HOST RESPONSES IN PERIODONTAL-DISEASES - CURRENT CONCEPTS
HOST RESPONSES IN PERIODONTAL-DISEASES - CURRENT CONCEPTS
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DOI：
10.1902/jop.1992.63.4s.338
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发表时间：
1992-04-01
影响因子：
4.3
通讯作者：
GENCO, RJ
中科院分区：
文献类型：
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作者：
GENCO, RJ
在牙周病中，细菌引发炎症宿主反应，与细菌的直接破坏性作用一起，导致大部分组织破坏。牙周炎性反应大体上是免疫学的，免疫生物学知识的爆炸性增长促进了我们对这些反应的理解，本文对其中一些知识进行了讨论。了解免疫细胞及其调节细胞表面分子(如MHC、CD抗原和受体)的作用，以及启动的效应系统(如吞噬细胞和细胞毒性T细胞)以及效应分子(如抗体、补体和细胞因子)的知识，有助于更好地理解牙周病的复杂发病机制。基质金属蛋白酶、蛋白多糖、激动素和过敏性毒素等介质，以及包括花生四烯酸代谢产物在内的低分子介质在牙周病中的作用已开始被阐明。开发基于宿主反应的诊断试验的重要研究途径是显而易见的。例如，牙周炎症过程中释放的组织产物，包括金属蛋白酶、弹力酶、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/补体轴对于牙周细菌的保护至关重要，这一系统的异常往往会导致牙周易感性的增加，这为开发评估风险的诊断试验提供了方法。包括转化生长因子-β、干扰素和IL-1受体拮抗剂在内的一组炎症负性调节因子为牙周病缓解期或愈合期的评估提供了潜在的可能性。最后，诸如人类白细胞抗原相关性和中性粒细胞异常的分子基础等因素可能为牙周病的易感性提供遗传标记。基于宿主反应措施的诊断因子为预测宿主的易感性提供了巨大的潜力，并可能与识别特定感染微生物的微生物诊断结合使用。
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.