ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2018
Immunohistochemical Localization of Fam83h During Fluorosis-induced Mouse Molar Development.
Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Multiomics Data Synthesis of FAM83H in Amelogenesis Imperfecta.International dental journal · 2026Pooled it
- TGF-β1/Smad3 Signaling Is Required to Alleviate Fluoride-Induced Enamel Hypomineralization.Biological trace element research · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The clinical and pathological features of fluorosis are similar to amelogenesis imperfecta (AI) caused by FAM83H mutations, suggesting that excess fluoride could have effects on the expression of Fam83h. Our previous study found that Fam83h was downregulated by fluorosis induction in ameloblasts; the purpose of this study was to underline the importance of understanding the relationship between fluoride administration and Fam83h expression in vivo. A total of 80 healthy female adult Kunming mice were randomly divided into control group or F group that induced the clinical features of fluorosis. Immunohistochemical staining on sections of the embryo mandible regions was performed at different developmental stages. Mouse primary ameloblast-like cells of the two groups at E13.5, E15.5, and E18.5 were cultured and examined for the expression of Fam83h. The expression of Fam83h in the F group was significantly lower than that in the control group; however, Fam83h was observed clearly in the whole enamel organ in the control group. Our findings shed new light on the potential effects of Fam83h in fluorosis using a mouse model and revealed that high fluoride decreased the expression of Fam83h. This may be one of the reasons for the occurrence of fluorosis.
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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.