Evidence map›Paper›PMID 28611683›Full record

ReviewFrontiers in physiology2017

Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis.

Hiroyuki Kanzaki, Satoshi Wada, Tsuyoshi Narimiya, Yuuki Yamaguchi, Yuta Katsumata, Kanako Itohiya, Sari Fukaya, Yutaka Miyamoto, Yoshiki Nakamura

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06261723 (Effect of Non-chirurgical Periodontal Treatment on the Innate and Adaptive Immunity From a Gender Perspective), which is not on this map. Cited by 99 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 2 pooled it
10.1field-weighted citation impact, top 1% 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.

NCT06261723 completednot on this mapstarted 2024, after this paper: background citation

Effect of Non-chirurgical Periodontal Treatment on the Innate and Adaptive Immunity From a Gender Perspective: Potential Therapeutic Implications of microRNAs

Typeobservational_patient_registrySponsorMilagros Rocha BarajasRan2024 to 2025Enrolled100ConditionsPeriodontal DiseasesArmsnon-chirurgical periodontal treatment
3 · Its place in the literature

Who cites it

99 citing papers in PubMed, 2 syntheses or guidelines pooled it, 181 citations in OpenAlex.

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39 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Hiroyuki KanzakiMaxillo-Oral Disorders, Tohoku University HospitalSendai, Japan.
Satoshi WadaDepartment of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.
Tsuyoshi NarimiyaDepartment of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.
Yuuki YamaguchiDepartment of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.
Yuta KatsumataDepartment of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.
Kanako ItohiyaDepartment of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.
Sari FukayaDepartment of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.
Yutaka MiyamotoDepartment of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.
Yoshiki NakamuraDepartment of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.
Tsurumi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontitis, an inflammatory disease that affects the tissues surrounding the teeth, is a common disease worldwide. It is caused by a dysregulation of the host inflammatory response to bacterial infection, which leads to soft and hard tissue destruction. In particular, it is the excessive inflammation in response to bacterial plaque that leads to the release of reactive oxygen species (ROS) from neutrophils, which, then play a critical role in the destruction of periodontal tissue. Generally, ROS produced from immune cells exhibit an anti-bacterial effect and play a role in host defense and immune regulation. Excessive ROS, however, can exert cytotoxic effects, cause oxidative damage to proteins, and DNA, can interfere with cell growth and cell cycle progression, and induce apoptosis of gingival fibroblasts. Collectively, these effects enable ROS to directly induce periodontal tissue damage. Some ROS also act as intracellular signaling molecules during osteoclastogenesis, and can thus also play an indirect role in bone destruction. Cells have several protective mechanisms to manage such oxidative stress, most of which involve production of cytoprotective enzymes that scavenge ROS. These enzymes are transcriptionally regulated via NRF2, Sirtuin, and FOXO. Some reports indicate an association between periodontitis and these cytoprotective enzymes' regulatory axes, with superoxide dismutase (SOD) the most extensively investigated. In this review article, we discuss the role of oxidative stress in the tissue destruction manifest in periodontitis, and the mechanisms that protect against this oxidative stress.

Indexed as

cytoprotective enzymesosteoclastoxidative stressperiodontitisROS

Identifiers

PMID28611683
PMCPMC5447763
OpenAlexW2617384658

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.