ArticleEuropean journal of oral sciences2011
Cell proliferation and apoptosis in enamelin null mice.
Article in European journal of oral sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Ganoin and acrodin formation on scales and teeth in spotted gar: A vital role of enamelin in the unique process of enamel mineralization.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2023Article
- Role of Cell Death in Cellular Processes During Odontogenesis.Frontiers in cell and developmental biology · 2021Review
- FAM20A is essential for amelogenesis, but is dispensable for dentinogenesis.Journal of molecular histology · 2019Article
- ENAM mutations and digenic inheritance.Molecular genetics & genomic medicine · 2019Article
- AMBN mutations causing hypoplastic amelogenesis imperfecta and Ambn knockout-NLS-lacZ knockin mice exhibiting failed amelogenesis and Ambn tissue-specificity.Molecular genetics & genomic medicine · 2019Article
- DENTAL ENAMEL FORMATION AND IMPLICATIONS FOR ORAL HEALTH AND DISEASE.Physiological reviews · 2017Review
- Ultrastructure of early amelogenesis in wild-type,Molecular genetics & genomic medicine · 2016Article
- Enamel ribbons, surface nodules, and octacalcium phosphate in C57BL/6Molecular genetics & genomic medicine · 2016Article
- Article
- The development of complex tooth shape in reptiles.Frontiers in physiology · 2014Article
- Dental enamel development: proteinases and their enamel matrix substrates.ISRN dentistry · 2013Review
- Gene Expression Profiling during Murine Tooth Development.Frontiers in genetics · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Enamelin is a secreted glycoprotein that is critical for dental enamel formation. Ameloblasts in enamelin (Enam) null mice develop atypical features that include the absence of a Tomes' process, expanded endoplasmic reticulum, apparent loss of polarity, and pooling of extracellular matrix in all directions, including between ameloblasts and the stratum intermedium. We hypothesized that ameloblast pathological changes may be associated with increased cell apoptosis. Our objective was to assess apoptotic activity in maxillary first molars of wild-type, Enam(+/-), and Enam(-/-) mice at postnatal days 5, 7, 9, 14, and 17. Mouse maxillae were characterized by light microscopy after terminal deoxynucleotidyl transferase (TdT)-mediated biotin-dUTP nick-end labelling (TUNEL) or 5-bromo-2'-deoxyuridine (BrdU) staining. Following the initial deposition of dentin matrix, ameloblasts became highly dysplastic and no enamel crystal ribbons were deposited. Ameloblast apoptosis was observed in the Enam null mice starting in the secretory stage and with no apparent alteration in cell proliferation. We conclude that in the absence of enamelin and subsequent shutdown of enamel formation, ameloblasts undergo pathological changes early in the secretory stage that are evident as radically altered cell morphology, detachment from the tooth surface, apoptosis, and formation of ectopic calcifications both outside and inside the dystrophic enamel organ.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.