TGF-β1 (transforming growth factor-β1) plays a central role in regulating proliferation, migration and differentiation of dental pulp cells during the repair process after tooth injury. Our previous study showed that p38 mitogen-activated protein kinase may act downstream of TGF-β1 signalling to effect the differentiation of dental pulp cells. However, the molecular mechanisms that trigger and regulate the process remain to be elucidated. TGF-β1 interacts with signalling pathways such as Wnt/β-catenin and Rho to induce diverse biological effects. TGF-β1 activates β-catenin signalling, increases β-catenin nuclear translocation and interacts with LEF/TCF to regulate gene expression. Morphologic changes in response to TGF-β1 are associated with activation of Rho GTPases, but are abrogated by inhibitors of Rho-associated kinase, a major downstream target of Rho. These results suggest that the Wnt/β-catenin and Rho pathways may mediate the downstream events of TGF-β1 signalling.