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Objective: Condylar hyperplasia (CH) in human temporomandibular joint (TMJ) always leads to facial asymmetry, which causes facial deformity and occlusal disturbance.However, The etiology of CH remains unknown.The aim of this study is to discussing the etiology of CH and the molecular mechanism in enhancing cellular differentiation of CH cartilage Material and methods: The expressions of Shh in CH cartilage was observed to confirm its increasing, then an IGF1-over expressing in condylar cartilage model will be set on transgenic rats to verify the cooperation between Shh and IGF-I in Promoting condylar hyperplasia cartilage overgrowth.Finally, the crosstalk between Shh pathway and IGF-I pathway and its regulating effects in different CH chondrocytes will be investigated.