Harder Sönke, Quabius Elgar Susanne, Ossenkop Lars, Kern Matthias
Department of Prosthodontics, Propaedeutics and Dental Materials, Christian-Albrechts University at Kiel, Arnold-Heller Str. 16, 24105 Kiel, Germany.
Clin Oral Investig. 2012 Oct;16(5):1377-84. doi: 10.1007/s00784-011-0646-4. Epub 2011 Dec 2.
The aim of this in vitro study was to assess lipopolysaccharide microleakage at conical implant-abutment connections of two-piece dental implants in terms of the expression levels of genes involved in lipopolysaccharide-mediated proinflammatory cytokine production.
Two implant systems with conical implant-abutment connections were inoculated with lipopolysaccharide and submerged in human whole blood. Positive-control blood samples (without implants) were stimulated with 4 μg/ml, 2 μg/ml, 200 ng/ml, and 20 ng/ml lipopolysaccharide. Sampling was performed after 1, 8, and 24 h of incubation. Changes of gene expression levels of Toll-like receptor 9, tumor necrosis factor-α, nuclear factor kappa light chain enhancer of activated B cells, interleukin-1β, and interferon-γ were assessed by real-time quantitative PCR. In addition, protein expression levels of interleukin-6, tumor necrosis factor-α, interleukin-1β, and interferon-γ were determined by immunoassay.
Changes in cytokine expression at the genomic and proteomic levels indicated lipopolysaccharide leakage at the interfaces of both tested implant systems, although some implants showed no sign of microleakage. Any tested concentration of lipopolysaccharide stimulated similar gene expression.
Conical implant-abutment connections of two-piece dental implants do not prevent microleakage on a molecular level. Changes in lipopolysaccharide-induced proinflammatory cytokine gene expression facilitate the detection of lipopolysaccharide microleakage at implant-abutment interfaces.
Small amounts of lipopolysaccharide released from intra-implant cavities can stimulate a detectable immunological response in human whole blood and may induce alveolar bone resorption via the osteoclast-activating pathway.
本体外研究旨在根据参与脂多糖介导的促炎细胞因子产生的基因表达水平，评估两件式牙种植体的锥形种植体-基台连接处的脂多糖微渗漏情况。
将两种具有锥形种植体-基台连接的种植系统接种脂多糖，并浸入人全血中。用4μg/ml、2μg/ml、200ng/ml和20ng/ml脂多糖刺激阳性对照血样（无种植体）。孵育1、8和24小时后进行采样。通过实时定量PCR评估Toll样受体9、肿瘤坏死因子-α、活化B细胞核因子κ轻链增强子、白细胞介素-1β和干扰素-γ的基因表达水平变化。此外，通过免疫测定法测定白细胞介素-6、肿瘤坏死因子-α、白细胞介素-1β和干扰素-γ的蛋白表达水平。
基因组和蛋白质组水平上细胞因子表达的变化表明，两种测试种植系统的界面处均存在脂多糖渗漏，尽管一些种植体没有微渗漏迹象。任何测试浓度的脂多糖均刺激相似的基因表达。
两件式牙种植体的锥形种植体-基台连接在分子水平上不能防止微渗漏。脂多糖诱导的促炎细胞因子基因表达变化有助于检测种植体-基台界面处的脂多糖微渗漏。
种植体内腔释放的少量脂多糖可在人全血中刺激可检测到的免疫反应，并可能通过破骨细胞激活途径诱导牙槽骨吸收。
