Vascular adhesion molecules in oral lichen planus.
OBJECTIVE
Because recruitment and retention of lymphoid cells appear to be critical components of the pathogenesis of lichen planus, we have compared the expression and distribution of a panel of vascular adhesion 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.


METHODS
Frozen sections of 12 clinically 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 vascular endothelium was evaluated semiquantitatively. Three microvascular zones or compartments were defined and evaluated separately.


RESULTS
Generally, different staining patterns were observed in association with the various endothelium-associated adhesion molecules. In normal controls, 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 frequently showed variations in intensity. In lichen planus, increased staining for ELAM-1, P-selectin, ICAM-1, and VCAM-1 was evident in one or more of the microvascular compartments. In the subepithelial vascular compartment where the infiltrate was the most dense, VCAM-1 appeared to show the greatest positive change. Almost all cells in the lichen planus infiltrates stained positive for ICAM-1, L-selectin, LFA-1, and VLA4, 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 subepithelial 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 retention in the active lichen planus lesion.
Regezi
J A
JA
Department of Stomatology, School of Dentistry, University of California, San Francisco, USA.
Dekker
N P
NP
MacPhail
L A
LA
Lozada-Nur
F
F
McCalmont
T H
TH
D000328:Adult; D000368:Aged; D018952:Antigens, CD34 / Q000032:analysis / Q000096:biosynthesis; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000096:biosynthesis*; D019040:E-Selectin / Q000032:analysis / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000737:chemistry / Q000276:immunology; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D039041:Integrin alpha4beta1; D016023:Integrins / Q000032:analysis / Q000096:biosynthesis; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis; D019041:L-Selectin / Q000032:analysis / Q000096:biosynthesis; D017676:Lichen Planus, Oral / Q000276:immunology* / Q000378:metabolism; D016169:Lymphocyte Function-Associated Antigen-1 / Q000032:analysis / Q000096:biosynthesis; D016177:Macrophage-1 Antigen / Q000032:analysis / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D009061:Mouth Mucosa / Q000737:chemistry / Q000276:immunology; D019007:P-Selectin / Q000032:analysis / Q000096:biosynthesis; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis; D016201:Receptors, Lymphocyte Homing / Q000032:analysis / Q000096:biosynthesis; D015854:Up-Regulation; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis
D018952:Antigens, CD34; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D039041:Integrin alpha4beta1; D016023:Integrins; D016169:Lymphocyte Function-Associated Antigen-1; D016177:Macrophage-1 Antigen; D019007:P-Selectin; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D016201:Receptors, Lymphocyte Homing; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D019041:L-Selectin