Salivary antioxidants as periodontal biomarkers in evaluation of tissue status and treatment outcome

Background and objective One of the major pathologic patterns in periodontitis represents an imbalance among the production of free radicals and local antioxidants resulting in periodontal tissue destruction. The objective of the study was to investigate the influence of non‐surgical periodontal tre...

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Published inJournal of periodontal research Vol. 49; no. 1; pp. 129 - 136
Main Authors Novakovic, N., Todorovic, T., Rakic, M., Milinkovic, I., Dozic, I., Jankovic, S., Aleksic, Z., Cakic, S.
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.02.2014
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ISSN0022-3484
1600-0765
1600-0765
DOI10.1111/jre.12088

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Abstract Background and objective One of the major pathologic patterns in periodontitis represents an imbalance among the production of free radicals and local antioxidants resulting in periodontal tissue destruction. The objective of the study was to investigate the influence of non‐surgical periodontal treatment on salivary antioxidants and to evaluate their capacity as biomarkers reflecting periodontal tissue condition and therapy outcome. Material and Methods Sixty‐three systemically healthy non‐smokers, including 21 periodontally healthy subjects (HC) and 42 patients with current chronic periodontitis fulfilled the inclusion criteria. Half of the patients received scaling and root planing (SRP) and the other half received only oral hygiene instructions. Full mouth clinical measurements, including gingival index (GI), plaque index (PI), periodontal pocket depth, clinical attachment level and saliva sampling were performed at baseline visit and 2 mo after treatment/baseline visit. Total antioxidant capacity (TAOC), albumins (ALB), uric acid (UA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were evaluated in saliva samples using commercial kits. Results All measured antioxidants were affected by treatment resulting in significant increase in TAOC (p < 0.005), ALB (p < 0.001), UA (p < 0.001) and GPX (p < 0.001) and decrease of SOD (p < 0.005) in response to SRP, where no differences were observed for any of parameters in the oral hygiene instructions group. Comparison of antioxidant levels between the HC and SRP group showed that before treatment ALB were significantly higher in HC when compared to the SRP group (p = 0.039), and GXP (p = 0.000) and SOD (p = 0.021) levels were significantly higher in the SRP group. Comparison of values after treatment showed that TAOC was significantly higher in the HC than in the SRP group (p = 0.001), but UA was, inversely, significantly higher in the SRP group (p = 0.034). All clinical parameters except clinical attachment level were significantly decreased after SRP and significant correlations were observed between SOD and GI (p = 0.017), SOD and PI (p = 0.011), GPX and GI (p = 0.003) and GPX and PI (p = 0.008). Conclusion Non‐surgical periodontal treatment affected salivary TAOC, ALB, UA, SOD and GPX; moreover, these biochemical parameters convincingly reflected periodontal status and tissue response on treatment.
AbstractList One of the major pathologic patterns in periodontitis represents an imbalance among the production of free radicals and local antioxidants resulting in periodontal tissue destruction. The objective of the study was to investigate the influence of non-surgical periodontal treatment on salivary antioxidants and to evaluate their capacity as biomarkers reflecting periodontal tissue condition and therapy outcome.BACKGROUND AND OBJECTIVEOne of the major pathologic patterns in periodontitis represents an imbalance among the production of free radicals and local antioxidants resulting in periodontal tissue destruction. The objective of the study was to investigate the influence of non-surgical periodontal treatment on salivary antioxidants and to evaluate their capacity as biomarkers reflecting periodontal tissue condition and therapy outcome.Sixty-three systemically healthy non-smokers, including 21 periodontally healthy subjects (HC) and 42 patients with current chronic periodontitis fulfilled the inclusion criteria. Half of the patients received scaling and root planing (SRP) and the other half received only oral hygiene instructions. Full mouth clinical measurements, including gingival index (GI), plaque index (PI), periodontal pocket depth, clinical attachment level and saliva sampling were performed at baseline visit and 2 mo after treatment/baseline visit. Total antioxidant capacity (TAOC), albumins (ALB), uric acid (UA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were evaluated in saliva samples using commercial kits.MATERIAL AND METHODSSixty-three systemically healthy non-smokers, including 21 periodontally healthy subjects (HC) and 42 patients with current chronic periodontitis fulfilled the inclusion criteria. Half of the patients received scaling and root planing (SRP) and the other half received only oral hygiene instructions. Full