Abnormal osteopontin and matrix extracellular phosphoglycoprotein localization, and odontoblast differentiation, in X-linked hypophosphatemic teeth

@article{Salmon2014AbnormalOA,
  title={Abnormal osteopontin and matrix extracellular phosphoglycoprotein localization, and odontoblast differentiation, in X-linked hypophosphatemic teeth},
  author={B. Salmon and C. Bardet and B. R. Coyac and B. Baroukh and J. Naji and P. Rowe and S. Opsahl Vital and A. Linglart and M. McKee and C. Chaussain},
  journal={Connective Tissue Research},
  year={2014},
  volume={55},
  pages={79 - 82}
}
Abstract Mutations in phosphate-regulating gene (PHEX) lead to X-linked hypophosphatemic rickets (XLH), a genetic disease characterized by impaired mineralization in bones and teeth. In human XLH tooth dentin, calcospherites that would normally merge as part of the mineralization process are separated by unmineralized interglobular spaces where fragments of matrix proteins accumulate. Here, we immunolocalized osteopontin (OPN) in human XLH teeth, in a three-dimensional XLH human dental pulp… Expand
Osteopontin and the dento-osseous pathobiology of X-linked hypophosphatemia.
TLDR
Findings of an excess of inhibitory OPN near osteocytes and their cell processes, and in dentin, spatially correlates with the defective mineralization observed at these sites in the skeleton and teeth of XLH patients. Expand
Impaired mineral quality in dentin in X-linked hypophosphatemia
TLDR
Results indicate that like for bone and tooth cementum, there are impaired mineral quality and matrix changes in XLH dentin reflecting high sensitivity to systemic serum phosphate levels and possibly other local changes in the dentin matrix. Expand
Tissue-specific mineralization defects in the periodontium of the Hyp mouse model of X-linked hypophosphatemia.
TLDR
The results show a major XLH phenotype in oral mineralized tissues consistent with variations in patient susceptibility to periodontal disorders. Expand
Disrupted Protein Expression and Altered Proteolytic Events in Hypophosphatemic Dentin Can Be Rescued by Dentin Matrix Protein 1
TLDR
The hypothesis that hypophosphatemia resulting from PHEX loss-of-function affects the integrity of the organization of the dentin matrix is supported and it is suggested that exogenous DMP1 can restore physiological processing of matrix proteins, in addition to its canonical role in mineralization. Expand
Alterations of bone material properties in adult patients with X-linked hypophosphatemia (XLH).
TLDR
A model is proposed that possibly integrates the relationship between the observed mineralization disturbances, FGF23 secretion and the known osteopontin accumulation in XLH and the effects on bone material poorly characterized. Expand
Insights into Dental Mineralization from Three Heritable Mineralization Disorders.
TLDR
The distinct dental defects associated with the three heritable mineralization disorders reflect unique processes of the respective dental hard tissues, revealing insights into their development and clues about pathological mechanisms underlying such disorders. Expand
Basic fibroblast growth factor regulates phosphate/pyrophosphate regulatory genes in stem cells isolated from human exfoliated deciduous teeth
TLDR
This study reveals for the first time the effects of bFGF on Pi/PPi regulators in SHEDs and implicates these factors in how bF GF directs osteo/odontogenic differentiation and mineralization by these cells. Expand
Osteopontin regulates dentin and alveolar bone development and mineralization.
