title: Adhesion molecule expression in chronic inflammatory periodontal disease tissue.
abstract: Differences in lymphocyte populations have been demonstrated in gingivitis and periodontitis lesions. A differential expression of adhesion molecules may play a role in lymphocyte trafficking in these tissues. An indirect avidin biotin immunoperoxidase technique was used to stain a range of adhesion molecules in tissue sections of 21 gingival biopsies from both gingivitis and periodontitis subjects. These specimens were placed into three groups according to the size of the infiltrate. ICAM-1, PECAM-1 and LECAM-1 expression on mononuclear cells in the inflammatory infiltrates increased significantly with increasing size of infiltrate. Approximately 50% of these mononuclear cells were LFA-1+ and CD29+. When specimens were grouped according to their putative disease status there were no significant differences between mononuclear cell adhesion molecule expression in small infiltrates from either gingivitis or adult periodontitis subjects. This was also the case with larger lesions from both clinical groups. Therefore there does not appear to be a differential expression of adhesion molecules on lymphocytes in gingivitis and periodontitis tissue. Endothelial cells were positive for ICAM-1, PECAM-1, CD29, GMP-140 but negative for ELAM-1. Keratinocyte expression of ICAM-1 increased with increasing size of infiltrate although in heavy infiltrates, cells in the region of the junctional epithelium which were positive in small lesions, became ICAM-1 negative. The upper layers of the oral epithelium were positive for LECAM-1 in small infiltrates and with increasing size of infiltrate, the lower layers and many of the sulcular and junctional epithelium keratinocytes were positive.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Dentistry, University of Queensland, Australia.
authors.forename: E
authors.initials: E
authors.lastname: Gemmell
authors.forename: L J
authors.initials: LJ
authors.lastname: Walsh
authors.forename: N W
authors.initials: NW
authors.lastname: Savage
authors.forename: G J
authors.initials: GJ
authors.lastname: Seymour
mesh_terms: D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D016516:CD4-CD8 Ratio; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000276:immunology*; D002450:Cell Communication; D002908:Chronic Disease; D004727:Endothelium / Q000166:cytology / Q000276:immunology; D004846:Epithelial Attachment / Q000166:cytology / Q000276:immunology; D004847:Epithelial Cells; D004848:Epithelium / Q000276:immunology; D005891:Gingivitis / Q000276:immunology*; D007124:Immunoenzyme Techniques; D019012:Integrin beta1; D018799:Intercellular Adhesion Molecule-1; D015603:Keratinocytes / Q000276:immunology; D019041:L-Selectin; D016169:Lymphocyte Function-Associated Antigen-1 / Q000032:analysis; D010518:Periodontitis / Q000276:immunology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015815:Cell Adhesion Molecules; D019012:Integrin beta1; D016169:Lymphocyte Function-Associated Antigen-1; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D019041:L-Selectin