mouth clinical measurements, including gingival index (GI), plaque index (PI), periodontal pocket depth, clinical attachment level and saliva sampling were performed at baseline visit and 2 mo after treatment/baseline visit. Total antioxidant capacity (TAOC), albumins (ALB), uric acid (UA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were evaluated in saliva samples using commercial kits.All measured antioxidants were affected by treatment resulting in significant increase in TAOC (p < 0.005), ALB (p < 0.001), UA (p < 0.001) and GPX (p < 0.001) and decrease of SOD (p < 0.005) in response to SRP, where no differences were observed for any of parameters in the oral hygiene instructions group. Comparison of antioxidant levels between the HC and SRP group showed that before treatment ALB were significantly higher in HC when compared to the SRP group (p = 0.039), and GXP (p = 0.000) and SOD (p = 0.021) levels were significantly higher in the SRP group. Comparison of values after treatment showed that TAOC was significantly higher in the HC than in the SRP group (p = 0.001), but UA was, inversely, significantly higher in the SRP group (p = 0.034). All clinical parameters except clinical attachment level were significantly decreased after SRP and significant correlations were observed between SOD and GI (p = 0.017), SOD and PI (p = 0.011), GPX and GI (p = 0.003) and GPX and PI (p = 0.008).RESULTSAll measured antioxidants were affected by treatment resulting in significant increase in TAOC (p < 0.005), ALB (p < 0.001), UA (p < 0.001) and GPX (p < 0.001) and decrease of SOD (p < 0.005) in response to SRP, where no differences were observed for any of parameters in the oral hygiene instructions group. Comparison of antioxidant levels between the HC and SRP group showed that before treatment ALB were significantly higher in HC when compared to the SRP group (p = 0.039), and GXP (p = 0.000) and SOD (p = 0.021) levels were significantly higher in the SRP group. Comparison of values after treatment showed that TAOC was significantly higher in the HC than in the SRP group (p = 0.001), but UA was, inversely, significantly higher in the SRP group (p = 0.034). All clinical parameters except clinical attachment level were significantly decreased after SRP and significant correlations were observed between SOD and GI (p = 0.017), SOD and PI (p = 0.011), GPX and GI (p = 0.003) and GPX and PI (p = 0.008).Non-surgical periodontal treatment affected salivary TAOC, ALB, UA, SOD and GPX; moreover, these biochemical parameters convincingly reflected periodontal status and tissue response on treatment.CONCLUSIONNon-surgical periodontal treatment affected salivary TAOC, ALB, UA, SOD and GPX; moreover, these biochemical parameters convincingly reflected periodontal status and tissue response on treatment.
One of the major pathologic patterns in periodontitis represents an imbalance among the production of free radicals and local antioxidants resulting in periodontal tissue destruction. The objective of the study was to investigate the influence of non-surgical periodontal treatment on salivary antioxidants and to evaluate their capacity as biomarkers reflecting periodontal tissue condition and therapy outcome. Sixty-three systemically healthy non-smokers, including 21 periodontally healthy subjects (HC) and 42 patients with current chronic periodontitis fulfilled the inclusion criteria. Half of the patients received scaling and root planing (SRP) and the other half received only oral hygiene instructions. Full mouth clinical measurements, including gingival index (GI), plaque index (PI), periodontal pocket depth, clinical attachment level and saliva sampling were performed at baseline visit and 2 mo after treatment/baseline visit. Total antioxidant capacity (TAOC), albumins (ALB), uric acid (UA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were evaluated in saliva samples using commercial kits. All measured antioxidants were affected by treatment resulting in significant increase in TAOC (p < 0.005), ALB (p < 0.001), UA (p < 0.001) and GPX (p < 0.001) and decrease of SOD (p < 0.005) in response to SRP, where no differences were observed for any of parameters in the oral hygiene instructions group. Comparison of antioxidant levels between the HC and SRP group showed that before treatment ALB were significantly higher in HC when compared to the SRP group (p = 0.039), and GXP (p = 0.000) and SOD (p = 0.021) levels were significantly higher in the SRP group. Comparison of values after treatment showed that TAOC was significantly higher in the HC than in the SRP group (p = 0.001), but UA was, inversely, significantly higher in the SRP group (p = 0.034). All clinical parameters except clinical attachment level were significantly decreased after SRP and significant correlations were observed between SOD and GI (p = 0.017), SOD and PI (p = 0.011), GPX and GI (p = 0.003) and GPX and PI (p = 0.008). Non-surgical periodontal treatment affected salivary TAOC, ALB, UA, SOD and GPX; moreover, these biochemical parameters convincingly reflected periodontal status and tissue response on treatment.
