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A Study of Macrophages, Macrophage-related Cells, and Endothelial Adhesion Molecules in Recurrent Aphthous Ulcers in HIV-positive Patients

Department of Stomatology, School of Dentistry, Division of Oral Pathology, University of California, San Francisco, California 94143-0424

L.A. Macphail

Department of Stomatology, School of Dentistry, Division of Oral Pathology, University of California, San Francisco, California 94143-0424

D.W. Richards

Department of Stomatology, School of Dentistry, Division of Oral Pathology, University of California, San Francisco, California 94143-0424

J.S. Greenspan

Department of Stomatology, School of Dentistry, Division of Oral Pathology, University of California, San Francisco, California 94143-0424

The purpose of this immunohistochemical study was to investigate the presence and distribution of macrophages (CDllc+ and CD68+) and macrophage-related dendritic cells (factor XIIIa+ and CD36+) in early and late aphthous ulcers associated with HIV infection. To substantiate a mechanism by which these cells may move from the vascular compartment to tissue spaces, we also investigated expression of ELAM (endothelial leukocyte adhesion molecule), ICAM-1 (intercellular adhesion molecule), and CD18 (leukocyte function antigen). Numerous CD 1 lc+ and CD68+ macrophages were seen in early lesions, though larger numbers of CD68+ cells were present in older lesions. No significant increases in factor XIIIa+ dendrocytes were seen in either early or late lesions, though dendrocytes appeared enlarged. CD36+ cells and CD18+ leukocytes were more numerous in early than in late aphthous ulcers. ELAM and ICAM expression was most intense on endothelial cells in early aphthous ulcers, with staining intensity fading toward the lesion periphery. Control specimens showed weaker ELAM and ICAM staining than did the ulcer specimens. Keratinocytes did not express ICAM. By virtue of their numbers, macrophages and macrophage subtypes appear to have a significant role in both the early and late stages of this disease. Although factor XIIIa-expressing dendrocytes may not have been more numerous in the ulcers, they appeared to be "activated" because of their prominence in the lesions and their occasional co-expression of CD68 antigen (KP1+). They may have a minor role in antigen processing, phagocytosis, and fibroplasia. ELAM and ICAM expression by endothelial cells provides a mechanism by which macrophages and other leukocytes can be recruited to the site of the lesion. This mechanism appears to be functional in HIV-positive patients.

Journal of Dental Research, Vol. 72, No. 12, 1549-1553 (1993)
DOI: 10.1177/00220345930720120301


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