Effects of interleukin 1 on the proceeding process in apical periodontitis

作为对IL-1在牙周炎发病过程中的基础性研究，本文采用培养系统成纤维细胞、成骨细胞和软骨细胞进行生化和免疫学研究。此外，我们还探讨了根管渗出物来源的IL-1样因子与根尖牙周炎临床症状的关系。所得结果如下：1。在sds-page还原条件下，经muramyl dipeptide （MDP）刺激的豚鼠成纤维细胞获得的胸腺细胞活化因子（FTAF）在分子量为20000 ~ 35000的范围内出现，在PH为3.5 ~ 4.7的范围内迁移，表明FTAF为酸性分子。人重组IL-1、IL-1和TNF显著抑制糖胺聚糖的合成，并刺激培养软骨细胞中蛋白聚糖的分解。6种不同的抗IL-1单克隆抗体可中和IL-1诱导的糖胺聚糖合成抑制和蛋白聚糖分解刺激。IL-1诱导的组织学变化表现为成骨细胞变平，与骨表面的物理分离。发现IL-1可能通过作用于骨微环境中的破骨细胞前体而引起骨表面附着。此外，高纯度IL-1的制备激活了破骨前细胞向破骨细胞的分化。在根尖牙周炎患者根管渗出液中检测到分子量为10000的il -1样因子。结果表明，经牙髓治疗后，il -1样因子的活化消失。此外，il -1样因子的作用可被抗il -1抗血清特异性中和。

As a fundamental study on IL-1, the proceeding process in periodontitis was examined biochemically and immunologically using fibroblasts, osteoblasts and chondrocytes in cultured system. Moreover, we clinically invstigated into the relationship between IL-1 like factor derived from exudate of root canal and clinical symptoms in apical periodontitis. The results obtained were as follows.1. Thymocyte activating factor (FTAF) derived from guinea pig fibroblast stimulated with muramyl dipeptide (MDP) appeared at molecular weight range of 20,000 to 35,000 under reducing condition of sds-page, and migrated at PH range of 3.5 to 4.7, indicating acidic molecule of FTAF.2.Human recombinant IL-1 , IL-1 and TNF strikingly inhibited the synthesis of glycosaminoglycan and stimulated breakdown of proteoglycan in cultured chondrocytes. Six different anti-IL-1 monoclonal antibodies neutralized IL-1 -induced inhibition of glycosaminoglycan synthesis and stimulation of proteoglycan breakdown.3.Histological changes induced by IL-1 showed a flattening of the osteoblast, and a physical separation from the underlying bone surface. It was found that IL-1 may cause attachment to the bone surface by an action on osteoclast precursors in the bone microenvironment. Moreover, highly-purified preparations of IL-1 activated differentiation of preosteoclasts into osteoclasts.4.IL-1-like factor with molecular weight 10,000 was detected in exudate of root canal in patients with apical periodontitis. It was demonstrated that the activation of IL-1-like factor disappeared after endodontic therapy. Moreover, the effect of IL-1-like factor was specifically neutralized by anti-IL-1 antisera.