Background and objective One of the major pathologic patterns in periodontitis represents an imbalance among the production of free radicals and local antioxidants resulting in periodontal tissue destruction. The objective of the study was to investigate the influence of non‐surgical periodontal treatment on salivary antioxidants and to evaluate their capacity as biomarkers reflecting periodontal tissue condition and therapy outcome. Material and Methods Sixty‐three systemically healthy non‐smokers, including 21 periodontally healthy subjects (HC) and 42 patients with current chronic periodontitis fulfilled the inclusion criteria. Half of the patients received scaling and root planing (SRP) and the other half received only oral hygiene instructions. Full mouth clinical measurements, including gingival index (GI), plaque index (PI), periodontal pocket depth, clinical attachment level and saliva sampling were performed at baseline visit and 2 mo after treatment/baseline visit. Total antioxidant capacity (TAOC), albumins (ALB), uric acid (UA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were evaluated in saliva samples using commercial kits. Results All measured antioxidants were affected by treatment resulting in significant increase in TAOC (p < 0.005), ALB (p < 0.001), UA (p < 0.001) and GPX (p < 0.001) and decrease of SOD (p < 0.005) in response to SRP, where no differences were observed for any of parameters in the oral hygiene instructions group. Comparison of antioxidant levels between the HC and SRP group showed that before treatment ALB were significantly higher in HC when compared to the SRP group (p = 0.039), and GXP (p = 0.000) and SOD (p = 0.021) levels were significantly higher in the SRP group. Comparison of values after treatment showed that TAOC was significantly higher in the HC than in the SRP group (p = 0.001), but UA was, inversely, significantly higher in the SRP group (p = 0.034). All clinical parameters except clinical attachment level were significantly decreased after SRP and significant correlations were observed between SOD and GI (p = 0.017), SOD and PI (p = 0.011), GPX and GI (p = 0.003) and GPX and PI (p = 0.008). Conclusion Non‐surgical periodontal treatment affected salivary TAOC, ALB, UA, SOD and GPX; moreover, these biochemical parameters convincingly reflected periodontal status and tissue response on treatment.
Author Milinkovic, I.
Jankovic, S.
Novakovic, N.
Rakic, M.
Todorovic, T.
Cakic, S.
Dozic, I.
Aleksic, Z.
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  surname: Novakovic
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  surname: Todorovic
  fullname: Todorovic, T.
  organization: Department of Biochemistry, Faculty of Dental Medicine, University of Belgrade, Belgrade, Serbia
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  givenname: M.
  surname: Rakic
  fullname: Rakic, M.
  email: mia.rakic@gmail.com
  organization: Department for Periodontology and Oral Medicine, Faculty of Dental Medicine, University of Belgrade, Belgrade, Serbia
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  surname: Milinkovic
  fullname: Milinkovic, I.
  organization: Department for Periodontology and Oral Medicine, Faculty of Dental Medicine, University of Belgrade, Belgrade, Serbia
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  surname: Cakic
  fullname: Cakic, S.
  organization: Department for Periodontology and Oral Medicine, Faculty of Dental Medicine, University of Belgrade, Belgrade, Serbia
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Issue 1
Keywords antioxidants
biomarkers
superoxide dismutase
albumin
periodontitis
uric acid
glutathione peroxidase
total antioxidant status
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PublicationPlace United States
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PublicationTitle Journal of periodontal research
PublicationTitleAlternate J Periodont Res
PublicationYear 2014
Publisher Blackwell Publishing Ltd
Publisher_xml – name: Blackwell Publishing Ltd
References Page RC, Kornman K. The pathogenesis of human periodontitis: an introduction. Periodontol 2000 1997;14:9-11.
