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VOLUME 20 , ISSUE 8 ( August, 2019 ) > List of Articles

ORIGINAL RESEARCH

Clinical and Biochemical Valuation of Enzymatic and Nonenzymatic Stress Markers Following Full-mouth Disinfection in Aggressive Periodontitis

Rajeev Arunachalam, Vini Rajeev, Ramesh Kumaresan, Sarath B Kurra

Keywords : Aggressive periodontitis, Antioxidants, Biomarkers, Full-mouth disinfection

Citation Information : Arunachalam R, Rajeev V, Kumaresan R, Kurra SB. Clinical and Biochemical Valuation of Enzymatic and Nonenzymatic Stress Markers Following Full-mouth Disinfection in Aggressive Periodontitis. J Contemp Dent Pract 2019; 20 (8):952-956.

DOI: 10.5005/jp-journals-10024-2622

License: CC BY-NC 4.0

Published Online: 01-04-2019

Copyright Statement:  Copyright © 2019; The Author(s).


Abstract

Introduction: Assessment of host response to inflammation will throw light on the critical role of antioxidants (AOs) and free radicle damage in the etiology of periodontal disease. The purpose of the study was to assess the level of plasma oxidative stress in those having aggressive periodontal disease before and after full-mouth disinfection. Objectives were to find the influence of full-mouth disinfection analyzing the level of thiobarbituric acid reactive substances (TBARSs), thereby quantifying the lipid peroxidation (LPO) and also the activities of reduced glutathione (GSH), glutathione peroxidase (GPX), and catalase (CAT), valuing the AO defense systems in health and disease. Materials and methods: The valuation composed of 30 subjects with aggressive periodontal disease and 30 healthy controls. Clinical assessment included following periodontal parameters: plaque index (PI), papillary bleeding index (PBI), probing pocket depth (PPD), and clinical attachment level (CAL). Levels of bone loss were assessed by taking full-mouth periapical radiographs. Initial periodontal therapy comprises of full-mouth disinfection which includes subgingival scaling and root planing within 24 hours combined with adjunctive chlorhexidine chemotherapy for aggressive periodontitis subject's at sites indicated. The parameters (clinical) were evaluated at the baseline and 8 weeks after initial periodontal therapy at six sites of teeth indicated. Plasma samples were taken and evaluated by standard procedures as defined in the literature. All the values were weighed and related. Results: Strong positive associations were detected among periodontal parameters and TBARS, enzymatic/nonenzymatic AO levels (p < 0.05), and pre- and postperiodontal management. The plasma levels of patients with aggressive periodontitis had high levels of TBARS and displayed a substantial escalation in the activities of GSH and GPX levels in the plasma matched to the healthy individuals (p < 0.05). Conclusion: This paper evaluated ROS activity and AO defense before and after treatment to stimulate added periodontal investigation in this part which will give an insight into the therapeutic options with foreseeable results.

