Department of Orthodontics, School of Stomatology, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Tongji University, Shanghai, China.
J Periodontal Res. 2020 Oct;55(5):667-675. doi: 10.1111/jre.12753. Epub 2020 Apr 22.
Though impacts of traumatic occlusion (TO) on periodontal tissues and roles of cystathionine γ-lyase (Cth) gene in the regulation of bone homeostasis have been studied by many, no consensus has been reached so far on whether TO deteriorates the periodontium and precise roles of Cth in occlusal trauma. Therefore, this study aims to investigate the impacts of TO on periodontal tissues and the involvement of Cth gene.
Eighty C57BL/6 wild-type (WT) mice and Cth knockout (Cth ) mice, 8 weeks old, were used in this study. The TO model was established using composite resin bonding on the left maxillary molar for one, two, and three weeks, respectively. Morphological and histological changes in the periodontium were assessed by micro-computed tomography (micro-CT), hematoxylin and eosin (H&E) staining, and tartrate-resistant acid phosphatase (TRAP) staining. Osteoclast-related genes were analyzed by real-time polymerase chain reaction (qPCR).
It was found that decreased alveolar bone height, expanded bone resorption area, and increased width of periodontal ligament (PDL) occurred in TO models, accompanied by an increased number of osteoclasts in a time-dependent manner by micro-CT and histological staining. Osteoclast-related genes including Ctsk, Mmp9, Rank, Trap, and Rankl/Opg were also up-regulated after one week of modeling. The up-regulated expressions of Cth gene and its protein CTH were observed in TO mouse models. After 1, 2, or 3 weeks of modeling, WT mice showed more severe alveolar bone resorption, wider PDL, higher osteoclast count, and higher levels of osteoclast-related genes Ctsk, Rank, and Rankl/Opg than Cth mice.
TO causes a reduction in alveolar bone height and PDL morphological disorder with their severity increases in a time-dependent manner. Cth aggravates periodontal damage caused by TO.
尽管创伤性咬合（TO）对牙周组织的影响以及胱硫醚γ-裂解酶（Cth）基因在骨稳态调节中的作用已被许多人研究过，但迄今为止，关于 TO 是否会使牙周组织恶化以及 Cth 在咬合创伤中的确切作用，尚未达成共识。因此，本研究旨在探讨 TO 对牙周组织的影响以及 Cth 基因的参与。
本研究使用 80 只 8 周龄 C57BL/6 野生型（WT）小鼠和 Cth 基因敲除（Cth）小鼠。分别使用复合树脂在左侧上颌磨牙上黏附 1、2 和 3 周来建立 TO 模型。使用微计算机断层扫描（micro-CT）、苏木精和伊红（H&E）染色和抗酒石酸酸性磷酸酶（TRAP）染色评估牙周组织的形态和组织学变化。通过实时聚合酶链反应（qPCR）分析破骨细胞相关基因。
研究发现，TO 模型中牙槽骨高度降低、骨吸收面积扩大、牙周膜（PDL）增宽，且破骨细胞数量随时间呈依赖性增加，通过 micro-CT 和组织学染色证实。骨吸收相关基因 Ctsk、Mmp9、Rank、Trap 和 Rankl/Opg 也在建模 1 周后上调。在 TO 小鼠模型中观察到 Cth 基因及其蛋白 CTH 的上调表达。在建模 1、2 或 3 周后，WT 小鼠比 Cth 小鼠表现出更严重的牙槽骨吸收、更宽的 PDL、更高的破骨细胞计数以及更高水平的破骨细胞相关基因 Ctsk、Rank 和 Rankl/Opg。
TO 导致牙槽骨高度降低和 PDL 形态紊乱，其严重程度随时间呈依赖性增加。Cth 加重了 TO 引起的牙周损伤。
