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Xeno-Free Biomimetic-Scaffold Supports hiPSC-Derived Dental Organoid Formation and Tooth Regeneration

ABSTRACT: Tooth regeneration remains an unmet clinical challenge due to the structural complexity of dental tissues and the requirement for precise epithelial–mesenchymal interactions during development. Here, we present a xeno-free, biomimetic strategy for dental organoid engineering by integrating human induced pluripotent stem cell (hiPSC)–derived oral epithelial cells (OECs) and neural crest cells (NCCs) within a biodegradable chitosan–alginate (CA) scaffold. The CA scaffold provides a mechanically compliant and highly porous 3D microenvironment that supports hiPSC maintenance, lineage-specific differentiation, and spatial organization. Recombined OECs and NCCs self-organized into dental organoids that recapitulated key features of early odontogenesis, including coordinated epithelial–mesenchymal interactions, progressive expression of odontogenic markers (DSPP and AMBN), and time-dependent mineral deposition. Transcriptomic profiling revealed activation of gene programs associated with odontogenesis, amelogenesis, and craniofacial morphogenesis. Upon orthotopic implantation into a rat maxillary molar extraction site, cell-laden scaffolds supported cell survival, early tooth-like tissue organization, and localized mineralized matrix formation in vivo. Together, these results establish a xeno-free, scaffold-based platform for dental organoid formation and early tooth regeneration, providing a translational framework for stem cell–based dental tissue engineering and regenerative therapies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE319198 | GEO | 2026/02/18

REPOSITORIES: GEO

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Project description:Embryologically the tooth is derived from both the ectoderm and neural crest (ectomesenchyme). It is often used as a model to study how epithelialmesenchymal interactions can control differentiation and morphogenesis. During early development organs of ectodermal origin share both a set of signalling molecules and exhibit common morphological features, subsequently proceeding along separate developmental programs. Tooth development is a continuous process that can be divided into the initiation -, bud -, cap -, and bell-stages. In mice, tooth development begins at embryonic day 11.5 (E11.5), by thickening of the dental epithelium, while mineralization of enamel and dentin in first molar starts at postnatal day 0 (P0) (5). A multistep and complex process of the gene expression are involved in the early stage of tooth development. So far expression of more than 1300 genes and/or proteins have been detected during tooth germ development by microarrays/immunocytochemistry/in situ hybridization. Studies with mutant mice have identified a number of genes that regulate tooth development and morphology. For example, deficiency of Lef-1 or P63 arrests tooth development at early stages. Deficiency of Msx1 or Pax9 results in arrest of tooth development at the bud stage , while deficiency of Runx2/Cbfa1 or Sp3 inhibits cyto-differentiation of ameloblasts and/or odontoblasts. Shh is required for normal growth and morphogenesis, but is not essential for cyto-differentiation of the ameloblast and odontoblast populations. Ameloblastin and amelogenin knock-out mice develop severe enamel hypoplasia with abnormal ameloblast differentiation. Recently, new connections between retinoid metabolism and PPAR responses have been identified. It has also been shown that endogenous retinoic acid is necessary for the initiation of odontogenesis , and that some of the genes that catalyze the oxidation of retinaldehyde into retinoic acid, exhibit distinct patterns of expression in developing murine teeth. Little is known about functions of PPAR-a as regards tooth germs or mature teeth. It is, however, likely that mitochondrial oxidative metabolism well as fatty acid metabolism is enhanced in late odontogenesis. These are metabolic activities which in other tissues are stimulated by PPAR-a agonists. For this reason it was of interest to carry out comparative gene expression profiling of the first molar tooth germs of PPAR-a knock-out mouse and of the corresponding wild-type mice. The results suggest marked differences in gene expression, parts of which may be associated with an observed hypomineralization of enamel in the mature PPAR-a knock-out murine tooth.

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Xeno-Free Biomimetic-Scaffold Supports hiPSC-Derived Dental Organoid Formation and Tooth Regeneration

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