GINGIVAL FLUID IL-1 AND IL-6 LEVELS IN REFRACTORY PERIODONTITIS
GINGIVAL FLUID IL-1 AND IL-6 LEVELS IN REFRACTORY PERIODONTITIS
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DOI：
10.1111/j.1600-051x.1993.tb00348.x
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发表时间：
1993-03-01
影响因子：
6.7
通讯作者：
ALLISON, AC
中科院分区：
文献类型：
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作者：
REINHARDT, RA;MASADA, MP;ALLISON, AC
对与传统牙周治疗（难治性）无反应的患者相关的选定牙龈细菌和细胞因子谱进行了评估。将 10 名治疗后临床附着丧失发生率高的受试者（> 2% 位点/年，丧失大于或等于 3 毫米）与 10 名年龄、种族和龈上牙菌斑匹配、治疗后临床附着丧失低（< 0.5% 位点/年）的患者进行比较，相对于具有最深探测深度的 2 位点/患者的以下参数：(1) 存在 3 种选定的牙周病原体通过选择性培养测定龈下菌斑中的伴放线杆菌、牙龈卟啉单胞菌、腐蚀艾肯氏菌），以及（2）通过双位点 ELISA 测定与骨吸收相关的 3 种细胞因子（IL-1 α、IL-1 β、IL-6）的龈沟液 (GCF) 水平。结果表明，难治性受试者部位与稳定受试者部位之间的任何临床测量（临床附着丧失的发生率除外）、任何细菌病原体存在下或 GCF 细胞因子水平均无显着差异。然而，当比较每个患者产生最大总 GCF 细胞因子的位点时，来自难治性患者的位点产生显着更多的 IL-6（30.1 +/- 4.0 与 15.4 +/- 2.8 nM，p < 0.01）。龈下存在的3种细菌病原体中的每一种都与升高的GCF IL-1浓度相关。这些数据表明，牙龈IL-1和IL-6的产生对于与牙周炎相关的局部和全身因素的反应是不同的，并且IL-6可能在难治性牙周炎的识别和机制中发挥作用。
Selected gingival bacteria and cytokine profiles associated with patients who did not respond to conventional periodontal therapy (refractory) were evaluated. 10 subjects with a high incidence of post-active treatment clinical attachment loss (> 2% sites/year lost greater-than-or-equal-to 3 mm) were compared to 10 age-, race-, and supragingival plaque-matched patients with low post-treatment clinical attachment loss (< 0.5% sites/year) relative to the following parameters at 2 sites/patient with the deepest probing depths: (1) presence of 3 selected periodontal pathogens (Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Eikenella corrodens) in subgingival plaque as determined by selective culturing, and (2) gingival crevicular fluid (GCF) levels of 3 cytokines associated with bone resorption (IL-1 alpha, IL-1 beta, IL-6) as determined by two-site ELISA. Results indicated no significant differences in any clinical measurement (except incidence of clinical attachment loss), in the presence of any bacterial pathogen, or in GCF cytokine levels between refractory subject sites versus stable subject sites. However, when sites producing the greatest total GCF cytokine/patient were compared, sites from refractory patients produced significantly more IL-6 (30.1 +/- 4.0 versus 15.4 +/- 2.8 nM, p < 0.01). The subgingival presence of each of the 3 bacterial pathogens was associated with elevated GCF IL-I concentrations. These data suggest that gingival IL-1 and IL-6 production is different in response to local and systemic factors associated with periodontitis, and that IL-6 may play a role in the identification and mechanisms of refractory periodontitis.