目的:探讨慢性牙周炎患者牙周基础治疗前、后龈沟液(GCF)中β-防御素2(HBD-2)及其与白细胞介素-1β(IL-1β)表达水平的关系.方法:选择慢性牙周炎患者10例为慢性牙周炎组,按纳入标准选取20位点分别在牙周基础治疗前及治疗后1个月分别收集GCF并记录临床指标.以牙周健康者12例的24位点GCF为健康对照组.GCF采集后记录采集点出血指数(BI)和探诊深度(PD).采用酶联免疫吸附法测定GCF中HBD-2及IL-1β含量.结果:健康对照组GCF中HBD-2表达水平高于慢性牙周炎组(P<0.05);慢性牙周炎组牙周基础治疗前、后HBD-2表达水平差异无统计学意义(P>0.05).牙周基础治疗前,慢性牙周炎组IL-1β的表达水平高于健康对照组(P<0.001),慢性牙周炎组牙周基础治疗后IL-1β表达水平低于治疗前.牙周基础治疗后,BI、PD均较治疗前小(P<0.001).与HBD-2、IL-1β表达水平无关(P>0.05).结论:慢性牙周炎患者牙周基础治疗后GCF中IL-1β的表达水平较治疗前低,GCF中HBD-2在牙周基础治疗前、后表达水平无差异;与GCF中的HBD-2、IL-1β表达水平无关。
Objective:To investigate the change of Human β-Defensin-2 (HBD-2) and interleukln-1β(IL-1β) expressions in gingival crevicular fluid(GCF) of chronic periodontitis (CP) after base treatment, and to explore the relationship between HBD-2 and IL-1β in GCF. Methods: 10 patients with chronic periodontitis were selected as chronic periodontitis group. According to the admission criterion, GCF was collected and clinical index was recorded in appointed 20 sites after treatment a month later. Meanwhile, the GCF respectively collected in appointed 24 sites of 12 cases people with healthy periodontitis was healthy control group. Next,Bleeding index (BI) and probing depth (PD) were recorded after GCF collection. Finally, The levels of HBD-2 and IL-1β in GCF were quantified by ELISA. Results:Though the expressions of HBD-2 in healthy controls were higher than that of chronic periodontitis group( P〈0.05), the HBD-2 expression of chronic periodontitis group was no difference after treatment or not. ( P〈0.05). And the results of treat- ment showed that the IL-1β expression of chronic periodontitis was lower than ever, thought the IL-1β expression of Chronic periodontitis was higher than the normal control's, before treatment. And the value of BI and PD was smaller after treatment. ( P〈0. 001). Correlation study showed that it's no relationship between HBD-2 and IL-1β. Conclusion: For chronic periodontitis, the expression of IL-1β in GCF was lower after treatment, and it's no difference on HBD-2 expression. It is no corelationship between HBD-2 and IL-1β in GCF.