ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2013
Tooth root dentin mineralization defects in a mouse model of hypophosphatasia.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 108 citations in OpenAlex.
- Article
- NEFL is associated with inhibition of odontoblastic process in odontohypophosphatasia.Journal of bone and mineral metabolism · 2026Article
- Mineral-targeted alkaline phosphatase improves bone graft-mediated alveolar bone defect healing in mice.Journal of periodontology · 2026Article
- Impact of oral phosphate supplements and active vitamin D treatment on dentoalveolar features of X-linked hypophosphatemia.JBMR plus · 2026Article
- Hypophosphatasia-pathophysiological understanding, preclinical data looking beyond the skeleton, and upcoming treatments.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Review
- ENPP1 inhibition as a therapeutic approach for later-onset hypophosphatasia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- Article
- Metabolic programming in tooth development: a regulatory network from energy substrates to signaling instructions.Frontiers in cell and developmental biology · 2026Review
- Proof-of-principle for enhanced dentoalveolar mineralization using exogenous tissue-nonspecific alkaline phosphatase in theJBMR plus · 2025Article
- Inhibition of histone deacetylase 3 in dental mesenchyme regulates the development of tooth root.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Article
- Article
- Polystyrene substrate effects on human dental pulp cell behavior: implications for in vitro culture optimization.BMC oral health · 2025Article
- Preclinical evaluation of the efficacy and safety of adeno-associated virus 8-tissue-nonspecific alkaline phosphatase-D10 in Alpl-/- and AlplPrx1/Prx1 mouse models for the treatment of early and late-onset hypophosphatasia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Article
- Review
- Fabrication of Hard Tissue Constructs from Induced Pluripotent Stem Cells for Exploring Mechanisms of Hereditary Tooth/Skeletal Dysplasia.International journal of molecular sciences · 2025Article
- Establishment of human periodontal ligament cell lines withFrontiers in cell and developmental biology · 2025Article
- Delayed Tooth Development and the Impaired Differentiation of Stem/Progenitor Cells in Incisors from Type 2 Diabetes Mice.International journal of molecular sciences · 2024Article
- Inherited phosphate and pyrophosphate disorders: New insights and novel therapies changing the oral health landscape.Journal of the American Dental Association (1939) · 2024Review
- Dental impact of anti-fibroblast growth factor 23 therapy in X-linked hypophosphatemia.International journal of oral science · 2023Article
- Dental characteristics of patients with four different types of skeletal dysplasias.Clinical oral investigations · 2023Article
12 more citing papers are in PubMed but not listed here.
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10 authors at 5 institutions in 2 countries.
Funding
Abstract
Tissue-nonspecific alkaline phosphatase (TNAP) is expressed in mineralizing tissues and functions to reduce pyrophosphate (PP(i) ), a potent inhibitor of mineralization. Loss of TNAP function causes hypophosphatasia (HPP), a heritable disorder marked by increased PP(i) , resulting in rickets and osteomalacia. Tooth root cementum defects are well described in both HPP patients and in Alpl(-/-) mice, a model for infantile HPP. In Alpl(-/-) mice, dentin mineralization is specifically delayed in the root; however, reports from human HPP patients are variable and inconsistent regarding dentin defects. In the current study, we aimed to define the molecular basis for changes in dentinogenesis observed in Alpl(-/-) mice. TNAP was found to be highly expressed by mature odontoblasts, and Alpl(-/-) molar and incisor roots featured defective dentin mineralization, ranging from a mild delay to severely disturbed root dentinogenesis. Lack of mantle dentin mineralization was associated with disordered and dysmorphic odontoblasts having disrupted expression of marker genes osteocalcin and dentin sialophosphoprotein. The formation of, initiation of mineralization within, and rupture of matrix vesicles in Alpl(-/-) dentin matrix was not affected. Osteopontin (OPN), an inhibitor of mineralization that contributes to the skeletal pathology in Alpl(-/-) mice, was present in the generally unmineralized Alpl(-/-) mantle dentin at ruptured mineralizing matrix vesicles, as detected by immunohistochemistry and by immunogold labeling. However, ablating the OPN-encoding Spp1 gene in Alpl(-/-) mice was insufficient to rescue the dentin mineralization defect. Administration of bioengineered mineral-targeting human TNAP (ENB-0040) to Alpl(-/-) mice corrected defective dentin mineralization in the molar roots. These studies reveal that TNAP participates in root dentin formation and confirm that reduction of PP(i) during dentinogenesis is necessary for odontoblast differentiation, dentin matrix secretion, and mineralization. Furthermore, these results elucidate developmental mechanisms underlying dentin pathology in HPP patients, and begin to explain the reported variability in the dentin/pulp complex pathology in these patients.
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