ADHESION MOLECULE EXPRESSION IN CHRONIC INFLAMMATORY PERIODONTAL-DISEASE TISSUE

Citation
E. Gemmell et al., ADHESION MOLECULE EXPRESSION IN CHRONIC INFLAMMATORY PERIODONTAL-DISEASE TISSUE, Journal of Periodontal Research, 29(1), 1994, pp. 46-53
Citations number
46
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
ISSN journal
00223484
Volume
29
Issue
1
Year of publication
1994
Pages
46 - 53
Database
ISI
SICI code
0022-3484(1994)29:1<46:AMEICI>2.0.ZU;2-D
Abstract
Differences in lymphocyte populations have been demonstrated in gingiv itis 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 biops ies from both gingivitis and periodontitis subjects. These specimens w ere placed into three groups according to the size of the infiltrate. ICAM-1, PECAM-1 and LECAM-1 expression on mononuclear cells in the inf lammatory infiltrates increased significantly with increasing size of infiltrate. Approximately 50% of these mononuclear cells were LFA-1+ a nd CD29+. When specimens were grouped according to their putative dise ase status there were no significant differences between mononuclear c ell adhesion molecule expression in small infiltrates from either ging ivitis or adult periodontitis subjects. This was also the case with la rger lesions from both clinical groups. Therefore there does not appea r to be a differential expression of adhesion molecules on lymphocytes in gingivitis and periodontitis tissue. Endothelial cells were positi ve for ICAM-1, PECAM-1, CD29, GMP-140 but negative for ELAM-1. Keratin ocyte expression of ICAM-1 increased with increasing size of infiltrat e although in heavy infiltrates, cells in the region of the junctional epithelium which were positive in small lesions, became ICAM-1 negati ve. 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 keratinocyt es were positive. The basal epithelium and keratinocytes in the lower layers were CD29+ and in larger infiltrates, the upper layers were als o positive. This study suggests that if specific homing of different l ymphocyte clones occurs in gingivitis compared with periodontitis, thi s is not reflected in the pattern of adhesion molecule expression obse rved in this investigation. The present study may help to elucidate th e roles played by endothelial cells and keratinocytes in lymphocyte tr afficking in inflamed tissues.