Abstract
Short root anomaly (SRA) is a dental disorder that presents an abnormal root morphology with short and blunt dental roots. In this situation, many dental treatments face a difficult challenge, especially orthodontic and prosthodontic treatments. Therefore, an understanding of how SRA develops is urgently needed. Here we describe that the abnormal expression of nuclear factor I C-type (Nfic), osterix (Osx), hedgehog (Hh), bone morphogenetic proteins (BMPs), transforming growth factor-β (TGF-β), Smad, Wnt, β-catenin, and dickkopf-related protein 1 (DKK1) leads to SRA. These factors interact with each other and constitute complicated signaling network in tooth formation. Specifically, BMP signaling inhibits the activity of Wnt/β-catenin directly or by inducing Osx via Runx2-dependent and Runx2-independent pathways. And Osx is a main inhibitor of Wnt/β-catenin signaling. In return, Wnt/β-catenin signaling has an antagonistic action of BMP pathway and a stimulation of Runx2. We highlight the importance of Wnt/β-catenin signaling in the pathological mechanisms. Either suppression or overactivation of this signaling influences the normal odontogenesis. Finally, we list rescue experiments on animal models, which have been reported to restore the interrupted cell differentiation and impaired tooth formation. We hope to find potential treatments for SRA based on these evidences in the future.
Published Version
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