Lossdörfer S, Götz W, Jäger A
Department of Orthodontics, Dental Clinic, University of Bonn, Germany.
J Periodontal Res. 2006 Dec;41(6):519-26. doi: 10.1111/j.1600-0765.2006.00899.x.
Periodontal ligament (PDL) cells show traits that are typical of osteoblasts, such as osteoblastic marker gene expression and the ability to respond to parathyroid hormone (PTH) stimulation in an osteoblast-like manner with respect to differentiation and local factor production. In the present study, we hypothesized that human PDL cells might respond to PTH stimulation with changes in proliferation and cell survival and thereby provide another mechanism by which PTH might affect the reparative potential of PDL cells. We speculated that the maturation state of the cells and the mode of PTH(1-34) administration would have an impact on the cellular response.
PDL cells were challenged with PTH(1-34) intermittently or continuously at different maturation states. Cell number, 5-bromo-2-deoxyuridine (BrdU) incorporation, DNA fragmentation, nitric oxide production and the duration of the PTH(1-34) effect were determined.
Intermittent PTH(1-34) treatment of preconfluent cells caused a significant increase in proliferation and DNA fragmentation, whereas in more mature cells, proliferation was less enhanced while apoptosis was more pronounced than in immature cells. Continuous PTH(1-34) exposure did not alter proliferation in any maturation state but increased DNA fragmentation in preconfluent cells. PTH(1-34) prevented etoposide-induced apoptosis after 6 h but no longer after 24 h. Nitric oxide production was unaffected.
These results indicate that human PDL cells respond to PTH(1-34) with changes in proliferative and apoptotic signaling in a maturation-state-dependent manner. Besides changes in local factor production, these findings provide a further possible mechanism to support the idea that PDL cells possess the potential to be involved in the regulation of dental hard tissue repair.
牙周膜（PDL）细胞表现出成骨细胞的典型特征，如成骨细胞标志物基因表达以及在分化和局部因子产生方面以成骨细胞样方式响应甲状旁腺激素（PTH）刺激的能力。在本研究中，我们假设人牙周膜细胞可能通过增殖和细胞存活的变化对PTH刺激作出反应，从而为PTH影响牙周膜细胞修复潜能提供另一种机制。我们推测细胞的成熟状态和PTH（1-34）给药方式会对细胞反应产生影响。
在不同成熟状态下，用PTH（1-34）间歇性或持续性刺激牙周膜细胞。测定细胞数量、5-溴-2-脱氧尿苷（BrdU）掺入量、DNA片段化、一氧化氮产生以及PTH（1-34）作用的持续时间。
对未汇合细胞进行间歇性PTH（1-34）处理导致增殖和DNA片段化显著增加，而在更成熟的细胞中，增殖增强较少，而凋亡比未成熟细胞更明显。持续暴露于PTH（1-34）在任何成熟状态下均未改变增殖，但增加了未汇合细胞中的DNA片段化。PTH（1-34）在6小时后可预防依托泊苷诱导的凋亡，但24小时后则不再起作用。一氧化氮产生不受影响。
这些结果表明，人牙周膜细胞以成熟状态依赖的方式通过增殖和凋亡信号变化对PTH（1-34）作出反应。除了局部因子产生的变化外，这些发现为支持牙周膜细胞具有参与牙硬组织修复调节潜能的观点提供了进一步的可能机制。
