VASCULAR ADHESION MOLECULES IN ORAL LICHEN-PLANUS

Citation
Ja. Regezi et al., VASCULAR ADHESION MOLECULES IN ORAL LICHEN-PLANUS, Oral surgery, oral medicine, oral pathology, oral radiology and endodontics, 81(6), 1996, pp. 682-690
Citations number
39
Categorie Soggetti
Pathology,Surgery,"Dentistry,Oral Surgery & Medicine
ISSN journal
10792104
Volume
81
Issue
6
Year of publication
1996
Pages
682 - 690
Database
ISI
SICI code
1079-2104(1996)81:6<682:VAMIOL>2.0.ZU;2-A
Abstract
Objective, Because recruitment and retention of lymphoid cells appear to be critical components of the pathogenesis of lichen planus, we hav e compared the expression and distribution of a panel of vascular adhe sion molecules (ELAM-1, P-selectin, ICAM-1, VCAM-1, PECAM-1, CD34) and leukocyte adhesion molecule ligands (LFA-1, Mac-1, VLA4, L-selectin) in biopsies of this disease. Study design, Frozen sections of 12 clini cally and histologically confirmed cases of lichen planus and 9 normal control tissues were evaluated immunohistochemically with a standard 1-day avidin-biotin peroxidase technique. Staining intensity of vascul ar endothelium was evaluated semiquantitatively. Three microvascular z ones or compartments were defined and evaluated separately. Results, G enerally, different staining patterns were observed in association wit h the various endothelium-associated adhesion molecules. In normal con trols, PECAM was intensely expressed and VCAM-1 was weakly expressed. Intermediate staining was associated with ELAM-1, P-selectin, ICAM-1, and CD34. Staining within the three microvascular compartments frequen tly showed variations in intensity. In lichen planus, increased staini ng for ELAM-1, P-selectin, ICAM-1, and VCAM-1 was evident in one or mo re of the microvascular compartments, In the subepithelial vascular co mpartment where the infiltrate was the most dense, VCAM-1 appeared to show the greatest positive change, Almost all cells in the lichen plan us infiltrates stained positive For ICAM-1, L-selectin, LFA-1, and VLA 4, and large numbers of cells also exhibited VCAM-1, PECAM-1, and Mac- 1 immunoreactivity. Conclusions. It appears that upregulation of ELAM- 1, ICAM-1, and VCAM-1 (especially by endothelial cells in the subepith elial vascular plexus) could play a role in the pathogenesis of lichen planus. The expression of leukocyte receptors L-selectin, LFA-1, and VLA4 by most of the cells in the lichen planus infiltrate suggest that these molecules may be responsible for recruitment as well as retenti on in the active lichen planus lesion.