Replacing Shox2 with human SHOX leads to the congenital osteoarthritis-like disease of temporomandib

• 作 者: Li Xihai Chen Houhuang Shao Xiang Wu Guangwen Zheng Chunsong Xu Huifeng Ye Jinxia Liu Xianxiang Yehongzhi
• 机 构: Academy of Integrative Medicine,Fujian University of Traditional Chinese Medicine,Fuzhou 350122,Chin
• 出 处: 中国中医药研究促进会骨伤科分会2017年学术年会第四届全国中医关节病论坛
• 发表日期: 2017年4期
• 关键词: temporomandibular joint extracellular matrix matrix metalloproteinases hedgehog

　　The temporomandibular joint(TMJ),a unique synovial joint whose development differs from the formation of other synovial joints,develops from two distinct mesenchymal condensations that grow toward each other and ossify through different mechanisms.The Shox(short stature homeobox)gene plays an important role in the TMJ development,and our previous report showed that the Shox2SHOX KI/KI mice developed an interesting phenotype of TMJ defect,congenital dysplasia and premature wear out of the articular disc,clinically defined as TMJ disorders.In this study,we used Shox2SHOX K1/KI mice models to investigate the mechanism of congenital osteoarthritis-like disease during post-natal TMJ growth in mice.We found that the Shox2SHOX KI/KI mice developed a severe wasting syndrome from post-natal day 7(P7).Histological examination indicated that the size of condyle and glenoid fossa of the Shox2SHOX KI/KI mice became smaller in the second week after the birth.The condyle of the Shox2SHOX KI/KI mice showed a reduced level of Collagen type Ⅱand Ihh,however,an increased level of Collagen type Ⅰ.Dramatically up-regulated of matrix metalloproteinase 9(MMP9)and MMP13 in the glenoid fossa was also observed.These combinatory cellular and molecular defects appear to contribute to the observed the phenotype of the Shox2SHOX KI/K1 mice TMJ.