Dai Jiewen, Ouyang Ningjuan, Zhu Xiaofang, Huang Li, Shen Guofang
Department of Oral & Cranio-maxillofacial Science, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, No.639 Zhizaoju Road, Shanghai 200011, China.
Department of Oral & Cranio-maxillofacial Science, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, No.639 Zhizaoju Road, Shanghai 200011, China.
J Craniomaxillofac Surg. 2016 Mar;44(3):294-300. doi: 10.1016/j.jcms.2015.12.006. Epub 2015 Dec 21.
The exact mechanisms of traumatic temporomandibular joint ankylosis (TTMJA) are largely unknown. In this study, we explore the role of injured condylar cartilage in the development of TTMJA.
One-month-old male mice were divided into two groups. In group 1, condylar cartilage was partially removed in the right joint using a small scissors to induce ankylosis. In group 2, condylar cartilage was completely removed in the same right joint using a small scissors to induce ankylosis. The phenotypes were observed using gross observation, micro-computed tomography scans and histological examination.
The results revealed a great deal of ectopic cartilage and bone formation in the right periarticular region in all mice in group 1, whereas there was only a small amount of ectopic cartilage present in 26.7% of the mice in group 2. Additionally, there was stronger expression of FGF9 and weaker expression of OPN in the right temporomandibular joint region in group 2 at 7 days after surgery.
These results suggest that the injured cartilage, not the injured bone, plays a crucial role in the development of TTMJA. In addition, it offers a useful TTMJA animal model to study the molecular mechanisms of TTMJA based on the gene manipulation technology, such as gene knock-out and knock-in as well as transgenic or gene mutation.
创伤性颞下颌关节强直(TTMJA)的确切机制在很大程度上尚不清楚。在本研究中,我们探讨损伤的髁突软骨在TTMJA发生发展中的作用。
将1月龄雄性小鼠分为两组。在第1组中,使用小剪刀在右侧关节部分切除髁突软骨以诱导关节强直。在第2组中,使用小剪刀在同一右侧关节完全切除髁突软骨以诱导关节强直。通过大体观察、显微计算机断层扫描和组织学检查观察表型。
结果显示,第1组所有小鼠右侧关节周围区域有大量异位软骨和骨形成,而第2组26.7%的小鼠仅存在少量异位软骨。此外,术后7天第2组右侧颞下颌关节区域FGF9表达较强,OPN表达较弱。
这些结果表明,损伤的软骨而非损伤的骨在TTMJA的发生发展中起关键作用。此外,基于基因敲除、基因敲入以及转基因或基因突变等基因操作技术,它为研究TTMJA的分子机制提供了一种有用的TTMJA动物模型。