Jacobs Collin, Walter Christian, Ziebart Thomas, Grimm Sarah, Meila Dan, Krieger Elena, Wehrbein Heinrich
Department of Orthodontics, University Medical Center, Johannes Gutenberg University Mainz, Augustusplatz 2, 55131, Mainz, Germany,
Clin Oral Investig. 2014 Apr;18(3):901-8. doi: 10.1007/s00784-013-1032-1. Epub 2013 Jul 14.
Mechanical loading is a potential activator of inflammation and able to stimulate factors for periodontal and alveolar bone destruction. Aim of this study was to investigate the inflammatory response and synthesis of proteinases by human periodontal ligament fibroblast (HPdLF) dependent on different strengths of static tensile strain (STS).
HPdLFs were loaded with different STS strengths (1, 5, and 10 %) in vitro. Gene expressions of cyclooxygenase (COX)-2 and interleukin (IL)-6 were analyzed by quantitative real-time polymerase chain reaction. Production of IL-6, prostaglandin E2 (PGE2), matrix metalloproteinase (MMP)-8, and tissue inhibitors of matrix metalloproteinase (TIMP)-1 were measured by enzyme-linked immunosorbent assay. Receptor activator of nuclear factor-kappa ligand (RANKL) synthesis was detected by immunocytochemical staining.
Ten percent STS led to an increased gene expression of IL-6 and COX-2 (34.4-fold) in HPdLF, and 1 and 5 % STS slightly reduced the gene expression of IL-6. Synthesis of IL-6 was significantly reduced by 1 % STS and stimulated by 10 % STS. Ten percent STS significantly induced PGE2 production. RANKL was not detectable at any strength of STS. MMP-8 synthesis showed significantly higher values only at 10 % STS, but TIMP-1 was stimulated by 5 and 10 % STS, resulting into highest TIMP-1/MMP-8 ratio at 5 % STS.
High-strength STS is a potent inducer of periodontal inflammation and MMP-8, whereas low-strength STS shows an anti-inflammatory effect. Moderate-strength STS causes the highest TIMP-1/MMP-8 ratio, leading to appropriate conditions for reformation of the extracellular matrix.
Furthermore, this study points out that the strength of force plays a pivotal role to achieve orthodontic tooth movement without inducing periodontal inflammation and to activate extracellular matrix regeneration.
机械负荷是炎症的潜在激活因素,能够刺激导致牙周和牙槽骨破坏的因子。本研究的目的是调查人牙周膜成纤维细胞(HPdLF)依赖于不同强度的静态拉伸应变(STS)时的炎症反应和蛋白酶合成情况。
体外对HPdLF施加不同强度的STS(1%、5%和10%)。通过定量实时聚合酶链反应分析环氧化酶(COX)-2和白细胞介素(IL)-6的基因表达。通过酶联免疫吸附测定法测量IL-6、前列腺素E2(PGE2)、基质金属蛋白酶(MMP)-8和基质金属蛋白酶组织抑制剂(TIMP)-1的产生。通过免疫细胞化学染色检测核因子κB受体激活剂配体(RANKL)的合成。
10%的STS导致HPdLF中IL-6和COX-2的基因表达增加(34.4倍),1%和5%的STS略微降低了IL-6的基因表达。1%的STS显著降低IL-6的合成,而10%的STS则刺激其合成。10%的STS显著诱导PGE2的产生。在任何强度的STS下均未检测到RANKL。仅在10%的STS下MMP-8合成显示出显著更高的值,但5%和10%的STS刺激TIMP-1的产生,导致在5%的STS下TIMP-1/MMP-8比率最高。
高强度的STS是牙周炎症和MMP-8的有效诱导剂,而低强度的STS显示出抗炎作用。中等强度的STS导致最高的TIMP-1/MMP-8比率,为细胞外基质的重塑创造了适宜条件。
此外,本研究指出力的强度对于在不引发牙周炎症的情况下实现正畸牙齿移动以及激活细胞外基质再生起着关键作用。