title: Salivary antioxidants in patients with type 1 or 2 diabetes and inflammatory periodontal disease: a case-control study.
abstract: BACKGROUND
  The purpose of this study was to evaluate and compare salivary concentrations of reduced, oxidized glutathione, uric acid, ascorbic acid, and total antioxidant capacity in subjects with diabetes and systemically healthy subjects with inflammatory periodontal disease.
  
  
  METHODS
  Sixteen patients with type 1 diabetes mellitus (DM), 25 patients with type 2 DM, and 24 systemically healthy patients, all with inflammatory periodontal disease, were recruited. Whole-saliva samples were obtained, and full-mouth clinical periodontal measurements, including plaque index, probing depth, gingival recession, clinical attachment level, and bleeding on probing, were recorded at six sites per tooth. Saliva flow rate and salivary levels of reduced and oxidized glutathione, vitamin C, uric acid, and total antioxidant capacity were determined. Data were analyzed statistically by non-parametric tests.
  
  
  RESULTS
  The subjects with type 2 DM had fewer teeth and more sites with probing depths >4 mm than the patients with type 1 DM (both P <0.01). The mean salivary reduced-glutathione concentration was lower in patients with type 1 DM than in the other two groups (both P <0.05). No significant differences in the salivary concentrations of the other antioxidants measured were found among the groups (P >0.05). Oxidized glutathione levels in the patients with type 1 DM were significantly lower than in the systemically healthy group (P = 0.007). In both groups with diabetes, salivary reduced-glutathione levels correlated positively with probing depth, and total antioxidant capacity correlated with salivary flow rate (P <0.01).
  
  
  CONCLUSIONS
  The decrease in salivary reduced-glutathione levels in patients with type 1 DM may have a role in periodontal tissue destruction by predisposing tissues to oxidative stress.
authors.affiliation: Department of Periodontology, School of Dentistry, Ege University, Izmir, Turkey.
authors.forename: Pinar
authors.initials: P
authors.lastname: Gümüş
authors.forename: Nurcan
authors.initials: N
authors.lastname: Buduneli
authors.forename: Sevki
authors.initials: S
authors.lastname: Cetinkalp
authors.forename: Samuel I
authors.initials: SI
authors.lastname: Hawkins
authors.forename: Diane
authors.initials: D
authors.lastname: Renaud
authors.forename: Denis F
authors.initials: DF
authors.lastname: Kinane
authors.forename: David A
authors.initials: DA
authors.lastname: Scott
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000032:analysis*; D001205:Ascorbic Acid / Q000032:analysis; D016022:Case-Control Studies; D003774:Dental Plaque Index; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D005260:Female; D005884:Gingival Hemorrhage / Q000378:metabolism; D005889:Gingival Recession / Q000378:metabolism; D005978:Glutathione / Q000032:analysis; D019803:Glutathione Disulfide / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology; D017622:Periodontal Attachment Loss / Q000378:metabolism; D010514:Periodontal Pocket / Q000378:metabolism; D010518:Periodontitis / Q000378:metabolism*; D012463:Saliva / Q000737:chemistry* / Q000378:metabolism; D012636:Secretory Rate / Q000502:physiology; D014527:Uric Acid / Q000032:analysis; D055815:Young Adult
chemical_list: D000975:Antioxidants; D014527:Uric Acid; D005978:Glutathione; D001205:Ascorbic Acid; D019803:Glutathione Disulfide