Children Salter's typeⅢ and Ⅳ growth plate injuries always induce the skeletal deformity because of bony bridge formation. However, the underlying cellular and molecular changes of the remaining cartilage adjacent to the injury site are still unclear. The purpose of this investigation was to understand the molecular mechanisms of bony bridge formation. The in vivo cellular and molecular changes in the adjacent cartilage were studied in the rat growth plate injury models. Consisted with the histological changes, both Terminal deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling (TUNEL) assay and in situ hybridization experiment using Col2a1 probe showed there was the sub-injury cartilage region adjacent to the original injury site. Despite the sub-injury region remained normal cartilage structure and Collagen typeⅩ in the extracellular matrix, the chondrocytes within this region showed the dislocation with the cartilage lacunas, and the strand breaks of cleaved DNA in TUNEL assay. That these chondrocytes didn't express Col2a1 mRNA further confirmed they were dead cells. Along with the degradation of sub-injury cartilage, some fibroblast-like cells presented to the cartilaginous region between the sub-injury region and uninjured cartilage. In situ hybridization experiment for Patched 1 (Ptch1), indicator of Indian Hedgehog (IHH) signaling, indicated these fibroblast-like cells could respond to Hh signaling. These results suggest that the bony bridge formation involves series of changes of chondrocytes and Ihh signaling may be involved in the formation of the transient perichondrium-like structure between the sub-injury cartilage and normal cartilage, and partially contribute to the bony bridge formation. Investigating the underlying cellular and molecular changes after the transphyseal injury will contribute us to explore a prevention treatment in the future clinic.