Evidence map›Paper›PMID 41554959›Full record

ArticleScientific reports2026

Therapeutic potency and the related mechanism of deinoxanthin in experimental animal and cell models of periodontitis.

Govinda Bhattarai, Yu-Hyeon An, Saroj Kumar Shrestha, Shankar Rijal, Seung-Moon Park, Sung-Ho Kook, Jeong-Chae Lee, Young-Mi Jeon

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Govinda Bhattarai *Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences, Jeonbuk National University, Jeonju, 54896, Republic of Korea.
Yu-Hyeon An *Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences, Jeonbuk National University, Jeonju, 54896, Republic of Korea.
Saroj Kumar Shrestha *Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL, 35233, USA.
Shankar RijalDepartment of Bioactive Material Sciences and Research Center of Bioactive Materials, Jeonbuk National University, Jeonju, 54896, Republic of Korea.
Seung-Moon ParkDepartment of Bioenvironmental Chemistry, Jeonbuk National University, Jeonju, 54896, Republic of Korea.
Sung-Ho KookDepartment of Bioactive Material Sciences and Research Center of Bioactive Materials, Jeonbuk National University, Jeonju, 54896, Republic of Korea.
Jeong-Chae LeeCluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences, Jeonbuk National University, Jeonju, 54896, Republic of Korea. jeongchae@jbnu.ac.kr.
Young-Mi JeonCluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences, Jeonbuk National University, Jeonju, 54896, Republic of Korea. young@jbnu.ac.kr.

Funding

National Research Foundation of Korea 2021R1A2C2006032National Research Foundation of Korea RS-2023-00277774National Research Foundation of Korea RS-2024-00338143
6 · The paper itself

Abstract

Periodontitis is a chronic inflammatory disease that leads to the destruction of periodontal tissue, ultimately resulting in tooth loss. Studies have aimed to develop biomaterials that effectively prevent inflammatory responses and oxidative stress in the progression of periodontitis, without adverse side effects. Here, we explored whether Deinococcus radiodurans-derived deinoxanthin (DEIX) protects against alveolar bone loss and connective tissue degradation in an experimental rat model of periodontitis and investigated the related mechanisms using human-derived periodontal ligament cells (hPDLCs) and THP-1 cells. Oral supplementation with DEIX (25 mg/kg body weight, once per day for 14 consecutive days) protected rats against ligature-mediated periodontal destruction. That protection involved the DEIX-induced restoration of the ligature-stimulated disorders, including overproduction of inflammatory mediators, accumulation of reactive oxygen species, and imbalance between osteoclast and osteoblast activity in the inflamed periodontium. In vitro experiments supported the associated mechanisms by which the direct addition of DEIX (20 µM) recovers lipopolysaccharide (LPS, 2 µg/mL)-stimulated inflammatory responses in hPDLCs and THP-1 cells. RNA sequence profiling from the DEIX and/or LPS-exposed hPDLCs further supported the protective mechanisms of DEIX on LPS-stimulated inflammatory and oxidative damage. Collectively, this study highlights the potential of DEIX to protect against inflammatory periodontal tissue destruction and demonstrates its clinical utility for patients with chronic periodontitis.

Indexed as

PeriodontitisAlveolar Bone LossAnimalsDisease Models, AnimalHumansLipopolysaccharidesMaleOxidative StressPeriodontal LigamentRatsReactive Oxygen SpeciesTHP-1 CellsLipopolysaccharidesReactive Oxygen SpeciesDeinoxanthinInflammatory disorderOxidative stressPeriodontitisProtective mechanismRNA sequence profiling

Identifiers

PMID41554959
PMCPMC12891702

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.