Immunologic dysfunction in the pathogenesis of periodontal diseases.
Immunologic dysfunction in the pathogenesis of periodontal diseases.
复制标题
牙周病发病机制中的免疫功能障碍。
DOI：
10.1111/j.1600-051x.1987.tb00989.x
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发表时间：
1987
影响因子：
6.7
通讯作者：
Shenker,BJ
中科院分区：
文献类型：
--
作者：
Shenker,BJ
尽管我们对牙周病发病机制和病因学的理解取得了重大进展，但免疫系统对这种疾病的性质和贡献仍不清楚。一些研究提供了保护性或破坏性作用的证据。这些相互矛盾的发现很难调和，因为大多数解释倾向于认为免疫系统具有静态的贡献作用（即保护性或破坏性）。目前关于免疫反应作用的理论并没有解决这些相互矛盾的发现，也没有解决这些患者面对持续感染时令人愉快的免疫反应的矛盾观察。在本文中，我们根据现有数据提出了一个模型，用于说明免疫系统对牙周病发病机制的贡献。该模型归因于免疫反应的动态作用。正如其他传染病中所记录的那样，例如，在牙周病进展的最早阶段，完全有可能出现免疫功能障碍的状态；随后可能会出现一段活跃的免疫反应（体液和/或细胞），这将代表延迟或抑制的反应。该模型与最近的发现一起讨论，即几种可疑的牙周病原体能够产生免疫抑制剂。关于宿主对口腔病原体的免疫反应及其与牙周病的进展和严重程度的相关性（或缺乏相关性）的许多明显矛盾的临床观察结果可以在该模型中得到解释。
Despite significant progress in our understanding of the pathogenesis and etiology of periodontal diseases, the nature and contribution of the immune system to this disorder remains unclear. Several studies provide evidence for either a protective or destructive rôle. These conflicting findings are difficult to reconcile, since most interpretations tend to argue for a static contributory rôle (i.e., either protective or destructive) of the immune system. Current theories on the role of the immune response do not address these conflicting findings as well as the contradictory observation of a delectable immune response in the face of persistent infection in these patients. In this article, we present a model, based on available data, for the contribution of the immune system to the pathogenesis of periodontal disease. This model ascribes a dynamic role for the immune response. As documented in other infectious diseases, it is entirely possible, for example, that a state of immunologic dysfunction may occur in the earliest stages of periodontal disease progression; this may then be followed by a period of active immune reactivity (humoral and/or cellular) that would represent either a delayed or depressed response. This model is discussed in conjunction with recent findings that several suspected periodontal pathogens are capable of producing immuno‐suppressive agents. Many of the apparently contradictory clinical observations concerning the host immune response to oral pathogens and its correlation (or lack of) with both the progression and severity of periodontal disease may be accounted for in this model.