Immune defense mechanisms of the dentin/pulp complex. An immunological and molecular biological analysis

牙本质/牙髓复合物的免疫防御机制。

• 批准号: 11470402
• 负责人: OKIJI Takashi
• 金额: $ 9.86万
• 依托单位: NIIGATA UNIVERSITY (2001)Tokyo Medical and Dental University (1999-2000)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2001
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-11470402/
• 关键词: dendritic cell; macrophage; HLA-DR; inflammatory cytokines; inducible nitric oxide synthase; cvclooxvgenase-2; dental caries; pulpitis; 歯髄; 共刺激分子; 免疫組織化学; 分子生物学; サイトカイン; inducible nitric oxide synthase; RT-PCR

Immunohistochemical and molecular biological analyzes were conducted in order to investigate the roles of pulpal densritic cells (DCs) in the pathogenesis of pulpal diseases. Results obtained were as follows:1. In human teeth bearing pulp exposure-free dentinal caries, HLA-DR-expressing pulpal DCs exhibited a localized accumulation beneath the affected dentinal tubules. The accumulation was evident in teeth with a shallow carious lesion. The majority of'the pulpal DCs expressed CD14 and CD68. In teeth with a deep carious lesion, expression of CD83 and CD86 was detected on some DCs. T cells showed a marked increase in teeth with shallow dentinal caries. These T cells were mostly memory cells expressing CD45RO, and some of them co-expressed CD25, a marker for activated T cells. However, B cells showed an increase only in teeth with deep dentinal caries. These results suggest that DC-T cell interaction and subsequent activation of T cells are involved in the initial pathogenesis of pulpal diseases.2. Expression of inducible nitric oxide synthase (iNOS) mRNA in LPS-induced pulpitis of rat upper incisors peaked at 6 hrs, which was detected by means of reverse transcription polymerase chain reaction (RT-PCR). Immunohistochemical staining for rat iNOS revealed that most of the iNOS-positive cells were macrophages. The expression of mRNAs for cyclooxygenase-2 (COX-2) and pro-inflammatory cytokines peaked at 3 to 6 hrs, whereas IL-10 (anti-inflammatory cytokine) mRNA was first detected at 6 hrs. Administration of an iNOS inhibitor caused drastic decrease in the expression of mRNAs for COX-2 and inflammatory cytokines in the inflamed pulp. These results indicate that NO generated by macrophages may regulate the pulpal inflammatory reactions.

通过免疫组织化学和分子生物学分析，探讨牙髓致密细胞（DCs）在牙髓疾病发病中的作用。实验结果如下：1。在患有无牙髓暴露的牙本质龋齿的人牙齿中，表达hla - dr的牙本质dc在受影响的牙本质小管下表现出局部积累。在牙齿中有明显的堆积，并有浅的龋损。大多数髓质dc表达CD14和CD68。在龋深病变的牙齿中，CD83和CD86在部分dc上表达。T细胞在浅牙本质龋齿中明显增加。这些T细胞大多是表达CD45RO的记忆细胞，其中一些共表达CD25，这是激活T细胞的标记物。然而，B细胞仅在深牙本质龋中增加。这些结果表明，DC-T细胞的相互作用和随后的T细胞活化参与了牙髓疾病的初始发病机制。逆转录聚合酶链反应（RT-PCR）检测诱导型一氧化氮合酶（iNOS） mRNA在lps诱导的大鼠上门牙牙髓炎6 h时表达达到峰值。免疫组化染色显示，iNOS阳性细胞以巨噬细胞居多。环氧化酶-2 （COX-2）和促炎细胞因子mRNA的表达在3 ~ 6小时达到峰值，而IL-10（抗炎细胞因子）mRNA的表达在6小时首次检测到。注射一种iNOS抑制剂导致发炎牙髓中COX-2 mrna和炎性细胞因子的表达急剧下降。这些结果表明巨噬细胞产生的NO可能调节牙髓炎症反应。

项目成果

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Takashi Koji 等人：“牙髓炎和根尖周炎的起源”《牙科世界展望》独立卷 1 新牙髓病学 (New Endodontics)。

A.M.M. Kamal, T. Okiji 他: "Responses of class II molecule-expressing cells and macrophages to cavity preparation and restoration with 4 META/MHA-TBB resin"International Endodontic Journal. (発売予定).

A.M.M. Kamal、T. Okiji 等人：“II 类分子表达细胞和巨噬细胞对使用 4 META/MHA-TBB 树脂制备和修复牙洞的反应”《国际牙髓杂志》（待发布）。

Kaneko T: "Ultrastructural analysis of MHC class II molecule-expressing cell in experimentally induced periapical lesions in the rat"Journal of Endodontics. 27. 337-342 (2001)

Kaneko T：“实验诱导大鼠根尖周病变中 MHC II 类分子表达细胞的超微结构分析”牙髓学杂志。

Kan L, et al.: "Localization and density of myeloid leukocytes in the periodontal ligament of normal rat molars"Archives of Oral Biology. 46(6). 509-520 (2001)

Kan L 等人：“正常大鼠磨牙牙周韧带中骨髓白细胞的定位和密度”口腔生物学档案。

Okiji T: "Seltzer and Bender's Dental Pulp"Quintessense publishing (in press). (2002)

Okiji T：“Seltzer 和 Bender 的牙髓”Quintessense 出版（正在印刷中）。