AchTG femurs showed suppressed growth compared with wild type (0.29 ± 0.10 mm vs. 0.46 ± 0.06 mm, respectively; p < 0.05), particularly in cartilage. PTH treatments improved the growth velocity in the femurs of the AchTG (0.50 ± 0.06 mm; p < 0.01 vs. control). This was associated with the inhibition of both differentiation and apoptosis in chondrocytes.
Our data suggest that PTH inhibits differentiation and apoptosis in chondrocytes and improves bone growth. These effects thus counterbalance the effects of FGFR3 mutations. PTH therefore is a potential therapeutic agent for achondroplasia.
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