Gutteridge JMC. Biological origin of free radicals and mechanisms of antioxidant protection. Chem Biol Interact 1994;9:133-140.
Halliwell B. Oral inflammation and reactive species: a missed opportunity? Oral Dis 2000;6:136-137.
Kaklamanos EG, Tsalikis L. A review on peri-implant crevicular fluid assays potential in monitoring and predicting peri-implant tissue responses. J Int Acad Periodontol 2002;4:49-59.
Lee JM, Garon E, Wong DT. Salivary diagnostics. Orthod Craniofac Res 2009;12:206-211.
Panjamurthy K, Manoharan S, Ramachandran CR. Lipid peroxidation and antioxidant status in patients with periodontitis. Cell Mol Biol Lett 2005;10:255-264.
Moore S, Calder KA, Miller NJ, Rice-Evans CA. Antioxidant activity of saliva and periodontal disease. Free Radic Res 1994;21:417-425.
Woodford FP, Whitehead TP. Is measuring serum antioxidant capacity clinically useful? Ann Clin Biochem 1998; 35 (Pt 1):48-56.
Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6.
Herrera D, Sanz M, Jepsen S, Needleman I, Roldan S. A systematic review on the effect of systemic antimicrobials as an adjunct to scaling and root planing in periodontitis patients. J Clin Periodontol 2002;29:136-159.
Brock GR, Butterworth CJ, Matthews JB, Chapple ILC. Local and systemic total antioxidant capacity in periodontitis and health. J Clin Periodontol 2004;31:515-521.
Löe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and severity. Acta Odontol Scand 1963;21:533-551.
Chapple ILC, Brock GR, Milward MR, Ling N, Matthews JB. Compromised GCF total antioxidant capacity in periodontitis: cause or effect? J Clin Periodontol 2007;34:103-110.
Dias IHK, Matthews JB, Chapple ILC, Wright HJ, Dunston CR, Griffiths HR. Activation of the neutrophil respiratory burst by plasma from periodontitis patients is mediated by pro-inflammatory cytokines. J Clin Periodontol 2011;38:1-7.
Silness J, Löe H. Periodontal disease in pregnancy. II. Correlation between oral hygiene and periodontal condition. Acta Odontol Scand 1964;22:121-135.
Chapple IL, Milward MR, Dietrich T. The prevalence of inflammatory periodontitis is negatively associated with serum antioxidant concentrations. J Nutr 2007;137:657-664.
Güncü GN, Tözüm TF, Güncü MB et al. Myeloperoxidase as a measure of polymorphonuclear leukocyte response in inflammatory status around immediately and delayed loaded dental implants: a randomized controlled clinical trial. Clin Implant Dent Relat Res 2008;10:30-39.
Borges I Jr, Moreira EA, Filho DW, de Oliveira TB, da Silva MB, Fröde TS. Proinflammatory and oxidative stress markers in patients with peri-odontal disease. Mediators Inflamm 2007;2007:45794. doi:10.1155/2007/45794
Cochran DL. Inflammation and bone loss in periodontal disease. J Periodontol 2008;79:1569-1576.
Iwasaki M, Yoshihara A, Hirotomi T, Ogawa H, Hanada N, Miyazaki H. Longitudinal study on the relationship between serum albumin and periodontal disease. J Clin Periodontol 2008;35:291-296.
Chapple ILC. Reactive oxygen species and antioxidants in inflammatory diseases. J Clin Periodontol 1997;24:287-296.
