title: Immunohistochemical analysis of CD1a-labeled Langerhans cells in human dental periapical inflammatory lesions--correlation with inflammatory cells and epithelial cells.
abstract: OBJECTIVE
  Distribution and density of CD1a-labeled Langerhans cells (LCs) were examined in human dental periapical inflammatory lesions, and compared with inflammatory cell infiltration or epithelial cell proliferation.
  
  
  METHODS
  Eighty three periapical lesions (26 apical granulomas (AGs), 8 epitheliated granulomas (EGs), 34 radicular cysts (RCs), 15 residual radicular cysts (RRCs)) were collected. As control, specimens of periodontal ligaments including Malassez epithelial rests were curetted from 21 teeth. LC densities were measured and various degrees of inflammatory cell infiltration were examined immunohistochemically. Labeling indices for the cellular proliferation markers Ki-67 antigen and DNA topoisomerase II alpha were calculated in the epithelial components.
  
  
  RESULTS
  LCs were found in all periapical lesions but not in Malassez epithelial rests. LCs were more abundant in epithelial components than in subepithelial layers. Intraepithelial LCs were more frequent in RCs than in RRCs, whereas subepithelial LCs were less frequent in RRCs than in AGs and EGs. T lymphocytes consistently outnumbered macrophages, plasma cells and B lymphocytes. The range of the CD4/CD8-positive cell ratio differed according to the lesions. Increased LC density was associated with the severity of CD3-positive cell infiltration. Ki-67- and Topo II-LI showed various degrees of epithelial immunoreactivity. There was a significant correlation between LC density and proliferative potential of the epithelium in periapical lesions.
  
  
  CONCLUSIONS
  These findings suggested that LCs appeared to be associated with T lymphocyte infiltration and proliferative potential of the epithelial tissue in periapical lesions.
authors.affiliation: Division of Maxillofacial and Plastic Surgery, Department of Oro-Maxillofacial Surgical Science, Tohoku University Graduate School of Dentistry, Sendai, Japan. takahiro@mail.cc.tohoku.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Kumamoto
authors.forename: K
authors.initials: K
authors.lastname: Ooya
authors.forename: K
authors.initials: K
authors.lastname: Motegi
mesh_terms: D000328:Adult; D018949:Antigens, CD1 / Q000032:analysis*; D000951:Antigens, Neoplasm; D001402:B-Lymphocytes / Q000276:immunology / Q000473:pathology; D017252:CD3 Complex / Q000032:analysis; D016516:CD4-CD8 Ratio; D002452:Cell Count; D002455:Cell Division; D004250:DNA Topoisomerases, Type II / Q000032:analysis; D004268:DNA-Binding Proteins; D004847:Epithelial Cells / Q000276:immunology; D004848:Epithelium / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000032:analysis; D019394:Ki-67 Antigen / Q000032:analysis; D007801:Langerhans Cells / Q000276:immunology*; D018655:Lymphocyte Count; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D010483:Periapical Diseases / Q000276:immunology* / Q000473:pathology; D010484:Periapical Granuloma / Q000276:immunology / Q000473:pathology; D010513:Periodontal Ligament / Q000276:immunology / Q000473:pathology; D010950:Plasma Cells / Q000276:immunology / Q000473:pathology; D011842:Radicular Cyst / Q000276:immunology / Q000473:pathology; D018709:Statistics, Nonparametric; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology
chemical_list: D018949:Antigens, CD1; D000951:Antigens, Neoplasm; C419393:CD1a antigen; D017252:CD3 Complex; D004268:DNA-Binding Proteins; D007527:Isoenzymes; D019394:Ki-67 Antigen; D004250:DNA Topoisomerases, Type II