HOST-BACTERIAL INTERACTIONS IN PERIODONTAL DISEASE

牙周炎是牙周组织的慢性炎症性疾病 以疾病活动的爆发和更长时间的 缓解。 结扎引起的牙周炎提供了一个类似的模型， 微生物菌群，其中疾病的速度可以加快。 的诱导 通过免疫增强免疫反应之前，通常 牙周病微生物（例如B.牙龈炎）可以 延迟或减少其殖民化，从而影响发展 和/或牙周炎的严重程度。 如果免疫可以提供一些 保护程度，它将提供一个更好的了解 牙周炎的发病机制，并将潜在的价值， 治疗 本研究的目的是研究免疫接种对儿童健康的影响 与宿主细菌相互作用的主要可培养微生物 在猴子模型中发展为牙周炎的过程中。 具体 目标是： 1.分离龈下优势可培养菌群， 血清和龈沟液抗体水平，这些生物体， 在从牙龈炎进展到牙龈炎的过程中，通过ELISA 结扎引起晚期牙周炎及其关系 观察 2.检查用牙龈拟杆菌免疫猴子的效力 通过监测临床、组织学、细菌学 和体液反应。 将 确定是否由B定殖。牙龈炎，患病率 疾病的进展和/或程度是从一组 假免疫、结扎猴和一组B.牙龈免疫 未结扎的猴子

Periodontitis is a chronic inflammatory disease of the periodontium characterized by bursts of disease activity and longer periods of remission. Ligature-induced periodontitis provides a model with a similar microflora in which the rate of disease can be accelerated. Induction of a heightened immune response via immunization prior to the usual establishment of a periodontopathic organism (such as B. gingivalis) may delay or reduce its colonization and thereby influence the development and/or severity of periodontitis. If immunization could provide some degree of protection, it would provide a better understanding of the pathogenesis of periodontitis and would potentially be of value in treatment. The purpose of this investigation is to study the influence of immunization with a predominant cultivable microorganism on host bacterial interactions during the progression to periodontitis in a monkey model. The specific aims are to: 1. Isolate the predominant cultivable subgingival microflora, determine the serum and gingival crevicular fluid antibody levels to these organisms in cynomolgus monkeys by ELISA during the progression from gingivitis to ligature-induced, advanced periodontitis and describe relationships observed. 2. Examine the efficacy of monkey immunization with Bacteroides gingivalis isolated from monkeys by monitoring the clinical, histological, bacterial and humoral responses during ligature-induced periodontitis. It will be determined if the colonization by B. gingivalis, the rate of disease progression and/or the extent is of disease is modified from a group of sham-immunized, ligated monkeys and a group of B. gingivalis immunized non-ligated monkeys.