Injured condylar cartilage leads to traumatic temporomandibular joint ankylosis

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• 作者：Jiewen Dai^a ; ^{daijiewen@163.com" class="auth_mail" title="E-mail the corresponding author} ; Ningjuan Ouyang^a ; Xiaofang Zhu^a ; Li Huang^b ; Guofang Shen^a ; ^{maxillofacsurg@163.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Condylar cartilage ; Traumatic ; Temporomandibular joint ankylosis
• 刊名：Journal of Cranio-Maxillofacial Surgery
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：44
• 期：3
• 页码：294-300
• 全文大小：3751 K

文摘

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.

Material and methods

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.

Results

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.

Conclusions

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.