title: Analysis of human leukocyte antigens in patients with internal derangement of the temporomandibular joint.
abstract: OBJECTIVE
  Spondyloarthropathy includes the subcategory of reactive arthritis (ReA). Spondyloarthropathies are commonly associated with certain human leukocyte antigen (HLA) alleles. Because we identified bacteria associated with ReA within the temporomandibular joint (TMJ), we now evaluate the frequency of HLA alleles in patients with TMJ pathology.
  
  
  METHODS
  HLA typing of 129 patients (121 females and 8 males) performed by standard microcytotoxicity technique. Thirty patients had only class I (HLA-A and -B loci) evaluated. Ninety-nine patients had both class I and class II (HLA-DR loci) evaluated. Identification of alleles at the C locus was not performed. The antigenic frequency in the study group was compared to US white control subjects using a 2-tailed Fisher's exact test with a Bonferroni multiple comparison adjustment.
  
  
  RESULTS
  The following class I HLA alleles, -A1 (32%), -A2 (50%), -A3 (33%), -B7 (23%), -B14 (14%), -B35 (20%), and -B44 (36%), including the B7 cross-reactive group (CREG) (49%) and class II alleles -DR1 (25%) and -DR4 (34%), were found to have an increased frequency in our patient group.
  
  
  CONCLUSIONS
  Our study shows an increased frequency of several alleles that have been previously associated with arthropathy, and the alleles of the B7 CREG, in patients with TMJ pathology. Patients with these alleles may have an increased risk for the development of internal derangement of the TMJ as a consequence of the bacterial/infectious agents and host interactions with the subsequent cytokine/inflammatory response being influenced by their HLA phenotype.
authors.affiliation: Baylor University Medical Center Transplantation Laboratory, Dallas, TX, USA. chenry@pol.net
authors.forename: Charles H
authors.initials: CH
authors.lastname: Henry
authors.forename: Afzal
authors.initials: A
authors.lastname: Nikaein
authors.forename: Larry M
authors.initials: LM
authors.lastname: Wolford
mesh_terms: D000483:Alleles; D016918:Arthritis, Reactive / Q000276:immunology; D016022:Case-Control Studies; D002874:Chromosome Mapping; D003429:Cross Reactions; D004198:Disease Susceptibility; D005260:Female; D006680:HLA Antigens / Q000032:analysis*; D015234:HLA-A Antigens / Q000032:analysis; D015788:HLA-A1 Antigen / Q000032:analysis; D015789:HLA-A2 Antigen / Q000032:analysis; D015791:HLA-A3 Antigen / Q000032:analysis; D015235:HLA-B Antigens / Q000032:analysis; D059909:HLA-B14 Antigen; D015797:HLA-B35 Antigen / Q000032:analysis; D059948:HLA-B44 Antigen; D015793:HLA-B7 Antigen / Q000032:analysis; D006684:HLA-DR Antigens / Q000032:analysis; D015798:HLA-DR1 Antigen / Q000032:analysis; D015804:HLA-DR4 Antigen / Q000032:analysis; D006801:Humans; D004204:Joint Dislocations / Q000276:immunology*; D016013:Likelihood Functions; D008297:Male; D000091402:Prohibitins; D013223:Statistics as Topic; D019224:Temporomandibular Joint Disc / Q000276:immunology*; D013705:Temporomandibular Joint Disorders / Q000276:immunology
chemical_list: D006680:HLA Antigens; D015234:HLA-A Antigens; D015788:HLA-A1 Antigen; D015789:HLA-A2 Antigen; D015791:HLA-A3 Antigen; D015235:HLA-B Antigens; D059909:HLA-B14 Antigen; D015797:HLA-B35 Antigen; D059948:HLA-B44 Antigen; D015793:HLA-B7 Antigen; D006684:HLA-DR Antigens; D015798:HLA-DR1 Antigen; D015804:HLA-DR4 Antigen; C000717331:PHB2 protein, human; D000091402:Prohibitins