gland: basis for a ‘feedback’ of the immune response on circadian timing. J Pineal Res 2006;41(4):344–350. DOI: 10.1111/j.1600-079X.2006.00373.x.
  38. Pontes GN, Cardoso EC, Carneiro-Sampaio MM, et al. Injury switches melatonin production source from endocrine (pineal) to paracrine (phagocytes) - melatonin in human colostrum and colostrum phagocytes. J Pineal Res 2006;41(2):136–141. DOI: 10.1111/j.1600-079X.2006.00345.x.
  39. Choi EY, Jin JY, Lee JY, et al. Melatonin inhibits Prevotella intermedia lipopolysaccharide-induced production of nitric oxide and interleukin-6 in murine macrophages by suppressing NF-κB and STAT1 activity. J Pineal Res 2011;50(2):197–206. DOI: 10.1111/j.1600-079X.2010.00829.x.
  40. Huang SH, Cao XJ, Wei W. Melatonin decreases TLR3-mediated inflammatory factor expression via inhibition of NF-kappa B activation in respiratory syncytial virus-infected RAW264.7 macrophages. J Pineal Res 2008;45(1):93–100. DOI: 10.1111/j.1600-079X.2008.00560.x.
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