Scientists at King’s College London have shown that our teeth possess a far greater capacity for self-repair than previously thought. When very small doses of tideglusib – a glycogen-synthase-kinase-3 (GSK-3) inhibitor first tested for Alzheimer’s disease – are placed on an exposed dental pulp, the drug switches on Wnt/β-catenin signalling in resident stem cells. Those cells quickly differentiate into odontoblast-like cells that secrete new dentin, the hard tissue lying beneath enamel. In rat molars the treatment filled experimentally drilled lesions up to ten times larger than the holes that teeth can normally repair on their own, completely replacing the biodegradable collagen sponge carrier with natural dentin within four weeks.
Chemical analysis confirmed that the regenerated dentin shows the same carbonate-to-phosphate and mineral-to-matrix ratios as healthy dentin, not bone, preserving tooth strength. Importantly, drug activity stayed localised to the coronal pulp; gene-expression tests detected no Wnt activation in the root pulp, suggesting a good safety margin. Standard drilling is still needed to remove decay, yet the findings indicate that, after cleaning, a dentist could encourage the tooth to rebuild itself instead of inserting an inert cement filling.
Tideglusib’s success adds momentum to the broader goal of human tissue regeneration. Follow-on studies are exploring light-cured hydrogels and nanofibre scaffolds that deliver the drug more precisely and could translate easily to everyday dental practice.
Journal of Dental Research – “Translation Approach for Dentine Regeneration Using GSK-3 Antagonists” (DOI: 10.1177/0022034520908593)
In mice and rats, 1 µM tideglusib or 20 µM CHIR99021 placed on a collagen sponge over an exposed pulp triggered robust Wnt signalling, restricted to the damaged coronal pulp, and produced a dense dentin bridge that completely filled defects up to 0.9 mm². Raman spectroscopy showed the regenerated tissue was chemically indistinguishable from native dentin, supporting clinical translation.
0 Comments