The Role of Immune Regulatory Mechanisms in the Pathogenesis of Periapical Periodontitis

慢性根尖周炎是根管系统感染的细菌与宿主免疫细胞相互作用的慢性破坏性疾病。局部宿主反应导致根尖周病变中大量促炎和抗炎细胞因子和介质的释放。我们定量了根尖周渗出液中IL-1β和IL-1 ra的水平，并表明IL-1 ra介导的拮抗作用阻断了局部产生的IL-1活性。IL-1 ra：IL-1β比值降低导致根尖周病变急性炎症活动增强。我们的定量分析还显示，从症状性根尖周病变的根尖周渗出液中IL-8的产生增加。IL-8与NO水平呈显著正相关。进行半定量RT-PCR分析以确定根尖周组织标本中促炎和抗炎细胞因子和生长因子信息的表达。结果表明，考克斯 关于我们 IL-2和IL-8的信息存在于所有测试的样品中，并提示根尖周病变中促炎介质的产生上调。另一方面，在大多数样品中检测到抗炎细胞因子、IL-10和TGF-β1 mRNA。我们还发现在大多数测试样本中存在IGF-1和EGF信息。体外研究还表明，人单核细胞长期暴露于牙龈卟啉单胞菌LPS导致LPS耐受性的诱导，这导致细胞功能的选择性上调或下调。我们的数据还表明IL-10以自分泌方式介导牙龈卟啉单胞菌LPS耐受单核细胞中IL-6的下调。这些结果表明，在慢性炎症性疾病根尖周炎的调节中的促炎和抗炎细胞因子和介质的潜在参与。总之，解剖这些细胞因子和介质的确切作用，对根尖周发病机制的影响，可能会提供新的诊断程序和治疗药物的发展机会。少

Chronic periapical periodontitis is a chronic destructive disease characterized by an interaction of bacteria infected in the root canal system and the host immune cells. The local host response results in the release of wide array of the pro-and anti-inflammatory cytokines and mediators in the periapical lesion. We quantified the levels of IL-1β and IL-1ra in periapical exudates, and indicated that IL-1ra-mediated antagonism occurred to block locally produced IL-1 activity. Decreased IL-1ra : IL-1β ratio resulted in an acute and higher inflammatory activity in periapical lesion. Our quantitative analysis also revealed increased IL-8 production in the periapical exudate from symptomatic periapical lesion. A significantly positive correlation was found between IL-8 and nitric oxide levels. Semi-quantitative RT-PCR analysis was performed to determine the expression of pro- and anti-inflammatory cytokine and growth factor messages in the periapical tissue specimen. Results showed that COX … More -2 and IL-8 messages were present in all samples tested, and suggested up-regulated production of pro-inflammatory mediators in periapical lesions. On the other hand, anti-inflammatory cytokines, IL-10 and TGF-β1 mRNA was detected in most samples. We also showed the presence of IGF-1 and EGF messages in the majority of test specimens. In vitro studies also revealed that the chronic exposure of human monocytes to Porphyromonas gingivalis LPS resulted in the induction of LPS tolerance that resulted in the selective up-or down-regulation of cell functions. Our data also suggested that IL-10 mediate IL-6 down-regulation in P. gingivalis LPS-tolerant monocytes in an autocrine manner. These results suggest the potential involvement of both the pro-and anti-inflammatory cytokines and mediators in the regulation of chronic inflammatory disease periapical periodontitis. In conclusion, dissection of the precise role of these cytokines and mediators that have an impact on perapical pathogenesis may provide opportunities for the development of new diagnostic procedures and therapeutic agents. Less