Maeda A, Soejima K, Bandow K, Kuroe K, Kakimoto K, Miyawaki S, Okamoto A, Matsuguchi T
Department of Orthodontics, Field of Developmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
J Dent Res. 2007 Jul;86(7):629-34. doi: 10.1177/154405910708600709.
During orthodontic tooth movement, mechanical stresses induce inflammatory reactions in the periodontal ligament (PDL). We hypothesized that chemokines released from PDL cells under mechanical stress regulate osteoclastogenesis, and investigated the profiles and mechanisms of chemokine expression by human PDL cells in response to mechanical stress. In vitro, shear stress and pressure force rapidly increased the gene and protein expressions of IL-8/CXCL8 by PDL cells. Consistently, amounts of IL-8 in the gingival crevicular fluid of healthy individuals increased within 2 to 4 days of orthodontic force application. The PDL cells constitutively expressed low levels of IL-1beta, which were not further increased by mechanical stress. Interestingly, neutralization of IL-1beta abolished IL-8 induction by mechanical stresses, indicating that IL-1beta is essential for IL-8 induction, presumably though autocrine or paracrine mechanisms. Finally, experiments with signal-specific inhibitors indicated that MAP kinase activation is essential for IL-8 induction.
在正畸牙齿移动过程中，机械应力会诱导牙周韧带（PDL）发生炎症反应。我们推测，机械应力作用下PDL细胞释放的趋化因子会调节破骨细胞生成，并研究了人PDL细胞响应机械应力时趋化因子表达的情况及机制。在体外，剪切应力和压力能迅速增加PDL细胞中IL-8/CXCL8的基因和蛋白表达。同样，在施加正畸力后的2至4天内，健康个体龈沟液中的IL-8含量增加。PDL细胞组成性表达低水平的IL-1β，机械应力不会使其进一步增加。有趣的是，中和IL-1β可消除机械应力诱导的IL-8产生，这表明IL-1β对于IL-8的诱导至关重要，推测可能是通过自分泌或旁分泌机制。最后，使用信号特异性抑制剂进行的实验表明，MAP激酶激活对于IL-8的诱导至关重要。
