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Related Experiment Video

Updated: Jan 23, 2026

Development of a Direct Pulp-capping Model for the Evaluation of Pulpal Wound Healing and Reparative Dentin Formation in Mice
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Mutant Dentin Sialophosphoprotein Causes Dentinogenesis Imperfecta.

T Liang1, H Zhang1, Q Xu1

  • 11 Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University College of Dentistry, Dallas, TX, USA.

Journal of Dental Research
|June 8, 2019
PubMed
Summary

A mutation in dentin sialophosphoprotein (DSPP) causes dentinogenesis imperfecta (DGI) in mice. Mutant DSPP accumulates in odontoblasts, leading to abnormal dentin formation and pulp chamber changes resembling human DGI types II and III.

Keywords:
extracellular matrixgeneticsmineralized tissue/developmentodontoblast(s)odontogenesistooth development

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Area of Science:

  • Biochemistry
  • Genetics
  • Dental Science

Background:

  • Dentin sialophosphoprotein (DSPP) is crucial for dentin formation and is highly expressed by odontoblasts.
  • Mutations in DSPP are linked to dentinogenesis imperfecta (DGI), a group of inherited dentin disorders.
  • A specific proline-to-leucine substitution at position 19 in DSPP was investigated.

Purpose of the Study:

  • To investigate the effects of a specific DSPP mutation (P19L) on tooth development and dentin matrix formation.
  • To characterize the dental phenotype of a novel mouse model expressing mutant DSPP.
  • To elucidate the cellular and molecular mechanisms underlying DSPP-related dentin abnormalities.

Main Methods:

  • Generation and analysis of a DSPP-mutant mouse model (Dspp mice).
  • Histological examination of tooth structure, including pulp chamber morphology and dentin thickness.
  • Immunohistochemistry, in situ hybridization, and real-time PCR to assess DSPP expression and localization.
  • In vitro studies to evaluate mutant DSPP secretion and intracellular processing.

Main Results:

  • Dspp mice exhibited dental phenotypes mimicking human DGI types II and III, with altered pulp chamber size and dentin thickness.
  • Increased enamel attrition and excessive peritubular dentin deposition were observed in mutant mice.
  • Reduced DSPP expression in odontoblasts and impaired secretion of mutant DSPP, leading to intracellular accumulation within the endoplasmic reticulum.
  • Differential DSPP expression levels between roof- and floor-forming odontoblasts in both wild-type and mutant mice.

Conclusions:

  • Intracellular retention of mutant DSPP in odontoblasts is a key factor in the pathogenesis of DSPP-related dental abnormalities.
  • The P19L DSPP mutation leads to distinct dental phenotypes associated with impaired dentin matrix formation and odontoblast dysfunction.
  • This mouse model provides valuable insights into the molecular mechanisms of dentinogenesis imperfecta and potential therapeutic targets.