Cavanaugh P F, Meredith M P, Buchanan W, Doyle M J, Reddy M S, Jeffcoat M K
Procter and Gamble Company, Cincinnati, OH 45242, USA.
J Periodontal Res. 1998 Feb;33(2):75-82. doi: 10.1111/j.1600-0765.1998.tb02295.x.
The inflammatory mediators prostaglandin E2 (PGE2) and interleukin-1 beta (IL-1 beta) play critical roles in the inflammatory process leading to alveolar bone and connective tissue loss in periodontal disease. Data from a previously published 6-month clinical study demonstrated that twice daily use of 0.1% ketorolac tromethamine oral rinse prevented alveolar bone loss in adults with periodontitis. We further analyzed data from this study to examine the relationship between PGE2. IL-1 beta and bone loss. Patient mean PGE2 and IL-1 beta levels in gingival crevicular fluid (M-GCF) measured throughout the course of the study were directly compared to the maximum amount of alveolar bone height loss observed at a single study site in each patient. The maximum amount of bone loss measured was chosen for the analysis since the pattern of bone loss was clearly episodic in nature. A statistically significant correlation (r = 0.73, p = 0.001) exists between M-GCF PGE2 concentration and the maximum amount of bone height lost at individual patient study sites. The correlation between M-GCF IL-1 beta concentration and maximum bone height lost is also statistically significant (r = 0.66, p = 0.005). Over the 6-month duration of the study, both PGE2 and IL-1 beta were coordinately expressed in the placebo treatment group as reflected in the significant correlation between M-GCF concentrations of the 2 mediators (r = 0.81, p < 0.001). Treatment of patients with 0.1% ketorolac tromethamine twice daily for 6 months resulted in reductions of PGE2 in GCF and a negligible correlation between M-GCF PGE2 and M-GCF IL-1 beta (r = 0.42, p = 0.088). This lack of a strong association between the 2 mediators in the ketorolac treatment group provides a direct biochemical readout of the anti-inflammatory efficacy of ketorolac tromethamine oral rinse in patients with periodontitis. Further studies are warranted to determine the full diagnostic potential of M-GCF levels of PGE2 and IL-1 beta for predicting risk of alveolar bone loss in patients with periodontitis and monitoring periodontal therapy effectiveness.
炎症介质前列腺素E2(PGE2)和白细胞介素-1β(IL-1β)在导致牙周病中牙槽骨和结缔组织丧失的炎症过程中起关键作用。一项先前发表的为期6个月的临床研究数据表明,每天两次使用0.1%酮咯酸氨丁三醇口腔含漱液可预防成人牙周炎患者的牙槽骨丧失。我们进一步分析了该研究的数据,以研究PGE2、IL-1β与骨丧失之间的关系。将研究过程中测量的患者龈沟液(M-GCF)中PGE2和IL-1β的平均水平,与每位患者单个研究部位观察到的牙槽骨高度丧失的最大量直接进行比较。选择测量的最大骨丧失量进行分析,因为骨丧失模式本质上明显是间歇性的。M-GCF中PGE2浓度与个体患者研究部位牙槽骨高度丧失的最大量之间存在统计学显著相关性(r = 0.73,p = 0.001)。M-GCF中IL-1β浓度与牙槽骨高度丧失最大值之间的相关性也具有统计学意义(r = 0.66,p = 0.005)。在为期6个月的研究中,安慰剂治疗组中PGE2和IL-1β均呈协同表达,这反映在两种介质的M-GCF浓度之间的显著相关性上(r = 0.81,p < 0.001)。每天两次用0.1%酮咯酸氨丁三醇治疗患者6个月,导致龈沟液中PGE2减少,且M-GCF中PGE2与M-GCF中IL-1β之间的相关性可忽略不计(r = 0.42,p = 0.088)。酮咯酸治疗组中这两种介质之间缺乏强关联,为酮咯酸氨丁三醇口腔含漱液对牙周炎患者的抗炎疗效提供了直接的生化指标。有必要进行进一步研究,以确定M-GCF中PGE2和IL-1β水平在预测牙周炎患者牙槽骨丧失风险和监测牙周治疗效果方面的全部诊断潜力。