HOST MEDIATORS IN GINGIVAL CREVICULAR FLUID - IMPLICATIONS FOR THE PATHOGENESIS OF PERIODONTAL-DISEASE
HOST MEDIATORS IN GINGIVAL CREVICULAR FLUID - IMPLICATIONS FOR THE PATHOGENESIS OF PERIODONTAL-DISEASE
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DOI：
10.1177/10454411920030010501
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发表时间：
1992-01-01
期刊：
影响因子：
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通讯作者：
NOVAK, MJ
中科院分区：
文献类型：
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作者：
LAMSTER, IB;NOVAK, MJ
在过去的几年里，相当多的研究从不同方面研究了牙周炎患者牙周液中宿主反应的不同方面，包括特异性标志物与牙周病活动期的关系。急性炎症反应的各种指标(溶酶体酶、β-葡萄糖醛酸酶和胶原酶、细胞质酶、天冬氨酸氨基转移酶、花生四烯酸代谢产物PGE2)与成人慢性牙周炎的临床附着丧失和动物模型的实验性牙周炎有关。相比之下，牙周炎患者体液免疫反应指标与活动性牙周病的关系不明确。此外，近年来在牙周病中发现了许多细胞免疫反应的指标(如IL-1-α、IL-1-β、肿瘤坏死因子-α)，但尚未研究它们与牙周病活动期的关系。来自GCF研究的证据表明，这些细胞的高反应性在某些形式的牙周病的活动期起着关键作用。PMN的代谢激活可能与许多潜在的破坏性反应有关。PMN对组织破坏的主要作用机制是PMN蛋白水解酶的释放和这些细胞产生的活性氧代谢产物的协同作用。PMN的启动，其中PMN的反应被不启动反应的介质增强，可能是沟隙环境中PMN激活的一个重要机制；例如，IL-1-β和TNF-α等细胞因子以及从龈下革兰氏阴性菌释放的脂多糖可以起到这一功能。这里提出的假设认为，除了与PMN定性或定量缺陷相关的严重形式的牙周病外，这些细胞的高反应性还可以观察到牙周组织的破坏。这些不同的结论不会造成两难境地，但可能代表着不再处于平衡状态的平衡的两端。
During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes beta-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-1-alpha, IL-1-beta, tumor necrosis factor-alpha), but their relationship to active phases of periodontal disease have not been studied.The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1-beta and TNF-alpha, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.