ArticleCells, tissues, organs2009
Phenotype characterization and DSPP mutational analysis of three Brazilian dentinogenesis imperfecta type II families.
Article in Cells, tissues, organs, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 15 citations in OpenAlex.
- Calcium phosphate polymer induced liquid precursor improves dentin bonding performance of primary teeth with dentinogenesis imperfecta type II.BMC oral health · 2026Article
- Isolated dentinogenesis imperfecta and dentin dysplasia: revision of the classification.European journal of human genetics : EJHG · 2015Review
- A novel DSPP mutation causes dentinogenesis imperfecta type II in a large Mongolian family.BMC medical genetics · 2010Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The aim of this study was to perform phenotype analysis and dentin sialophosphoprotein (DSPP) mutational analysis on 3 Brazilian families diagnosed with dentinogenesis imperfecta type II (DGI-II) attending the Dental Anomalies Clinic in Brasilia, Brazil. Physical and oral examinations, as well as radiographic and histopathological analyses, were performed on 28 affected and unaffected individuals. Clinical, radiographic and histopathological analyses confirmed the diagnosis of DGI-II in 19 individuals. Pulp stones were observed in ground sections of several teeth in 2 families, suggesting that obliteration of pulp chambers and root canals results from the growth of these nodular structures. Mutational DSPP gene analysis of representative affected family members revealed 7 various non-disease-causing alterations in exons 1-4 within the dentin sialoprotein domain. Further longitudinal studies are necessary to elucidate the progression of pulpal obliteration in the DGI-II patients studied as well as the molecular basis of their disease.
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