UNC Center for Oral and Systemic Diseases, North Carolina Oral Health Institute, UNC School of Dentistry, Durham, NC 27709, USA.
J Clin Periodontol. 2010 Apr;37(4):324-33. doi: 10.1111/j.1600-051X.2010.01543.x.
The goal of this study is to characterize the changes in 33 biomarkers within the gingival crevicular fluid during the 3-week induction and 4-week resolution of stent-induced, biofilm overgrowth mediated, experimental gingivitis in humans.
Experimental gingivitis was induced in 25 subjects for 21 days followed by treatment with a sonic powered toothbrush for 28 days. Clinical indices and gingival crevicular fluids were collected weekly during induction and biweekly during resolution. Samples were analysed using a bead-based multiplexing analysis for the simultaneous measurements of 33 biomarkers within each sample including cytokines, matrix-metalloproteinases (MMPs) and adipokines. Prostaglandin-E(2) was measured by enzyme-linked immunoadsorbant assay. Statistical testing using general linear models with structured covariance matrices were performed to compare stent to contralateral (non-stent) changes in clinical signs and in biomarker levels over time.
Gingivitis induction was associated with a significant 2.6-fold increase in interleukin 1-beta (IL-beta), a 3.1-fold increase in IL-1alpha and a significant decrease in multiple chemokines as well as MMPs-1, -3 and 13. All changes in clinical signs and mediators rebounded to baseline in response to treatment in the resolution phase.
Stent-induced gingivitis is associated with marked, but reversible increases in IL-alphaa and IL-1beta with suppression of multiple chemokines as well as selected MMPs.
本研究旨在描述在人类支架诱导的、生物膜过度生长介导的实验性牙龈炎的 3 周诱导期和 4 周缓解期内,龈沟液中 33 种生物标志物的变化。
将 25 名受试者的实验性牙龈炎诱导 21 天,然后用声波动力牙刷治疗 28 天。在诱导期每周和缓解期每两周收集临床指标和龈沟液。使用基于珠子的多重分析同时测量每个样本中的 33 种生物标志物,包括细胞因子、基质金属蛋白酶(MMPs)和脂肪因子。前列腺素 E(2)通过酶联免疫吸附测定法测量。使用具有结构化协方差矩阵的一般线性模型进行统计检验,以比较支架对临床体征和生物标志物水平随时间变化的双侧(非支架)变化。
牙龈炎诱导与白细胞介素 1-β(IL-1β)显著增加 2.6 倍、IL-1α 增加 3.1 倍以及多种趋化因子和 MMP-1、MMP-3 和 MMP-13 显著减少相关。在缓解阶段的治疗过程中,所有临床体征和介质的变化均反弹至基线。
支架诱导的牙龈炎与明显但可逆转的 IL-alphaa 和 IL-1β 增加有关,同时抑制多种趋化因子和选定的 MMP。