ArticleScientific reports2016
ClC-7 Deficiency Impairs Tooth Development and Eruption.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Spectrum and functions of ion channels and transporters in osteoclasts.Bone research · 2026Review
- Abnormal dental follicle cells: A crucial determinant in tooth eruption disorders (Review).Molecular medicine reports · 2024Review
- Molecular Mechanisms of Craniofacial and Dental Abnormalities in Osteopetrosis.International journal of molecular sciences · 2023Review
- Effect of periostin on bone metabolic and autophagy factors during tooth eruption in mice.Open life sciences · 2023Article
- GATA Binding Protein 4 Regulates Tooth Root Dentin DevelopmentInternational journal of biological sciences · 2020Article
- Aberrantly elevated Wnt signaling is responsible for cementum overgrowth and dental ankylosis.Bone · 2019Article
- ClC-7 Regulates the Pattern and Early Development of Craniofacial Bone and Tooth.Theranostics · 2019Article
- Dental care approach in patients with osteopetrosis.European archives of paediatric dentistry : official journal of the European Academy of Paediatric Dentistry · 2016Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CLCN7 gene encodes the voltage gated chloride channel 7 (ClC-7) in humans. The mutations in CLCN7 have been associated with osteopetrosis in connection to the abnormal osteoclasts functions. Previously, we found that some osteopetrosis patients with CLCN7 mutations suffered from impacted teeth and root dysplasia. Here we set up two in vivo models under a normal or an osteoclast-poor environment to investigate how ClC-7 affects tooth development and tooth eruption. Firstly, chitosan-Clcn7-siRNA nanoparticles were injected around the first maxillary molar germ of newborn mice and caused the delay of tooth eruption and deformed tooth with root dysplasia. Secondly, E13.5 molar germs infected with Clcn7 shRNA lentivirus were transplanted under the kidney capsule and presented the abnormal changes in dentin structure, periodontal tissue and cementum. All these teeth changes have been reported in the patients with CLCN7 mutation. In vitro studies of ameloblasts, odontoblasts and dental follicle cells (DFCs) were conducted to explore the involved mechanism. We found that Clcn7 deficiency affect the differentiation of these cells, as well as the interaction between DFCs and osteoclasts through RANKL/OPG pathway. We conclude that ClC-7 may affect tooth development by directly targeting tooth cells, and regulate tooth eruption through DFC mediated osteoclast pathway.
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