An international team of scientists, including researchers from the Biotechnology Center of the TU Dresden (BIOTEC), says it has found a new mechanism that could offer a potential solution to tooth repair. They discovered a new population of mesenchymal stromal cells in a continuously growing mouse incisor model. They have shown that these cells contribute to the formation of dentin, the hard tissue that covers the main body of a tooth. Importantly, the work showed that when these stem cells are activated, they send signals back to the mother cells of the tissue to control the number of cells produced, through a molecular gene called Dlk1.

This study (“Transit amplifying cells coordinate mouse incisor mesenchymal stem cell activation”), which was published in Nature Communications, reportedly is the first to show that Dlk1 is vital for this process to work. In the same study, the researchers also demonstrated that Dlk1 can enhance stem cell activation and tissue regeneration in a wound healing model.

This mechanism could provide an innovative solution for tooth repair, addressing problems such as tooth decay, crumbling, and trauma treatment. Further studies are needed to validate the results for clinical applications to determine the appropriate duration and dose of treatment.

“Stem cells (SCs) receive inductive cues from the surrounding microenvironment and cells. Limited molecular evidence has connected tissue-specific mesenchymal stem cells (MSCs) with mesenchymal transit amplifying cells (MTACs). Using mouse incisor as the model, we discover a population of MSCs nonboring to the MTACs and epithelial SCs. With Notch signaling as the key regulator, we disclose molecular proof and lineage tracing evidence showing the distinct MSCs contribute to incisor MTACs and the other mesenchymal cell lineages,” the investigators wrote.

“MTACs can feedback and regulate the homeostasis and activation of CL-MSCs through Delta-like 1 homolog (Dlk1), which balances MSCs-MTACs number and the lineage differentiation. Dlk1’s function on SCs priming and self-renewal depends on its biological forms and its gene expression is under dynamic epigenetic control. Our findings can be validated in clinical samples and applied to accelerate tooth wound healing, providing an intriguing insight of how to direct SCs towards tissue regeneration.”

“The discovery of this new population of stromal cells was very exciting and has enormous potential in regenerative medicine,” said Denis Corbeil, PhD, research group leader at BIOTEC.

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