Wei D, Zhang XL, Wang YZ, Yang CX, Chen G. Lipid peroxidation levels, total oxidant status and superoxide dismutase in serum, saliva and gingival crevicular fluid in chronic periodontitis patients before and after periodontal therapy. Aust Dent J 2010;55:70-78.
Sheikhi M, Bouhafs RL, Hammarstrom KJ, Jarstrand C. Lipid peroxidation caused by oxygen radicals from Fusobacterium-stimulated neutrophils as a possible model for the emergence of periodontitis. Oral Dis 2001;7:41-46.
Roche M, Rondeau P, Singh NR, Tarnus E, Bourdon E. The antioxidant properties of serum albumin. FEBS Lett 2008;582:1783-1787.
Graves D. Cytokines that promote periodontal tissue destruction. J Periodontol 2008;79:1585-1591.
Kornman K. Mapping the pathogenesis of periodontitis: a new look. J Periodontol 2008;79:1560-1568.
Skaleric U, Manthey CM, Mergenhagen SE, Gaspirc B, Wahl SM. Superoxide release and superoxide dismutase expression by human gingival fibroblasts. Eur J Oral Sci 2000;108:130-135.
Meier B, Radeke HH, Selle S et al. Human fibroblasts release reactive oxygen species in response to treatment with synovial fluid from patients suffering from arthritis. Free Radic Res Commun 1990;8:149-160.
Gustafsson A, Asman B. Increased release of free oxygen radicals from peripheral neutrophils in adult periodontitis after Fcg-receptor stimulation. J Clin Periodontol 1996;23:38-44.
Guentsch A, Preshaw PM, Bremer-Streck S, Klinger G, Glockmann E, Sigusch BW. Lipid peroxidation and antioxidant activity in saliva of periodontitis patients: effect of smoking and periodontal treatment. Clin Oral Investig 2008;12:345-352.
McCord JM. Human disease, free radicals, and the oxidant/antioxidant balance. Clin Biochem 1993;26:351-357.
Tulunoglu O, Alacam A, BaStug M, Yavuzer S. Superoxide dismutase activity in healthy and inflamed pulp tissues of permanent teeth in children. J Clin Pediatr Dent 1998;22:341-345.
Battino M, Ferreiro MS, Gallardo I, Newman HN, Bullon P. The antioxidant capacity of saliva. J Clin Periodontol 2002;29:189-194.
Waddington RJ, Moseley R, Embery G. Reactive oxygen species: a potential role in the pathogenesis of periodontal diseases. Oral Dis 2000;6:138-151.
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;40:378-384.
Sheikhi M, Gustafsson A, Jarstrand C. Cytokine, elastase and oxygen radical release by Fusobacterium nucleatum-activated leukocytes: a possible pathogenic factor in periodontitis. J Clin Periodontol 2000;27:758-762.
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References_xml – reference: Chapple ILC. Reactive oxygen species and antioxidants in inflammatory diseases. J Clin Periodontol 1997;24:287-296.
– reference: Cochran DL. Inflammation and bone loss in periodontal disease. J Periodontol 2008;79:1569-1576.
– reference: Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6.
– reference: McCord JM. Human disease, free radicals, and the oxidant/antioxidant balance. Clin Biochem 1993;26:351-357.
– reference: Brock GR, Butterworth CJ, Matthews JB, Chapple ILC. Local and systemic total antioxidant capacity in periodontitis and health. J Clin Periodontol 2004;31:515-521.
– reference: Wei D, Zhang XL, Wang YZ, Yang CX, Chen G. Lipid peroxidation levels, total oxidant status and superoxide dismutase in serum, saliva and gingival crevicular fluid in chronic periodontitis patients before and after periodontal therapy. Aust Dent J 2010;55:70-78.
– reference: Battino M, Ferreiro MS, Gallardo I, Newman HN, Bullon P. The antioxidant capacity of saliva. J Clin Periodontol 2002;29:189-194.
– reference: Guentsch A, Preshaw PM, Bremer-Streck S, Klinger G, Glockmann E, Sigusch BW. Lipid peroxidation and antioxidant activity in saliva of periodontitis patients: effect of smoking and periodontal treatment. Clin Oral Investig 2008;12:345-352.
