D'Aiuto F, Nibali L, Mohamed-Ali V, Vallance P, Tonetti M S
Department of Periodontology and Eastman Clinical Investigation Center, Eastman Dental Institute and Hospital, University College London, UK.
J Periodontal Res. 2004 Oct;39(5):294-9. doi: 10.1111/j.1600-0765.2004.00741.x.
Chronic periodontitis causes a low-grade systemic inflammatory response; its standard treatment, however, induces an acute inflammatory response. The aim of this study was to describe the systemic inflammatory reactions to an intensive periodontal treatment regimen.
Fourteen otherwise healthy subjects suffering from severe chronic periodontitis were enrolled in a 1 month pilot single-blind trial. Intensive periodontal treatment, consisting of full-mouth subgingival root debridement delivered within a 6-h period, was performed. Periodontal parameters were recorded before and 1 month after completion of treatment. Blood samples were taken at baseline and 1, 3, 5, 7 and 30 days after treatment. Interleukin-1 receptor antagonist (IL-1Ra), Interleukin-6 (IL-6) and C-reactive protein (CRP) serum concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Complete blood counts were also performed.
One day after treatment, mild neutrophilia and monocytosis (p < 0.05) and lymphopenia (p < 0.01) were accompanied by a sharp increase in inflammatory markers (IL-1Ra, IL-6, p < 0.01). A 10-fold increase in CRP (p < 0.001) was detected on day 1 and its kinetics followed a pattern of a classical acute phase response (significantly raised concentrations up to 1 week, p < 0.01). At 3-7 days after treatment, subjects presented also with a mild tendency towards a normocytic anaemic state (p < 0.01) and a degree of lympho-thrombocytosis (p < 0.05). The observed changes were similar to those expected following the well-characterized endotoxin-challenge model of inflammation.
Intensive periodontal treatment produced an acute systemic inflammatory response of 1 week duration and might represent an alternative to classic endotoxin-challenge or drug-induced models to study acute inflammation in humans.
慢性牙周炎会引发低度全身炎症反应；然而，其标准治疗会诱发急性炎症反应。本研究的目的是描述对强化牙周治疗方案的全身炎症反应。
14名患有重度慢性牙周炎的健康受试者参加了为期1个月的单盲试验。进行了强化牙周治疗，包括在6小时内完成全口龈下刮治。在治疗前和治疗完成后1个月记录牙周参数。在基线以及治疗后1、3、5、7和30天采集血样。通过酶联免疫吸附测定（ELISA）测定白细胞介素-1受体拮抗剂（IL-1Ra）、白细胞介素-6（IL-6）和C反应蛋白（CRP）的血清浓度。还进行了全血细胞计数。
治疗后1天，轻度中性粒细胞增多和单核细胞增多（p<0.05）以及淋巴细胞减少（p<0.01）伴随着炎症标志物（IL-1Ra、IL-6，p<0.01）的急剧增加。在第1天检测到CRP增加了10倍（p<0.001），其动力学遵循经典急性期反应模式（浓度显著升高直至1周，p<0.01）。在治疗后3至7天，受试者还表现出轻度的正细胞性贫血倾向（p<0.01）和一定程度的淋巴细胞血小板增多（p<0.05）。观察到的变化与在特征明确的内毒素激发炎症模型后预期的变化相似。
强化牙周治疗产生了持续1周的急性全身炎症反应，可能代表了经典内毒素激发或药物诱导模型之外用于研究人类急性炎症的另一种选择。
