• Shan-Li Pei, Rung-Shu Chen, and Min-Huey Chen.
• Graduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan; Department of Dentistry, National Taiwan University Hospital, Taipei, Taiwan.
• J Formos Med Assoc. 2024 Sep 1; 123 (9): 934941934-941.

Background/PurposeHuman nerve development is vital, affecting trauma recovery and dental issues. Early embryonic clues link nerves to tooth development via factors like Wnt and Hedgehog pathways. Centrosomes play a role, and centriole issues can disrupt oral development, as in oral facial digital syndrome type 1. This study aimed to delve deeper into the role and influence of centrioles on the development of dental nerves.MethodsCell migration assessed by co-culturing mouse neural tissue and human dental pulp stem cells (DPSCs). Centrioles were fluorescently stained, and their positions observed with confocal microscopy. Centrinone was employed to inhibit centriole activity, evaluating its impact on cell mobility under activity inhibition.ResultsAs the distance between nerve tissue and DPSCs decreased, more DPSCs had centrioles near nerve tissue. Co-culture with nerve tissue increased DPSCs migration toward it. In contrast, DPSCs cultured alone or with fibroblasts showed weaker migration, indicating neural tissue's attractive influence. The addition of 125 nM centrinone halted cell migration and centriole polymerization. After centrinone removal over two days, centrioles returned to normal, suggesting continued motility inhibition.ConclusionCentrioles direct cell movement and polarization. There are two scenarios: centrioles at the cell center with the nucleus moving backward (as in NIH3T3 cells) and both cells and centrioles moving forward (as in DPSCs). DPSCs' attraction to neural tissue may shed light on nerve guidance by tooth germs, aiding embryonic cell differentiation into nerves. However, further in vivo and in vitro studies are needed to confirm the specific mechanism.Copyright © 2024 Formosan Medical Association. Published by Elsevier B.V. All rights reserved.

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