– reference: Graves D. Cytokines that promote periodontal tissue destruction. J Periodontol 2008;79:1585-1591.
– reference: Skaleric U, Manthey CM, Mergenhagen SE, Gaspirc B, Wahl SM. Superoxide release and superoxide dismutase expression by human gingival fibroblasts. Eur J Oral Sci 2000;108:130-135.
– reference: Kaklamanos EG, Tsalikis L. A review on peri-implant crevicular fluid assays potential in monitoring and predicting peri-implant tissue responses. J Int Acad Periodontol 2002;4:49-59.
– reference: Herrera D, Sanz M, Jepsen S, Needleman I, Roldan S. A systematic review on the effect of systemic antimicrobials as an adjunct to scaling and root planing in periodontitis patients. J Clin Periodontol 2002;29:136-159.
– reference: Sheikhi M, Bouhafs RL, Hammarstrom KJ, Jarstrand C. Lipid peroxidation caused by oxygen radicals from Fusobacterium-stimulated neutrophils as a possible model for the emergence of periodontitis. Oral Dis 2001;7:41-46.
– reference: Chapple ILC, Brock GR, Milward MR, Ling N, Matthews JB. Compromised GCF total antioxidant capacity in periodontitis: cause or effect? J Clin Periodontol 2007;34:103-110.
– reference: 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;40:378-384.
– reference: Silness J, Löe H. Periodontal disease in pregnancy. II. Correlation between oral hygiene and periodontal condition. Acta Odontol Scand 1964;22:121-135.
– reference: Gutteridge JMC. Biological origin of free radicals and mechanisms of antioxidant protection. Chem Biol Interact 1994;9:133-140.
– reference: Borges I Jr, Moreira EA, Filho DW, de Oliveira TB, da Silva MB, Fröde TS. Proinflammatory and oxidative stress markers in patients with peri-odontal disease. Mediators Inflamm 2007;2007:45794. doi:10.1155/2007/45794
– reference: Sheikhi M, Gustafsson A, Jarstrand C. Cytokine, elastase and oxygen radical release by Fusobacterium nucleatum-activated leukocytes: a possible pathogenic factor in periodontitis. J Clin Periodontol 2000;27:758-762.
– reference: Gustafsson A, Asman B. Increased release of free oxygen radicals from peripheral neutrophils in adult periodontitis after Fcg-receptor stimulation. J Clin Periodontol 1996;23:38-44.
– reference: Halliwell B. Oral inflammation and reactive species: a missed opportunity? Oral Dis 2000;6:136-137.
– reference: Waddington RJ, Moseley R, Embery G. Reactive oxygen species: a potential role in the pathogenesis of periodontal diseases. Oral Dis 2000;6:138-151.
– reference: Lee JM, Garon E, Wong DT. Salivary diagnostics. Orthod Craniofac Res 2009;12:206-211.
– reference: Löe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and severity. Acta Odontol Scand 1963;21:533-551.
– reference: Kornman K. Mapping the pathogenesis of periodontitis: a new look. J Periodontol 2008;79:1560-1568.
– reference: Meier B, Radeke HH, Selle S et al. Human fibroblasts release reactive oxygen species in response to treatment with synovial fluid from patients suffering from arthritis. Free Radic Res Commun 1990;8:149-160.
– reference: Iwasaki M, Yoshihara A, Hirotomi T, Ogawa H, Hanada N, Miyazaki H. Longitudinal study on the relationship between serum albumin and periodontal disease. J Clin Periodontol 2008;35:291-296.
– reference: Tulunoglu O, Alacam A, BaStug M, Yavuzer S. Superoxide dismutase activity in healthy and inflamed pulp tissues of permanent teeth in children. J Clin Pediatr Dent 1998;22:341-345.
– reference: Dias IHK, Matthews JB, Chapple ILC, Wright HJ, Dunston CR, Griffiths HR. Activation of the neutrophil respiratory burst by plasma from periodontitis patients is mediated by pro-inflammatory cytokines. J Clin Periodontol 2011;38:1-7.
