Evidence map›Paper›PMID 31691738›Full record

ArticleJournal of applied oral science : revista FOB2019

Effects of 1,25-dihydroxyvitamin D3 on experimental periodontitis and AhR/NF-κB/NLRP3 inflammasome pathway in a mouse model.

Hao Li, Xinghua Zhong, Wei Li, Qi Wang

Open access · diamondAbstract readEvaluation Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of applied oral science : revista FOB, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 59 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Hao LiGuangxi Medical University, the Affiliated Hospital of Stomatology, Department of Prosthodontics, China.ORCID http://orcid.org/0000-0002-4633-8256
Xinghua ZhongGuangxi Medical University, the Affiliated Hospital of Stomatology, Department of Prosthodontics, China.
Wei LiSichuan University, West China Hospital of Stomatology, State Key Laboratory of Oral Diseases, China.
Qi WangSichuan University, West China Hospital of Stomatology, State Key Laboratory of Oral Diseases, China.
Guangxi Medical University · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vitamin D has been known to have important regulatory functions in inflammation and immune response and shows inhibitory effects on experimental periodontitis in animal models. However, the potential mechanism has yet to be clarified. Recent studies have highlighted Aryl hydrocarbon receptor (AhR) and its downstream signaling as a crucial regulator of immune homeostasis and inflammatory regulation.

objectiveThis study aimed to clarify the effect of 1,25-dihydroxyvitamin D3 (VD3) on experimental periodontitis and AhR/nuclear factor-κB (NF-κB)/NLR pyrin domain-containing 3 (NLRP3) inflammasome pathway in the gingival epithelium in a murine model. METHODOLOGY: We induced periodontitis in male C57BL/6 wild-type mice by oral inoculation of Porphyromonas gingivalis (P. gingivalis), and subsequently gave intraperitoneal VD3 injection to the mice every other day for 8 weeks. Afterwards, we examined the alveolar bone using scanning electron microscopy (SEM) and detected the gingival epithelial protein using western blot analysis and immunohistochemical staining.

resultsSEM images demonstrated that alveolar bone loss was reduced in the periodontitis mouse model after VD3 supplementation. Western blot analyses and immunohistochemical staining of the gingival epithelium showed that the expression of vitamin D receptor, AhR and its downstream cytochrome P450 1A1 were enhanced upon VD3 application. Additionally, VD3 decreased NF-κB p65 phosphorylation, and NLRP3, apoptosis-associated speck-like protein, caspase-1, interleukin-1β (IL-1β) and IL-6 protein expression.

conclusionsThese results implicate the alleviation of periodontitis and the alteration of AhR/NF-κB/NLRP3 inflammasome pathway by VD3 in the mouse model. The attenuation of this periodontal disease may correlate with the regulation of AhR/NF-κB/NLRP3 inflammasome pathway by VD3.

Indexed as

Alveolar Bone LossAnimalsBlotting, WesternBone Density Conservation AgentsCalcitriolCaspase 1GingivaImmunohistochemistryInterleukin-1betaInterleukin-6MaleMice, Inbred C57BLNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinPeriodontitisPorphyromonas gingivalisBone Density Conservation AgentsCalcitriolCaspase 1Interleukin-1betaInterleukin-6NF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, Aryl Hydrocarbon

Identifiers

PMID31691738
PMCPMC6831029
OpenAlexW2986597555

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.