Genco R J
Department of Oral Biology, School of Dental Medicine, State University of New York, Buffalo.
J Periodontol. 1992 Apr;63(4 Suppl):338-55. doi: 10.1902/jop.1992.63.4s.338.
In periodontal diseases, bacteria trigger inflammatory host responses which, along with the direct destructive effects of the bacteria, cause most of the tissue destruction. Periodontal inflammatory responses are, by and large, immunologic, and our understanding of these reactions has been advanced by the explosion of knowledge in immunobiology, some of which is discussed in this review. Understanding the role of immune cells and their regulatory cell surface molecules such as the MHC, CD antigens, and receptors, as well as knowledge of effector systems set into motion such as phagocytes and cytotoxic T-cells, and the effector molecules such as antibodies, complement, and cytokines, have led to better understanding of the complex pathogenesis of periodontal disease. The role of mediators including the matrix metalloproteinases, proteoglycans, the kinins and anaphylatoxins, and low molecular weight mediators including products of arachidonic metabolism is beginning to be elucidated in periodontal disease. Important avenues of research for development of diagnostic tests based upon host response are apparent. For example, tissue products released during periodontal inflammation including the metalloproteinases, elastase, cytokines, prostaglandins, antibodies, and complement components may provide the basis for future diagnostic indicator tests. The recognition that the neutrophil/antibody/complement axis is critical for protection against periodontal bacteria and that abnormalities in this system often lead to increased periodontal susceptibility provide approaches for the development of diagnostic tests assessing risk. A group of factors which are negative regulators of inflammation including TGF-beta, gamma-interferon, and IL-1 receptor antagonist provide potential for assessment of periodontal disease in remission or in the healing phase. Finally, factors such as HLA associations and the molecular basis for neutrophil abnormalities may provide genetic markers for periodontal disease susceptibility. Diagnostic factors based upon host response measures offer great potential for predicting host susceptibility and will likely be used in combination with microbial diagnostics which identify specific infecting organisms.
在牙周疾病中，细菌引发宿主的炎症反应，这些反应连同细菌的直接破坏作用，导致了大部分组织损伤。大体而言，牙周炎症反应是免疫性的，免疫生物学知识的激增推动了我们对这些反应的理解，本文将讨论其中的一些知识。了解免疫细胞及其调节性细胞表面分子（如主要组织相容性复合体、CD抗原和受体）的作用，以及对诸如吞噬细胞和细胞毒性T细胞等启动的效应系统和诸如抗体、补体和细胞因子等效应分子的了解，有助于更好地理解牙周疾病复杂的发病机制。包括基质金属蛋白酶、蛋白聚糖、激肽和过敏毒素在内的介质的作用，以及包括花生四烯酸代谢产物在内的低分子量介质在牙周疾病中的作用正开始得到阐明。基于宿主反应开发诊断测试的重要研究途径已很明显。例如，牙周炎症期间释放的组织产物，包括金属蛋白酶、弹性蛋白酶、细胞因子、前列腺素、抗体和补体成分，可能为未来的诊断指标测试提供基础。认识到中性粒细胞/抗体/补体轴对抵御牙周细菌至关重要，且该系统的异常往往会导致牙周易感性增加，这为开发评估风险的诊断测试提供了途径。一组作为炎症负调节因子的因素，包括转化生长因子-β、γ-干扰素和白细胞介素-1受体拮抗剂，为评估处于缓解期或愈合期的牙周疾病提供了可能。最后，诸如人类白细胞抗原关联以及中性粒细胞异常的分子基础等因素，可能为牙周疾病易感性提供遗传标记。基于宿主反应测量的诊断因素在预测宿主易感性方面具有巨大潜力，并且可能会与识别特定感染生物体的微生物诊断方法结合使用。
