title: Individual composition of human leukocyte antigens and periodontopathogens in the background of periodontitis.
abstract: BACKGROUND
  Human leukocyte antigens (HLAs) are a basic precondition to induce the immune response to pathogens. Therefore, this study evaluates associations among periodontitis, five key periodontopathic bacteria, and HLAs to test their impact together with additional risk factors in multivariate analyses.
  
  
  METHODS
  Eighty-five patients with generalized aggressive periodontitis (GAgP) and 71 patients with generalized chronic periodontitis (CP) were compared to 88 periodontitis-free controls. HLA Class I and II typing was performed by polymerase chain reaction (PCR) with sequence-specific primers. Subgingival plaque specimens were detected by PCR with sequence-specific oligonucleotides. Risk-factor analyses were performed with respect to the cofactors age, sex, smoking, and plaque level by logistic regression.
  
  
  RESULTS
  In the total patient group (GAgP + CP), the adjusted odds ratio (OR) of periodontitis was decreased in cases who were carriers of HLA-B*57 (OR = 0.259, 95% confidence interval [CI] = 0.086 to 0.782), HLA-DQB1*08 (OR = 0.404, 95% CI = 0.187 to 0.871), or the combination HLA-DRB1*04;DRB4*;DQB1*0302 (OR = 0.407, 95% CI = 0.185 to 0.895). Moreover, individuals who expressed HLA-DRB1*04 (OR = 0.36, 95% CI = 0.148 to 0.886) or HLA-DRB1*04;DRB4*;DQB1*0302 (OR = 0.29, 95% CI = 0.092 to 0.884) had a decreased colonization risk with Aggregatibacter actinomycetemcomitans.
  
  
  CONCLUSIONS
  Certain HLA markers were negatively associated to the manifestation of a generalized periodontitis and/or the individual colonization of A. actinomycetemcomitans. The underlying mechanisms have to be investigated in future studies.
authors.affiliation: Department of Operative Dentistry and Periodontology, University School of Dental Medicine, Martin Luther University Halle-Wittenberg, Halle, Germany. stefan.reichert@medizin.uni-halle.de
authors.forename: Stefan
authors.initials: S
authors.lastname: Reichert
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Altermann
authors.forename: Jamal M
authors.initials: JM
authors.lastname: Stein
authors.forename: Hans-Günter
authors.initials: HG
authors.lastname: Schaller
authors.forename: Helmut K G
authors.initials: HK
authors.lastname: Machulla
authors.forename: Susanne
authors.initials: S
authors.lastname: Schulz
mesh_terms: D000328:Adult; D000367:Age Factors; D016976:Aggregatibacter actinomycetemcomitans / Q000302:isolation & purification; D010520:Aggressive Periodontitis / Q000276:immunology / Q000382:microbiology*; D001439:Bacteroides / Q000302:isolation & purification; D055113:Chronic Periodontitis / Q000276:immunology / Q000382:microbiology*; D015331:Cohort Studies; D003773:Dental Plaque / Q000382:microbiology; D003774:Dental Plaque Index; D005260:Female; D015235:HLA-B Antigens / Q000032:analysis; D059866:HLA-DQ beta-Chains / Q000032:analysis; D059811:HLA-DRB1 Chains / Q000032:analysis; D059845:HLA-DRB4 Chains / Q000032:analysis; D015395:Histocompatibility Antigens Class I / Q000032:analysis*; D000949:Histocompatibility Antigens Class II / Q000032:analysis*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016966:Porphyromonas gingivalis / Q000302:isolation & purification; D018713:Prevotella intermedia / Q000302:isolation & purification; D012307:Risk Factors; D012737:Sex Factors; D012907:Smoking; D016388:Tooth Loss / Q000145:classification; D048373:Treponema denticola / Q000302:isolation & purification
chemical_list: D015235:HLA-B Antigens; C103707:HLA-B57 antigen; D059866:HLA-DQ beta-Chains; C069051:HLA-DQB1 antigen; D059811:HLA-DRB1 Chains; C527195:HLA-DRB1*04 antigen; D059845:HLA-DRB4 Chains; D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II