Lamster Ira B, Smith Quenton T, Celenti Romanita S, Singer Robert E, Grbic John T
Division of Periodontics, School of Dental and Oral Surgery, Columbia University, New York, NY.
Department of Oral Sciences, School of Dentistry, University of Minnesota, Minneapolis, MN.
J Periodontol. 1994 May;65 Suppl 5S:511-520. doi: 10.1902/jop.1994.65.5s.511.
Advances in our understanding of the relationship between the microbial challenge and the host response in periodontal disease have led to the search for pathogenesisbased risk indicators or risk factors for disease progression. This evaluation is based on analysis of non-invasive or minimally invasive samples that allow measurement of the subgingival plaque microflora or the host response in gingival crevicular fluid (GCF), serum, or saliva. Studies conducted by us have indicated that in GCF, persistently elevated levels of β-glucuronidase (βG, a marker for primary granule release from polymorphonuclear leukocytes) are associated with clinical attachment loss in patients with periodontitis. This finding has been confirmed in a multicenter trial. We have also observed that a statistically significant positive correlation exists between βG in GCF and measures of the subgingival microbial challenge, but the correlation was less than 0.5, suggesting variations in the host response to the challenge. Furthermore, βG levels in GCF were inversely correlated with the IgG serum antibody titer to a panel of periodontal pathogens, suggesting the essentially protective function of the systemic humoral response in periodontal disease. Data in the literature support this concept. In addition, recent studies of the relationship of antibody isotypes in GCF to progression of clinical attachment loss have suggested that IgA in GCF has a protective function. This may relate to the lack of complement activation by IgA. Alternately, the development of IgA antigen-specific responses are T-cell dependent, and reductions in local levels of IgA may indicate a decrease in T-helper cell function. These data have allowed development of strategies for identifying individual risk profiles for patients with periodontal disease based on the host response to the microbial challenge. With identification of these risk indicators/risk factors for active periodontal disease, the next challenge is to provide clinicians with access to the tests and analyses that are required for this approach to periodontal diagnosis. Improved patient management should result from the incorporation of these tests into clinical practice. J Periodontol 1994;65:511-520.
我们对牙周病中微生物刺激与宿主反应之间关系的理解取得了进展，这促使人们寻找基于发病机制的疾病进展风险指标或危险因素。该评估基于对非侵入性或微创样本的分析，这些样本可用于测量龈下菌斑微生物群或龈沟液（GCF）、血清或唾液中的宿主反应。我们进行的研究表明，在GCF中，β-葡萄糖醛酸酶（βG，一种多形核白细胞初级颗粒释放的标志物）持续升高与牙周炎患者的临床附着丧失有关。这一发现已在一项多中心试验中得到证实。我们还观察到，GCF中的βG与龈下微生物刺激指标之间存在统计学上显著的正相关，但相关性小于0.5，这表明宿主对刺激的反应存在差异。此外，GCF中的βG水平与针对一组牙周病原体的IgG血清抗体滴度呈负相关，这表明全身体液反应在牙周病中具有基本的保护作用。文献中的数据支持这一概念。此外，最近关于GCF中抗体亚型与临床附着丧失进展关系的研究表明，GCF中的IgA具有保护作用。这可能与IgA缺乏补体激活有关。或者，IgA抗原特异性反应的发展是T细胞依赖性的，局部IgA水平的降低可能表明T辅助细胞功能下降。这些数据使得能够制定基于宿主对微生物刺激的反应来识别牙周病患者个体风险概况的策略。随着这些活动性牙周病风险指标/危险因素的确定，下一个挑战是为临床医生提供进行这种牙周诊断方法所需的检测和分析。将这些检测纳入临床实践应能改善患者管理。《牙周病学杂志》1994年；65:511 - 520。
