Yu V, Damek-Poprawa M, Nicoll S B, Akintoye S O
Department of Orthodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Biochem Biophys Res Commun. 2009 Sep 4;386(4):661-5. doi: 10.1016/j.bbrc.2009.06.106. Epub 2009 Jun 23.
The masticatory apparatus absorbs high occlusal forces, but uncontrolled parafunctional or orthodontic forces damage periodontal ligament (PDL), cause pulpal calcification, pulp necrosis and tooth loss. Morphology and functional differentiation of connective tissue cells can be controlled by mechanical stimuli but effects of uncontrolled forces on intra-pulpal homeostasis and ability of dental pulp stem cells (DPSCs) to withstand direct external forces are unclear. Using dynamic hydrostatic pressure (HSP), we tested the hypothesis that direct HSP disrupts DPSC survival and odontogenic differentiation. DPSCs from four teenage patients were subjected to HSP followed by assessment of cell adhesion, survival and recovery capacity based on odontogenic differentiation, mineralization and responsiveness to bone morphogenetic protein-2 (BMP-2). HSP down-regulated DPSC adhesion and survival but promoted differentiation by increasing mineralization, in vivo hard tissue regeneration and BMP-2 responsiveness despite reduced cell numbers. HSP-treated DPSCs displayed enhanced odontogenic differentiation, an indication of favorable recovery from HSP-induced cellular stress.
咀嚼器官能承受较高的咬合力量，但不受控制的副功能或正畸力量会损害牙周韧带（PDL），导致牙髓钙化、牙髓坏死和牙齿脱落。结缔组织细胞的形态和功能分化可受机械刺激控制，但不受控制的力量对牙髓内环境稳态以及牙髓干细胞（DPSC）承受直接外力能力的影响尚不清楚。我们使用动态静水压力（HSP）来检验直接HSP会破坏DPSC存活和牙源性分化这一假设。对四名青少年患者的DPSC施加HSP，然后基于牙源性分化、矿化以及对骨形态发生蛋白-2（BMP-2）的反应性来评估细胞黏附、存活和恢复能力。HSP下调了DPSC的黏附和存活，但通过增加矿化、体内硬组织再生以及BMP-2反应性促进了分化，尽管细胞数量减少。经HSP处理的DPSC显示出增强的牙源性分化，这表明能从HSP诱导的细胞应激中良好恢复。
