Investigation of periodontal ligament reaction upon excessive occlusal load - osteopontin induction among periodontal ligament cells

Investigation of periodontal ligament reaction upon excessive occlusal load - osteopontin induction among periodontal ligament cells
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DOI:
10.1111/j.1600-0765.2004.00773.x
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发表时间:
2005-02-01
影响因子:
3.5
通讯作者:
Miura, H
Miura, H
中科院分区:
医学3区
文献类型:
--
作者:
Kaku, M;Uoshima, K;Miura, H

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目的:通过观察牙周膜的组织学变化和骨桥蛋白的诱导,探讨牙周膜对咬合负荷过大的反应。本文还讨论了核因子kappaB受体激活剂配体(RANKL)参与骨桥蛋白诱导的可能性。背景:咬合负荷过大导致牙周膜破坏的确切机制尚不清楚。我们在体内建立了咬合负荷过大的实验模型。众所周知,骨桥蛋白是在机械负荷下产生的,被认为可以诱导破骨细胞迁移到吸收部位。RANKL是破骨细胞成熟的必需因子之一,在体外诱导细胞内骨桥蛋白的构造性诱导。方法:采用钢丝粘结的方法抬高大鼠左上第一磨牙的咬合面,造成咬合创伤。观察牙周膜的破坏情况,用免疫组织化学方法检测牙周膜细胞产生骨桥蛋白和RANKL的情况。结果:该模型可造成牙周膜的广泛破坏。从第3天到第7天,牙周膜明显受压,破骨细胞在根尖间隔处迁移。在一些破骨细胞、周围的成纤维细胞和邻近受压区的成骨细胞中检测到骨桥蛋白。RANKL在成骨细胞和破骨细胞周围观察1~7天。结论:我们的模型可用于研究过度咬合负荷时牙周膜破裂的详细情况。尽管间歇性咬合负荷的破骨细胞产生了细胞内骨桥蛋白,但该蛋白在细胞中的作用尚不清楚。破骨细胞中RANKL的分布与骨桥蛋白的产生无相关性。
Objective: The purpose of the present study was to investigate the reaction of the periodontal ligament to excessive occlusal loading by observing the histological changes and osteopontin induction. The possibility of ligand for receptor activator of nuclear factor kappaB (RANKL) participation in osteopontin induction was also discussed.Background: The precise mechanism of periodontal ligament breakdown by excessive occlusal loading remains unclear. We established an experimental model for excessive occlusal loading in vivo. Osteopontin is known to be produced upon mechanical loading and is considered to induce the migration of osteoclasts to the resorption site. RANKL is one of the essential factors for osteoclast maturation and induces the constitutive induction of intracellular osteopontin in vitro.Methods: The occlusal surface of the upper left first molars of rats was raised by steel wire bonding in order to induce occlusal trauma. The destruction of the periodontal ligament was observed and the production of osteopontin and RANKL by periodontal ligament cells was detected via immunohistochemistry.Results: Our model produced wide-ranging destruction of the periodontal ligament. From day 3 to day 7, prominent compression of the periodontal ligament and osteoclast migration were observed at the apical interradicular septum. Osteopontin was detected in some osteoclasts, surrounding fibroblasts, and osteoblasts adjacent to the compression area. RANKL was observed from day 1 to day 7 around the osteoblasts and osteoclasts.Conclusions: Our model was useful for the detailed investigation of periodontal ligament breakdown during excessive occlusal loading. Although intracellular osteopontin was produced in osteoclasts with intermittent occlusal loading, the role of this protein in the cells was not clear. No correlation between RANKL distribution and osteopontin production in osteoclasts could be found.