Shimizu N, Goseki T, Yamaguchi M, Iwasawa T, Takiguchi H, Abiko Y
Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
J Dent Res. 1997 Jul;76(7):1367-75. doi: 10.1177/00220345970760070601.
Although the severity of periodontal disease is known to be affected by host age, the pathological role of aging in periodontal disease, and especially that attributable to trauma from occlusion, has not been well-characterized. Interleukin (IL)-1 beta is a key mediator involved in periodontal diseases, a potent stimulator of bone resorption. Furthermore, it is produced by human periodontal ligament (PDL) cells in response to mechanical stress. To investigate the age-related changes in the biosynthetic capacity of IL-1 beta in PDL cells, we examined the effects of in vitro cellular aging with mechanical stress on IL-1 beta protein and gene expression by human PDL cells. Human PDL cells (young = 5th or 6th passage; old = 18-20th passage) were cultured on flexible-bottomed culture plates, and the cells were deformed at 6 cycles per min at 2 steps of tension force for 1 to 5 days. We found a two-fold increase in IL-1 beta production by old PDL cells subjected to mechanical tension compared with that by young PDL cells, although the constitutive levels of IL-1 beta were similar in both the young and old PDL cells. This increase was tension-dependent. IL- 1 beta mRNA was also detected in both cell types under basal conditions, and its expression was further enhanced by application of mechanical tension by use of reverse-transcription-polymerase chain-reaction (RT-PCR) and in situ hybridization methods. The increase in signal rate was higher in the old cells than in the young cells. IL-1 beta-converting enzyme mRNA remained unchanged. It is possible that a large amount of IL- 1 beta produced by PDL cells from an aged host in response to mechanical force may be positively related to the acceleration of alveolar bone resorption.
虽然已知牙周病的严重程度受宿主年龄影响，但衰老在牙周病中的病理作用，尤其是与咬合创伤相关的作用，尚未得到充分阐明。白细胞介素（IL）-1β是参与牙周病的关键介质，是骨吸收的强效刺激物。此外，它由人牙周膜（PDL）细胞在机械应力作用下产生。为了研究PDL细胞中IL-1β生物合成能力的年龄相关变化，我们检测了体外细胞衰老与机械应力对人PDL细胞IL-1β蛋白和基因表达的影响。人PDL细胞（年轻细胞=第5或6代；老年细胞=第18 - 20代）培养在底部可弯曲的培养板上，细胞在每分钟6个循环、分两步施加张力的条件下变形1至5天。我们发现，与年轻PDL细胞相比，受到机械张力的老年PDL细胞产生的IL-1β增加了两倍，尽管年轻和老年PDL细胞中IL-1β的基础水平相似。这种增加是张力依赖性的。在基础条件下，两种细胞类型中均检测到IL-1β mRNA，通过逆转录-聚合酶链反应（RT-PCR）和原位杂交方法，施加机械张力后其表达进一步增强。老年细胞中信号率的增加高于年轻细胞。IL-1β转换酶mRNA保持不变。老年宿主的PDL细胞在机械力作用下产生大量IL-1β，这可能与牙槽骨吸收加速呈正相关。