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  1. The American Academy of Periodontology. Proceedings of the World Workshop in Clinical Periodontics. Chicago: The American Academy of Periodontology; 1989.
  2. Laine ML, Crielaard W, et al. Genetic susceptibility to periodontitis. Periodontol 2000 2012 Feb;58(1):37–68. DOI: 10.1111/j.1600-0757.2011.00415.x.
  3. Kornman KS. Mapping the pathogenesis of periodontitis: a new look. J Periodontol 2008 Aug;79(8 Suppl):1560–1568. DOI: 10.1902/jop.2008.080213.
  4. Serhan CN, Yacoubian S, et al. Anti-inflammatory and proresolving lipid mediators. Ann Rev Pathol 2008;3:279–312. DOI: 10.1146/annurev.pathmechdis.3.121806.151409.
  5. Chapplle IL, Matthews JB. The role of reactive oxygen and antioxidant species in periodontal tissue destruction. Periodontol 2000 2007;43:160–232. DOI: 10.1111/j.1600-0757.2006.00178.x.
  6. Konopka T, Krol K, et al. Total antioxidant status and 8-hydroxy-2′-deoxyguanosine levels in gingival and peripheral blood of periodontitis patients. Arch Immunol Ther Exp (Warsz) 2007 Dec;55(6):417–425. DOI: 10.1007/s00005-007-0047-1.
  7. Kantarci A, Oyaizu K, et al. Neutrophil-mediated tissue injury in periodontal disease pathogenesis: Findings from localized aggressive periodontitis. J Periodontol 2003 Jan;74(1):66–75. DOI: 10.1902/jop.2003.74.1.66.
  8. Dias IH, Matthews JB, et al. Activation of the neutrophil respiratory burst by plasma from periodontitis patients is mediated by pro-inflammatory cytokines. J Clin Periodontol 2011 Jan;38(1):1–7. DOI: 10.1111/j.1600-051X.2010.01628.x.
  9. Matthews JB, Wright HJ, et al. Neutrophil hyper-responsiveness in periodontitis. J Dent Res 2007 Aug;86(8):718–722. DOI: 10.1177/154405910708600806.
  10. Brock GR, Butterworth CJ, et al. Local and systemic total antioxidant capacity in periodontitis and health. J Clin Periodontol 2004 Jul;31(7):515–521. DOI: 10.1111/j.1600-051X.2004.00509.x.
  11. Chapple IL, Brock GR, et al. Compromised GCF total antioxidant capacity in periodontitis: cause or effect? J Clin Periodontol 2007 Feb;34(2):103–110. DOI: 10.1111/j.1600-051X.2006.01029.x.
  12. Ohshima H, Pignatelli B, et al. Analysis of oxidized and nitrated proteins in plasma and tissues as biomarkers for exposure to reactive oxygen and nitrogen species. IARC Sci Publ 2002;156:393–394.
  13. Schisterman EF, Faraggi D, et al. Minimal and best linear combination of oxidative stress and antioxidant biomarkers to discriminate cardiovascular disease. Nutr Metab Cardiovasc Dis 2002 Oct;12(5): 259–266.
  14. Canakçi CF, Ciçek Y, et al. Reactive oxygen species and human inflammatory periodontal diseases. Biochemistry (Mosc) 2005 Jun;70(6):619–628.
  15. Luliano L, Micheletta F, et al. Measurement of oxysterols and tocopherol in plasma and tissue samples as indices of oxidant stress status. Anal Biochem 2003 Jan;312(2):217–223. DOI: 10.1016/s0003-2697(02)00467-0.
  16. Jacob RA, Aiello GM, et al. Moderate antioxidant supplementation has no effect on biomarkers of oxidative damage in healthy men with low fruit and vegetable intakes. J Nutr 2003 March;133(3):740–743. DOI: 10.1093/jn/133.3.740.
  17. Lim PS, Chang YM, et al. 8-Iso-Prostaglandin F2alpha as a useful clinical biomarker of oxidative stress in ESRD patients. Blood Purif 2002;20:537–542. DOI: 10.1159/000066962.
  18. Milbury P, Blumberg JB. Dietary antioxidants—human studies overview. In: Rodriguez H, Cutler RG. ed. Critical Reviews of Oxidative Stress and Aging: Advances in Basic science, Diagnostics and Intervention. River Edge, NJ: World Scientific Publishing; 2003. pp. 487–502.
  19. Tahara EB, Navarete FD, et al. Tissue-, substrate-, and site-specific characteristics of mitochondrial reactive oxygen species generation. Free Radic Biol Med 2009;46:1283–1297. DOI: 10.1016/j.freeradbiomed.2009.02.008.
  20. Dröge W. Free radicals in the physiological control of cell function. Physiol Rev 2002 Jan;82(1):47–95. DOI: 10.1152/physrev.00018.2001.
  21. Chapple IL. Reactive oxygen species and antioxidants in inflammatory diseases. J Clin Periodontol 1997 May;24(5):287–296.
  22. Sies H. Oxidative stress: oxidants and antioxidants. Exp Physiol 1997 Mar;82(2):291–295.
  23. Armitage GC. Development of a classification system for periodontal disease and conditions. Ann Periodontal 1999 Dec;4(1):1–6. DOI: 10.1902/annals.1999.4.1.1.
