Expression of the Cd54 (icam-1) and Cd11a (lfa-1) Adhesion Molecules in Oral Mucosal Inflammation

Previous studies of chronic dermatoses have suggested that expression of the CD54 cell surface antigen (intercellular adhesion molecule-1, ICAM-1) by keratinocytes is a feature of chronic inflammation. However, whether such expression is a prerequisite for intraepithelial migration of lymphocytes is unclear. The present study evaluated the expression of CD54 and its ligand, CD11a (lymphocyte function-associated antigen, LFA-1) in oral lesions of lichen planus, recurrent aphthous stomatitis, secondary Sjogren's syndrome and traumatic ulceration using an immunoperoxidase technique. In 33 of 56 lesions examined, substantial numbers of CD11a+ cells were present within oral mucosal epithelium despite an absence of detectable keratinocyte CD54 antigen expression. Consequently, CD54/CD11a adhesion interactions may not be critical in the initiation of oral mucosal inflammation

Increased submucosal factor XII la-positive dendrocytes in oral lichen planus

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71666/1/j.1600-0714.1994.tb01097.x.pd

Adhesion Molecule Expression in Chronic Inflammatory Periodontal-Disease Tissue

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. The basal epithelium and keratinocytes in the lower layers were CD29+ and in larger infiltrates, the upper layers were also positive. This study suggests that if specific homing of different lymphocyte clones occurs in gingivitis compared with periodontitis, this is not reflected in the pattern of adhesion molecule expression observed in this investigation. The present study may help to elucidate the roles played by endothelial cells and keratinocytes in lymphocyte trafficking in inflamed tissues