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Published on: September 12, 2017
Cell proliferation and apoptosis in enamelin null mice
Jan C-C Hu1, Rangsiyakorn Lertlam, Amelia S Richardson
1Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48108, USA. janhu@umich.edu
Enamelin deficiency in mice leads to abnormal ameloblast development and increased cell death during enamel formation. This highlights enamelin's crucial role in maintaining ameloblast health and proper enamel matrix deposition.
Area of Science:
- Biochemistry
- Developmental Biology
- Cell Biology
Background:
- Enamelin is a key glycoprotein in dental enamel formation.
- Enamelin null mice exhibit abnormal ameloblast features, including altered morphology and extracellular matrix deposition.
Purpose of the Study:
- To investigate the association between pathological changes in ameloblasts and increased apoptosis in enamelin null mice.
- To assess apoptotic activity in wild-type, heterozygous, and null mice at various postnatal developmental stages.
Main Methods:
- Light microscopy of mouse maxillae.
- Terminal deoxynucleotidyl transferase (TdT)-mediated biotin-dUTP nick-end labelling (TUNEL) for apoptosis detection.
- 5-bromo-2'-deoxyuridine (BrdU) staining for cell proliferation assessment.
Main Results:
- Ameloblasts in enamelin null mice showed dysplastic changes and failed to deposit enamel crystal ribbons.
- Increased ameloblast apoptosis was observed in enamelin null mice during the secretory stage.
- No significant alteration in ameloblast proliferation was detected.
Conclusions:
- Enamelin absence leads to ameloblast pathological changes, including altered morphology, detachment, and apoptosis, early in the secretory stage.
- The lack of enamelin disrupts enamel formation and results in ectopic calcifications.
- Enamelin is essential for maintaining ameloblast integrity and function during enamel development.
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