Pathogenic mechanisms in apical periodontitis : innate immunity, acquired immunity and dendritic cell maturation

本研究旨在加深对树突状细胞和免疫调节分子参与根尖周炎发病机制的认识。激光显微解剖和实时定量聚合酶链式反应显示，未封闭牙髓暴露可引起大鼠磨牙牙周膜MHC-II类分子CD86、CD83、TLR2和TLR4mRNAs表达上调。此外，利用大鼠磨牙全牙培养系统，发现常驻巨噬细胞和树突状细胞在内毒素刺激后上调CD14、TLR4和CX3CR1的表达。

This study aimed to advance the understanding of the involvement of dendritic cells and immunoregulatory molecules in the pathogenic mechanisms in apical periodontitis. Results demonstrated that unsealed pulp exposure caused the upregulation of MHC class II molecules, CD86, CD83, TLR2 and TLR4 mRNAs in the periodontal ligament of rat molars, as revealed by laser microdissection and real time PCR. Moreover, by employing a whole tooth culture system of the rat molar, it was demonstrated that resident macrophages and dendritic cells upregulated the expression of CD14, TLR4 and CX3CR1 following LPS stimulation.