Evidence map›Paper›PMID 29575674›Full record

ReviewOral diseases2019

Dentin dysplasia type I-A dental disease with genetic heterogeneity.

D Chen, X Li, F Lu, Y Wang, F Xiong, Q Li

Open access · hybridAbstract readReview
In one paragraph

Review in Oral diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. [Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2026
    Article
  4. Article
  5. [Case report of dentinogenesis imperfecta and review of literature].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Expert consensus on digital guided therapy for endodontic diseases.International journal of oral science · 2023
    Review
  14. Article
  15. Expressions of cytokeratin 14 and proliferating cell nuclear antigen in the Hertwig's epithelial root sheath of a Vps4b knockout mouse.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Haploinsufficiency ofFrontiers in physiology · 2020
    Article
  20. [Spatio-temporal expression of dentin sialophosphoprotein and collagen Ⅰ during molar tooth germ development in vps4b knockout mouse].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

D ChenDepartment of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID http://orcid.org/0000-0002-9627-4895
X LiDepartment of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID http://orcid.org/0000-0002-9291-6176
F LuDepartment of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Y WangDepartment of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
F XiongDepartment of Medical Genetics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Q LiDepartment of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CNSouthern Medical University · CN

Funding

National Natural Science Foundation of China 31371279National Natural Science Foundation of China 81470033
6 · The paper itself

Abstract

Hereditary dentin disorders include dentinogenesis imperfecta (DGI) and dentin dysplasia (DD), which are autosomal dominant diseases characterized by altered dentin structure such as abnormality in dentin mineralization and the absence of root dentin. Shields classified DGI into three subgroups and DD into two subtypes. Although they are all hereditary dentin diseases, they do not share the same causative genes. To date, the pathogenic genes of DGI type I, which is considered a clinical manifestation of syndrome osteogenesis imperfecta, include COL1A1 and COL1A2. Mutations of the DSPP gene, which encodes the dentin sialophosphoprotein, a major non-collagenous protein, are responsible for three isolated dentinal diseases: DGI-II, DGI-III, and DD-II. However, DD-I appears to be special in that researchers have found three pathogenicity genes-VPS4B, SSUH2, and SMOC2-in three affected families from different countries. It is believed that DD-I is a genetically heterogeneous disease and is distinguished from other types of dentin disorders. This review summarizes the DD-I literature in the context of clinical appearances, radiographic characteristics, and functions of its pathogenic genes and aims to serve clinicians in further understanding and diagnosing this disease.

Indexed as

ATPases Associated with Diverse Cellular ActivitiesCaenorhabditis elegans ProteinsCalcium-Binding ProteinsDentin DysplasiaDentinogenesis ImperfectaDiagnosis, DifferentialEndosomal Sorting Complexes Required for TransportGenetic HeterogeneityHumansPhosphoprotein PhosphatasesATPases Associated with Diverse Cellular ActivitiesCaenorhabditis elegans ProteinsCalcium-Binding ProteinsEndosomal Sorting Complexes Required for TransportPhosphoprotein PhosphatasesSMOC2 protein, humanSSUP-72 phosphatase, C elegansVPS4B protein, humandentin dysplasiapathogenic genesSMOC2SSUH2VPS4B

Identifiers

PMID29575674
PMCPMC7818184
OpenAlexW2911871362

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.