ArticleDevelopmental biology2013
Inactivation of Tgfbr2 in Osterix-Cre expressing dental mesenchyme disrupts molar root formation.
Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 77 citations in OpenAlex.
- Depletion of macrophages during early postnatal development leads to disrupted tooth root development and altered Gli1⁺ MSC trajectory.Cell death & disease · 2026Article
- Gli2 and Gli3 synergistically mediate HH-TGF-β crosstalk in mesenchymal progenitor cells to orchestrate tooth root morphogenesis.International journal of oral science · 2026Article
- Bone matrix proteins: regulators of skeletal remodeling and repair.Journal of bone and mineral metabolism · 2026Review
- Mechanisms of primary failure of eruption: a new model of multidimensional framework.Progress in orthodontics · 2025Review
- A novel PTH1R mutation causes primary failure of eruption via the cAMP-PI3K/AKT pathway.Progress in orthodontics · 2025Article
- Abnormal dental follicle cells: A crucial determinant in tooth eruption disorders (Review).Molecular medicine reports · 2024Review
- Impaired Tertiary Dentin Secretion after Shallow Injury inInternational journal of molecular sciences · 2024Article
- TGF-β Signaling in Cranial Neural Crest Affects Late-Stage Mandibular Bone Resorption and Length.bioRxiv : the preprint server for biology · 2024Article
- A Wnt10a-Notch signaling axis controls Hertwig's epithelial root sheath cell behaviors during root furcation patterning.International journal of oral science · 2024Article
- The roles and regulatory mechanisms of TGF-β and BMP signaling in bone and cartilage development, homeostasis and disease.Cell research · 2024Review
- TGF-β signaling in the cranial neural crest affects late-stage mandibular bone resorption and length.Frontiers in physiology · 2024Article
- Effects of antiresorptive medications on tooth root formation and tooth eruption in paediatric patients.Orthodontics & craniofacial research · 2023Review
- Atp6i deficient mouse model uncovers transforming growth factor-β1 /Smad2/3 as a key signaling pathway regulating odontoblast differentiation and tooth root formation.International journal of oral science · 2023Article
- Immunomodulatory properties of mesenchymal stem cells/dental stem cells and their therapeutic applications.Cellular & molecular immunology · 2023Review
- Loss of Stat3 in OsterixCell & bioscience · 2023Article
- Activin receptor-like kinase 3: a critical modulator of development and function of mineralized tissues.Frontiers in cell and developmental biology · 2023Review
- Between a rock and a hard place: Regulation of mineralization in the periodontium.Genesis (New York, N.Y. : 2000) · 2022Review
- The Effects of Transforming Growth Factor-BioMed research international · 2022Article
- Article
- Role of the Demethylase AlkB Homolog H5 in the Promotion of Dentinogenesis.Frontiers in physiology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
It has been difficult to examine the role of TGF-ß in post-natal tooth development due to perinatal lethality in many of the signaling deficient mouse models. To address the role of Tgfbr2 in postnatal tooth development, we generated a mouse in which Tgfbr2 was deleted in odontoblast- and bone-producing mesenchyme. Osx-Cre;Tgfbr2(fl/fl) mice were generated (Tgfbr2(cko)) and post-natal tooth development was compared in Tgfbr2(cko) and control littermates. X-ray and μCT analysis showed that in Tgfbr2(cko) mice radicular dentin matrix density was reduced in the molars. Molar shape was abnormal and molar eruption was delayed in the mutant mice. Most significantly, defects in root formation, including failure of the root to elongate, were observed by postnatal day 10. Immunostaining for Keratin-14 (K14) was used to delineate Hertwig's epithelial root sheath (HERS). The results showed a delay in elongation and disorganization of the HERS in Tgfbr2(cko) mice. In addition, the HERS was maintained and the break up into epithelial rests was attenuated suggesting that Tgfbr2 acts on dental mesenchyme to indirectly regulate the formation and maintenance of the HERS. Altered odontoblast organization and reduced Dspp expression indicated that odontoblast differentiation was disrupted in the mutant mice likely contributing to the defect in root formation. Nevertheless, expression of Nfic, a key mesenchymal regulator of root development, was similar in Tgfbr2(cko) mice and controls. The number of osteoclasts in the bone surrounding the tooth was reduced and osteoblast differentiation was disrupted likely contributing to both root and eruption defects. We conclude that Tgfbr2 in dental mesenchyme and bone is required for tooth development particularly root formation.
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