– reference: Roche M, Rondeau P, Singh NR, Tarnus E, Bourdon E. The antioxidant properties of serum albumin. FEBS Lett 2008;582:1783-1787.
– reference: Chapple IL, Milward MR, Dietrich T. The prevalence of inflammatory periodontitis is negatively associated with serum antioxidant concentrations. J Nutr 2007;137:657-664.
– reference: Panjamurthy K, Manoharan S, Ramachandran CR. Lipid peroxidation and antioxidant status in patients with periodontitis. Cell Mol Biol Lett 2005;10:255-264.
– reference: Moore S, Calder KA, Miller NJ, Rice-Evans CA. Antioxidant activity of saliva and periodontal disease. Free Radic Res 1994;21:417-425.
– reference: Woodford FP, Whitehead TP. Is measuring serum antioxidant capacity clinically useful? Ann Clin Biochem 1998; 35 (Pt 1):48-56.
– reference: Page RC, Kornman K. The pathogenesis of human periodontitis: an introduction. Periodontol 2000 1997;14:9-11.
– reference: Güncü GN, Tözüm TF, Güncü MB et al. Myeloperoxidase as a measure of polymorphonuclear leukocyte response in inflammatory status around immediately and delayed loaded dental implants: a randomized controlled clinical trial. Clin Implant Dent Relat Res 2008;10:30-39.
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  article-title: Increased release of free oxygen radicals from peripheral neutrophils in adult periodontitis after Fcg‐receptor stimulation
  publication-title: J Clin Periodontol
– volume: 21
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  article-title: Periodontal disease in pregnancy. I. Prevalence and severity
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  article-title: Lipid peroxidation levels, total oxidant status and superoxide dismutase in serum, saliva and gingival crevicular fluid in chronic periodontitis patients before and after periodontal therapy
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  article-title: Mapping the pathogenesis of periodontitis: a new look
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  article-title: Compromised GCF total antioxidant capacity in periodontitis: cause or effect?
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  article-title: Reactive oxygen species: a potential role in the pathogenesis of periodontal diseases
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  article-title: Lipid peroxidation caused by oxygen radicals from ‐stimulated neutrophils as a possible model for the emergence of periodontitis
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  article-title: A systematic review on the effect of systemic antimicrobials as an adjunct to scaling and root planing in periodontitis patients
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  article-title: Longitudinal study on the relationship between serum albumin and periodontal disease
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  article-title: A review on peri‐implant crevicular fluid assays potential in monitoring and predicting peri‐implant tissue responses
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Snippet Background and objective One of the major pathologic patterns in periodontitis represents an imbalance among the production of free radicals and local...
One of the major pathologic patterns in periodontitis represents an imbalance among the production of free radicals and local antioxidants resulting in...
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StartPage 129
SubjectTerms Adult
albumin
Albumins - analysis
antioxidants
Antioxidants - analysis
biomarkers
Biomarkers - analysis
Chronic Periodontitis - metabolism
Chronic Periodontitis - therapy
Colorimetry - methods
Dental Devices, Home Care
Dental Plaque Index
Dental Scaling - methods
Female
Follow-Up Studies
glutathione peroxidase
Glutathione Peroxidase - analysis
Humans
Male
Oral Hygiene - education
Periodontal Attachment Loss - classification
Periodontal Attachment Loss - therapy
Periodontal Index
Periodontal Pocket - classification
Periodontal Pocket - therapy
periodontitis
Root Planing - methods
Saliva - chemistry
superoxide dismutase
Superoxide Dismutase - analysis
Toothbrushing - instrumentation
Toothbrushing - methods
total antioxidant status
Treatment Outcome
uric acid
Uric Acid - analysis
Title Salivary antioxidants as periodontal biomarkers in evaluation of tissue status and treatment outcome
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https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjre.12088
https://www.ncbi.nlm.nih.gov/pubmed/23710550
https://www.proquest.com/docview/1490727885
Volume 49
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