  24. Alpagot T, Wolff LF, et al. Risk indicators for periodontal disease in a racially diverse urban population. J Clin Periodontol 1996 Nov;23(11):982–988.
  25. Silness J, Loe H. Periodontal disease in pregnancy. Correlation between oral hygiene and periodontal condition. Acta Odontol Scand 1964 Feb;22:121–135.
  26. Muhlemann HR. Psychological and chemical mediators of gingival health. J Prev Dent 1997 Jul-Aug;4(4):6–17.
  27. Grant DA, Irving B, et al. Periodontics, 6th ed., CV Mosby and Co.; 1988. pp. 525–572.
  28. Carranza AF, Newman MG, et al. Clinical Periodontology, 9th ed., 2002. pp. 432–453.
  29. Quirynen M, De Soete M, et al. Benefit of “one-stage full-mouth disinfection” is explained by disinfection and root planing within 24 hours: a randomized controlled trial. J Clin Periodontol 2006 Sep;33(9):639–647. DOI: 10.1111/j.1600-051X.2006.00959.x.
  30. Ohkawa H, Ohishi N, et al. Assay for lipid peroxides in animal tissue by thiobarbituric acid reaction. Anal Biochem 1979 Jun;95(2):351–358. DOI: 10.1016/0003-2697(79)90738-3.
  31. Moron MS, Depierre JW, et al. Levels of glutathione reductase and glutathione –s-transferase activities in rat lung and liver. Biochim Biophys Acta 1979 Jan;582(1):67–78.
  32. Sinha AK. Calorimetric assay of catalase. Anal Biochem 1972 Jun;47(2):389–394. DOI: 10.1016/0003-2697(72)90132-7.
  33. Rotruck JT, Pope AL, et al. Selenium: Biochemical role as a compound of glutathione peroxidase purification and assay. Science 1973 Feb;179(4073):588–590. DOI: 10.1126/science.179.4073.588.
  34. Whyte G, Seymour GJ, et al. Chemiluminescence of peripheral polymorphonuclear leukocytes from adult periodontitis patients. J Clin Periodontol 1989 Feb;16(2):69–74.
  35. Sochaski M, Bartfay WJ, et al. Lipid peroxidation and protein modification in a Mouse model of chronic iron overload. Metabolism 2002;51(5):645–651. DOI: 10.1053/meta.2002.30530.
  36. Tsai CC, Chen HS, et al. Lipid peroxidation: a possible role in the induction and progression of chronic periodontitis. J Periodontal Res 2005 Oct;40(5):378–384. DOI: 10.1111/j.1600-0765.2005.00818.x.
  37. Borges Jr I, Moreira E, et al. Proinflammatory and oxidative stress markers in patients with periodontal disease. Mediators Inflamm 2007 2007:45794.
  38. Kolanjiappan K, Manoharan S, et al. Measurement of erythrocyte lipids, lipid peroxidation, antioxidants and osmotic fragility in cervical cancer patients. Clin Chim Acta 2002 Dec;326(1):143–149. DOI: 10.1016/s0009-8981(02)00300-5.
  39. Gutteridge JMC. Lipid peroxidation and antioxidants as biomarkers of tissue damage. Clin Chem 1995 Dec;41(12):1819–1828.
  40. Nagini S, Saroja M. Circulating lipid peroxides and antioxidants as biomarkers of tumour burden in patients with oral squamous cell carcinoma. J Biochem Mol Biol Biophys 2001;5:55–59.
  41. Guyton KZ, Kensler TW. Oxidative mechanisms in carcinogenesis. Br Med Bull 1993 July;49(3):523–544. DOI: 10.1093/oxfordjournals.bmb.a072628.
  42. Halliwell B, Gutteridge JMC. Free radicals, other reactive species and diseases. Free Radicals in Biology and Medicine, 3rd ed. Oxford, UK: Clarendon Press; 1999. pp. 617–783.
  43. Halliwell B, Gutteridge JMC. The chemistry of free radicals and related reactive species. Free Radicals in Biology and Medicine, 3rd ed. Oxford, UK: Clarendon Press; 1999. pp. 36–104.
  44. Chapple IL, Brock G, et al. Glutathione in gingival crevicular fluid and its relation to local antioxidant capacity in periodontal health and disease. Mol Pathol 2002 Dec;55(6):367–373. DOI: 10.1136/mp.55.6.367.
  45. Panjamurthy K, Manoharan S, et al. Lipid peroxidation and antioxidant status in patients with periodontitis. Cell Mol Biol Lett 2005;10(2): 255–264.
  46. Matés JM, Pérez-Gómez C, et al. Antioxidant enzymes and human diseases. Clin Biochem 1999;32:595–603.
  47. Sakallioğlu U, Aliyev E, et al. Reactive oxygen species scavenging activity during periodontal mucoperiosteal healing: an experimental study in dogs. Arch Oral Biol 2005 Dec;50(12):1040–1046. DOI: 10.1016/j.archoralbio.2005.03.012.
  48. Cheeseman KH, Slater TF. An introduction to free radical biochemistry. Br Med Bull 1993;49(3):481–493. DOI: 10.1093/oxfordjournals.bmb.a072625.
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