title: Density of CD1a-labeled Langerhans' cells in normal human gingiva and in nifedipine- and immunosuppressive medication-induced gingival overgrowth.
abstract: BACKGROUND
  The purpose of this study was to compare the distribution of Langerhans' cells in normal human gingiva and in nifedipine- and immunosuppressive medication-induced gingival overgrowth by means of an immunohistochemical study.
  
  
  METHODS
  Gingival samples were collected from 11 nifedipine-medicated cardiac patients, 22 triple-medicated (azathioprine, prednisolone, and cyclosporin A) renal transplant recipients, and 28 generally healthy individuals. Patients were grouped into the immunosuppression group, the combined immunosuppression and nifedipine group, the nifedipine group, and the generally healthy control group. Five microm-thick cryostat sections were stained with monoclonal antibody (mAb) for CD1a using an avidin-biotin-enzyme complex (ABC) method. Numbers of CD1a-labeled cells/mm2 were determined in 6 areas: oral epithelium, oral sulcular epithelium, sulcular epithelium, middle connective tissue, connective tissue beneath the oral epithelium, and connective tissue beneath the sulcular epithelium. Significances of differences between the groups were tested by means of the Kruskall-Wallis test, and significances of differences between pairs of results by the Mann-Whitney U-test and the t test.
  
  
  RESULTS
  Numbers of CD1a-labeled cells were significantly lower in the medicated groups than in controls in all 3 epithelial areas (P <0.0001) and in the connective tissue beneath the sulcular epithelium (P <0.0021). There were significantly fewer CD1a-labeled cells in the sulcular epithelium in the nifedipine group than in the other medication groups.
  
  
  CONCLUSIONS
  The reduced numbers of CD1a-labeled cells found in nifedipine-induced gingival overgrowth were similar to the reduced numbers of CD1a-labeled cells in gingival overgrowth associated with immunosuppressive medication.
authors.affiliation: Institute of Dentistry, University of Oulu, Finland.
authors.forename: P K
authors.initials: PK
authors.lastname: Nurmenniemi
authors.forename: H E
authors.initials: HE
authors.lastname: Pernu
authors.forename: M L
authors.initials: ML
authors.lastname: Knuuttila
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000009:adverse effects; D018949:Antigens, CD1 / Q000032:analysis*; D001379:Azathioprine / Q000009:adverse effects; D002121:Calcium Channel Blockers / Q000009:adverse effects*; D002452:Cell Count; D003238:Connective Tissue / Q000473:pathology; D016572:Cyclosporine / Q000009:adverse effects; D004846:Epithelial Attachment / Q000473:pathology; D004848:Epithelium / Q000473:pathology; D005260:Female; D005881:Gingiva / Q000473:pathology*; D019214:Gingival Overgrowth / Q000139:chemically induced / Q000473:pathology*; D006801:Humans; D007124:Immunoenzyme Techniques; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D016030:Kidney Transplantation; D007801:Langerhans Cells / Q000473:pathology*; D008297:Male; D009543:Nifedipine / Q000009:adverse effects*; D011239:Prednisolone / Q000009:adverse effects
chemical_list: D000893:Anti-Inflammatory Agents; D018949:Antigens, CD1; D002121:Calcium Channel Blockers; D007166:Immunosuppressive Agents; D016572:Cyclosporine; D011239:Prednisolone; D009543:Nifedipine; D001379:Azathioprine