TLDR
It is concluded that OPN has a non-redundant role regulating formation and mineralization of dentin and bone, influences tissue properties of PDL and pulp, but does not control acellular cementum apposition. Expand
Development of Enthesopathies and Joint Structural Damage in a Murine Model of X-Linked Hypophosphatemia
TLDR
Similar to adult patients with XLH, Hyp mice developed calcaneal enthesophytes, hip joint alterations, erosions of the sacroiliac joints and periarticular calcifications, and it is suggested that new bone formation is driven by altered mechanical strain. Expand
Compositional and microhardness findings in tooth affected by X-linked hypophosphatemic rickets
TLDR
Compositional and structural deficiencies were observed in deciduous tooth affected by XLHR and it was observed the absence of hydroxyapatite in the interglobular dentin by using Raman spectroscopy analysis. Expand
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References

SHOWING 1-10 OF 12 REFERENCES
MEPE-Derived ASARM Peptide Inhibits Odontogenic Differentiation of Dental Pulp Stem Cells and Impairs Mineralization in Tooth Models of X-Linked Hypophosphatemia
TLDR
It is demonstrated that the MEPE-derived ASARM peptide inhibits both odontogenic differentiation and matrix mineralization, while increasing MEPE expression, contributing to a partial mechanistic explanation of XLH pathogenesis. Expand
Dentin Alteration of Deciduous Teeth in Human Hypophosphatemic Rickets
TLDR
Alterations of the post-translational processing or partial degradation of some ECM appear as key factors in the formation of the defective hypophosphatemic dentin. Expand
Proteolytic processing of osteopontin by PHEX and accumulation of osteopontin fragments in Hyp mouse bone, the murine model of X‐linked hypophosphatemia
  • N. Barros, B. Hoac, +5 authors M. McKee
  • Chemistry, Medicine
  • Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2013
TLDR
Results identify full‐length OPN and its fragments as novel, physiologically relevant substrates for PHEX, suggesting that accumulation of mineralization‐inhibiting OPN fragments may contribute to the mineralization defect seen in the osteomalacic bone characteristic of XLH/HYP. Expand
MEPE, a new gene expressed in bone marrow and tumors causing osteomalacia.
TLDR
This paper describes the characterization and cloning of a gene that is a candidate for the tumor-secreted phosphaturic factor and has major similarities to a group of bone-tooth mineral matrix phospho-glycoproteins, including MEPE, which all map to a defined region in chromosome 4q. Expand
Abnormal presence of the matrix extracellular phosphoglycoprotein-derived acidic serine- and aspartate-rich motif peptide in human hypophosphatemic dentin.
TLDR
The results suggest that abnormal MEPE cleavage occurs when PHEX activity is deficient in humans, the ASARM peptide may be involved in the mineralization defects and the PHEX-MEPE interaction may be indirect, as ensuring a better phosphate and vitamin D environment to the mineralizing dentin prevents MEPE Cleavage. Expand
Six Genes Expressed in Bones and Teeth Encode the Current Members of the SIBLING Family of Proteins
TLDR
Analysis of human brain mRNA by RT-PCR has led to the discovery of two additional exons thereby making it more convincing that MEPE is a member of the SIBLING (Small Integrin-Binding LIgand, N-linked Glycoprotein) family. Expand
Phosphorylation‐dependent inhibition of mineralization by osteopontin ASARM peptides is regulated by PHEX cleavage
  • W. Addison, D. Masica, Jeffrey J Gray, M. McKee
  • Chemistry, Medicine
  • Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2010
TLDR
It is concluded that OPN ASARM inhibits mineralization by binding to hydroxyapatite in a phosphorylation‐dependent manner and that this inhibitor can be cleaved by PHEX, thus providing a mechanistic explanation for how loss of PHEX activity in X‐linked hyposphosphatemia can lead to extracellular matrix accumulation of ASARM resulting in the osteomalacia. Expand
Pyrophosphate Inhibits Mineralization of Osteoblast Cultures by Binding to Mineral, Up-regulating Osteopontin, and Inhibiting Alkaline Phosphatase Activity*
TLDR
PPi prevents mineralization in MC3T3-E1 osteoblast cultures by at least three different mechanisms that include direct binding to growing crystals, induction of Opn expression, and inhibition of Tnap activity. Expand
Osteoclasts differentiate from resident precursors in an in vivo model of synchronized resorption: a temporal and spatial study in rats.
TLDR
Results strongly suggest that the osteoclasts present on day 4 differentiated from the pool of TRAP(+, ED1(+), and NSE(+) cells present at the site on day 0, and osteogenic cells appeared to be as crucial in vivo for the acquisition of the TRAP phenotype as previously shown in vitro. Expand
ASARM mineralization hypothesis: A bridge to progress
  • W. Addison, M. McKee
  • Geology, Medicine
  • Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2010
TLDR
In vitro work on osteopontin peptide–mineral interactions demonstrates that phosphorylated OPN ASARM inhibits extracellular matrix mineralization in an osteoblast culture model and provides key novel findings related to peptide control of crystal growth relevant to bone biology. Expand
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