Pathogenic mechanisms of apical periodontal diseases : Kinetics of dendritic cells and immure functional molecules

本研究旨在探讨树突状细胞在根尖周炎发生发展中的作用。通过暴露未封闭牙髓诱导大鼠磨牙根尖周病变，应用免疫电镜观察根尖周病变后树突状细胞的超微结构、分布密度及免疫功能分子的表达。在活动性病变扩展期（扩展期），巨噬细胞占优势，仅检测到少量树突状细胞。然而，在病变稳定（慢性期）后，大多数表达MHC II类分子的细胞被鉴定为树突状细胞。在慢性期，树突状细胞和淋巴细胞之间的细胞间接触有时可见。树突状细胞的形态学变化也被注意到：细胞薄，短的胞质突起和发育不良的细胞器在扩张阶段占主导地位，而长的胞质突起的大细胞在慢性阶段占主导地位。慢性期树突状细胞可分为两个亚群：大部分树突状细胞表达CD 11 c，少数树突状细胞表达OX 62，胞体小而圆，胞质突起短。这些结果表明，树突状细胞，根据成熟/活化的阶段，由不同的亚群组成，参与病变慢性化作为抗原呈递细胞在响应慢性抗原挑战从感染根管。

This study aimed to investigate the role of dendritic cells in the development of apical periodontitis. Experimental periapical lesions were induced in rat molars by making unsealed pulp exposures, and ultrastructure, distributional density and immune functional molecule expression of dendritic cells were investigated by means of inmunoelectron microscopy. During the period of active lesion expansion (expanding stage), macrophages were dominant and only a small number of dendritic cells were detected. Following lesion stabilization (chronic stage), however, most of MHC class II molecule-expressing cells were identified as dendritic cells. Cell-to-cell contact between dendritic cells and lymphocytes was sometimes seen in the chronic stage. Morphological change of dendritic cells was also noted : cells with thin and short cytoplasmic processes and poorly developed organelles were predominant in the expanding stage, whereas large cells with long cytoplasmic processes were predominant in the chronic stage. Moreover, dendritic cells in the chronic stage were divided into two subpopulations according to the immunoreactivity to CD11c and OX62 : although most dendritic cells expressed CD11c, there were minor but definite subpopulation which expressed OX62 and had a small and round cell body with a small number of short cytoplasmic processes. These findings suggested that dendritic cells, composed of different subpopulations according to the stage of maturation/activation, are involved in lesion chronicity by acting as antigen presenting cells in response to chronic antigenic challenge from infected root canals.