Endothelial cell leukocyte adhesion molecule‐1 (ELAM‐1) and intercellular adhesion molecule‐1 (ICAM‐1) expression in gingival tissue during health and experimentally‐induced gingivitis

Abstract

The changes in vascular adhesion molecule expression and numbers of infiltrating leukocytes during a 21-day experimental gingivitis episode were investigated immunohistochemically. Monoclonal antibodies to ELAM-1 (1.2B6), ICAM-1 (6.5B5), CD3 (OKT3-pan-T cell) and neutrophils (PMN-elastase) were used to identify positive vessels and leukocytes within gingival biopsies taken on d 0, 7, 14 and 21. Vascular endothelium expressed ELAM-1 and ICAM-1 both in clinically 'healthy' tissue (d 0) and in experimentally inflamed tissue (d 7 to 21). Positive vessels were found mainly in the connective tissue subjacent to the junctional epithelium where the highest numbers of T cells and neutrophils were also seen. Although T cells were found in all tissue areas studied, neutrophils were largely concentrated in the junctional epithelium and the subjacent connective tissue but were absent from the oral epithelial region. As the experimental gingivitis developed, the number of T cells or neutrophils in the different tissue regions did not change significantly although the most intense vascular ICAM-1 and ELAM-1 staining redistributed to the CT adjacent to the junctional epithelium. A prominent feature was the intense ICAM-1 positive staining of the junctional epithelium and its absence in the closely adjacent oral epithelium, in both clinically 'healthy' and inflamed tissue. The gradient of ICAM-1 in junctional epithelium, with the strongest staining on the crevicular aspect plus the vascular expression of ELAM-1 and ICAM-1 in both clinically 'healthy' and inflamed tissue may be crucial processes which direct leukocyte migration towards the gingival crevice.

Effects of sodium bicarbonate on butyric acid-induced epithelial cell damage in vitro

“…The viability of cells treated in combination with sodium bicarbonate was improved significantly compared to cells treated with butyric acid alone; sodium bicarbonate alone had no effect on ICAM-1 expression. ICAM-1 expression in the epithelium is thought to play an important role in leukocyte transendothelial migration to areas of inflammation in gingival tissue (16)(17)(18). Our results indicated that sodium bicarbonate significantly Fig.…”

Lymphocyte-Fibroblast Interactions

“…For example, in the setting of chronic inflammation, ELAM-I is preferentially expressed on venules in the skin (Norris et al, 1991). Expression of ELAM-I's lymphocyte ligand, cutaneous lymphocyte-associated antigen (CLA), is largely limited to a skin-homing subset of memory/effector T-lymphocytes (Berg et al, 1991 (Moughal et al, 1992;Tonetti et al, 1994 sented by a cell that takes up and degrades it and displays the relevant immunogenic fragments in the context of MHC Class 11 products An antigen-presenting cell (APC) therefore must express MHC Class 11 antigens. It has been speculated that normally MHC Class 11 antigennegative cell types-including endothelial cells (De Waal et ci., 1983, Geppert andLipsky, 1985), astrocytes (Wong et ci., 1984), keratinocytes (Breathnach and Katz, 1983;Basham et cil., 1984), and fibroblasts (Pober et al, 1983;Geppertand Lipsky, 1985, Maureretal., 1985, 1987 Previous studies systematically examined APC function of MHC Class II-positive dermal fibroblasts which had been stimulated with IFN-y (Pober et cil, 1983, Geppert and Lipsky, 1985, Umetsu et al, 1985Maurer et cal., 1987).…”

Concentration- and time-dependent response of human gingival fibroblasts to fibroblast growth factor 2 immobilized on titanium dental implants

“…ICAM1, which is a widely expressed cell adhesion molecule [48][49][50] and belongs to the immunoglobulin super family, plays an important physiological role in routing polymorphonuclear neutrophils to the gingival sulcus efficiently and initiating a host response toward the implant. The expression of endothelial cell adhesion molecules (CAMs) for leukocytes, P-selectin, E-selectin, and ICAM1 is significantly upregulated in inflamed tissues by FGF2.…”