Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.
Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.
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DOI：
10.1111/j.1600-0765.1998.tb02313.x
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发表时间：
1998
影响因子：
3.5
通讯作者：
G. Salvi;C. E. Brown;K. Fujihashi;H. Kiyono;F. Smith;J. Beck;S. Offenbacher
中科院分区：
文献类型：
--
作者：
G. Salvi;C. E. Brown;K. Fujihashi;H. Kiyono;F. Smith;J. Beck;S. Offenbacher
根据修复文献，处于自然牙列和无牙列之间过渡阶段的受试者被称为“终末牙列”（TD）病例。本横断面调查的目的是描述两组终末牙列牙周炎患者的局部和全身炎症反应。8例重度成人终末牙列牙周炎（AP-TD）患者和8例早发性终末牙列牙周炎（EOP-TD）患者进入研究。我们的目的是测量龈沟液（GCF）和脂多糖（LPS）刺激的单核细胞培养上清液以及牙龈单核细胞信使RNA（mRNA）从活检样品确定的转录细胞因子的扩展电池。在GCF内，基于浓度的约10倍差异，有3个介质层（水平）。最高层包括前列腺素E2（PGE 2）、白细胞介素-1 β（IL-1 β）和白细胞介素-2（IL-2），中间层包括肿瘤坏死因子α（TNF α）和干扰素γ（IFN-γ），最低浓度水平为白细胞介素-4（IL-4）和白细胞介素-6（IL-6）。因此，GCF分析清楚地表明，在AP-TD和EOP-TD组中，单核细胞，即IL-1 β和PGE 2以及Th 1，即IL-2和IFN-γ，炎症介质水平在数量上超过Th 2介质，即IL-4和IL-6。与21名患有中度至晚期成人牙周炎的受试者的对照组相比，AP-TD和EOP-TD组中LPS刺激的单核细胞释放的IL-1 β、PGE 2和TNF α显著升高。牙龈单个核细胞的细胞因子mRNA表达显示，在AP-TD和EOP-TD组中，Th 1和Th 2细胞因子均表达，IL-4和IL-12水平较低。总之，我们的数据表明，这种横截面TD牙周炎模型可能反映与牙齿脱落相关的进行性牙周病。此外，虽然GCF中的Th 1细胞因子水平主导Th 2应答，但单核细胞活化提供了促炎介质的主要来源。此外，LPS刺激的外周血单核细胞表现出在终末牙列中的炎症介质分泌上调。
Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.