title: Treatment  outcome for IDDM patients in relation to glutamic acid decarboxylase autoantibodies and serum IgG to periodontal pathogens.
abstract: BACKGROUND
  Patients with insulin-dependent diabetes mellitus (IDDM) have elevated risk for periodontitis (PD) relative to subjects without diabetes. Whether refractory PD in IDDM patients is related to autoimmunity as indicated by serum glutamic acid decarboxylase autoantibody GAD Ab levels or to host bacterial immunity as reflected by serum antibody titers to periodontal pathogens is unknown.
  
  
  OBJECTIVE
  To determine if non-surgical periodontal treatment outcome differs between GAD Ab-seropositive and -seronegative IDDM patients by assessing the following parameters: (1) pretreatment serum levels of GAD Ab, (2) pretreatment serum IgG titers to key periodontal pathogens, and (3) changes in periodontal pocket probing depth (PDC) after treatment.
  
  
  METHODS
  Before and two months after periodontal treatment of 11 GAD Ab-seronegative and 7 -seropositive subjects, PDC was assessed and serum GAD Ab and IgG to Porphyromonas gingivalis (Pg), Bacteroides forsythus (BJ), and Actinobacillus actinomycetemcomitans (Aa) were studied using established radioligand precipitation and enzyme-linked immunosorbent assays, respectively.
  
  
  RESULTS
  The PDC decrease was significantly better for GAD Ab-seronegative subjects than for seropositive subjects (median 1.4 mm+/-0.5 s.d. versus 0.5 mm+/-0.3 s.d., p<0.03, Mann-Whitney). GAD Ab levels and PDC were positively correlated (r=+0.71, p<0.05) for sero-positive subjects but were neutral (r=-0.07) for seronegative subjects. Serum IgG to Pg and GAD Ab levels were positively associated (r2=0.42) in seropositive subjects. Logistic regression analysis confirmed that GAD Ab status was the primary discriminator for PDC (p<0.04).
  
  
  CONCLUSIONS
  Detection of elevated GAD Ab levels in combination with elevated IgG titers to Pg before treatment is indicative of IDDM patients with refractory PD.
authors.affiliation: Department of Oral Medicine, University of Washington, Seattle, USA.
authors.forename: T J
authors.initials: TJ
authors.lastname: Sims
authors.forename: A
authors.initials: A
authors.lastname: Lernmark
authors.forename: T
authors.initials: T
authors.lastname: Smith
authors.forename: R C
authors.initials: RC
authors.lastname: Page
authors.forename: G R
authors.initials: GR
authors.lastname: Persson
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans / Q000276:immunology; D000907:Antibodies, Bacterial / Q000097:blood*; D001323:Autoantibodies / Q000097:blood*; D001439:Bacteroides / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005500:Follow-Up Studies; D005891:Gingivitis / Q000382:microbiology / Q000628:therapy; D005968:Glutamate Decarboxylase / Q000097:blood / Q000276:immunology*; D006090:Gram-Negative Bacteria / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D016015:Logistic Models; D017622:Periodontal Attachment Loss / Q000382:microbiology / Q000628:therapy; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000382:microbiology / Q000628:therapy; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology* / Q000628:therapy; D016966:Porphyromonas gingivalis / Q000276:immunology; D018709:Statistics, Nonparametric; D016896:Treatment Outcome
chemical_list: D000907:Antibodies, Bacterial; D001323:Autoantibodies; D007074:Immunoglobulin G; D005968:Glutamate Decarboxylase