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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 KI/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 Ⅱ and 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/KI mice TMJ.