Growth plate cartilage is solely responsible for bone lengthening in children. Injury upon growth plate is often repaired by bony tissue which leads to bone growth defects such as limb length discrepancies or bone angulation deformity at later life. Earlier studies using an established rat growth plate injury model have identified a series of repair phases; inflammatory, fibrogenic, osteogenesis and remodelling repair phases. Currently, the cellular and molecular mechanisms involving the bony repair are unknown. A recent microarray study during the growth plate injury has shown BMP signalling activity during the growth plate injury repair. BMP signalling plays a vital role in regulating bone fracture repair. However, its role in the growth plate injury repair is unknown. This in vivo study investigated the potential roles of BMP signalling during the growth plate injury bony repair in rats using BMP inhibitor, human noggin recombinant protein, rhNoggin (delivered systemically using osmotic pump at 6 ug/ml for 14 days post growth plate injury) showed lower percentage of bone volume formation within the growth plate injury site for noggin-treated group on days 14 and 35 time-points through Micro-CT scan and analysis (n=4, P<0.05). Histological analysis revealed significant lower percentage of bone trabeculae formation when treated with rhNoggin protein for both D14 and D35 time-points (n=5, P<0.05). Immunohistochemical analysis on both treatment groups showed P-Smad1/5/8 immunopositive cells to be present however, the intensity and quantity were lesser when compared to the vehicle treated. Consistent with RT-qPCR, level of Runx2 and osteocalcin gene expression are lower when compared to the vehicle treated group at days 14 and 35 time-points although non-significant. These results suggest that BMP signalling is involved in regulating the bony repair during the growth plate injury repair by promoting osteoblast differentiation and osteogenesis.
17 May 2014 - 20 May 2014