An immunoelectron-microscopic study of class II major-histocompatibility complex molecule-expressing macrophages and dendritic cells in experimental rat periapical lesions

Previous studies have demonstrated that heterogeneous populations of class II major histocompatibility complex (MHC) molecule-expressing non-lymphoid cells, ultrastructurally classified as macrophages and dendritic cell (DC) cell-like cells, comprise the major immune cell population in experimental periapical lesions in rat molars. In this study, the temporal changes in re lative proportions of the two types of cells were examined, on the hypothes is that they are involved in different aspects of the pathogenesis of the l esions. The lesions were induced by making surgical pulp exposures in mandi bular first molars of 5-week-old Wistar rats. Observation periods were set at 0 (normal), 3, 14, 28, and 56 days. Non-lymphoid cells immunoreactive to OX6 (reactive to class II MHC molecules) were classified as macrophages an d DC cell-like cells according to their ultrastructure, and the frequencies of the two types of cells were assessed at each time-point. ED1 (reactive to nearly all macrophages and DCs) was also used to identify macrophages an d DC cell-like cells. At 3 days, most OX6 + cells and ED1 + cells in the pe riapical tissue had the ultrastructural appearance of newly recruited macro phages. At 14 days, when the lesion was actively expanding, there were sign ificantly more OX6 + macrophages than OX6 + DC cell-like cells (P < 0.01). However, at 28 days, when lesion expansion had ceased, DC cell-like cells s ignificantly outnumbered OX6 + macrophages (P < 0.01), this remained consta nt at 56 days. Cell-to-cell contact between OX6 + non-lymphoid cells and OX 6 - lymphocytes, suggesting a functional interaction, was most frequently s een at 28 days. These results support the notion that class II MHC molecule -expressing macrophages play some part in the initial lesion expansion, and suggest that DC cell-like cells may primarily be involved in immune defenc e against perpetuated antigenic challenges following lesion stabilization. (C) 2001 Elsevier Science Ltd. All rights reserved.