Evidence map›Paper›PMID 34363103›Full record

ArticleClinical oral investigations2022

Mechanisms of sphingosine-1-phosphate (S1P) signaling on excessive stress-induced root resorption during orthodontic molar intrusion.

Han Wang, Tiancheng Li, Xin Wang, Yuzhe Guan, Yukun Jiang, Shuo Chen, Shujuan Zou, Peipei Duan

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical oral investigations, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. RANKLInternational journal of oral science · 2023
    Article
  10. Article
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 at 2 institutions in 1 country.

Han WangState Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China School & Hospital of Stomatology, Sichuan University, No. 14, 3rd section of Renmin South Road, Chengdu, 610041, China.
Tiancheng LiState Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China School & Hospital of Stomatology, Sichuan University, No. 14, 3rd section of Renmin South Road, Chengdu, 610041, China.
Xin WangOral Diagnosis and Treatment Center, Aviation General Hospital, China Medical University, Beijing, China.
Yuzhe GuanState Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China School & Hospital of Stomatology, Sichuan University, No. 14, 3rd section of Renmin South Road, Chengdu, 610041, China.
Yukun JiangState Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China School & Hospital of Stomatology, Sichuan University, No. 14, 3rd section of Renmin South Road, Chengdu, 610041, China.
Shuo ChenState Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China School & Hospital of Stomatology, Sichuan University, No. 14, 3rd section of Renmin South Road, Chengdu, 610041, China.
Shujuan ZouState Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China School & Hospital of Stomatology, Sichuan University, No. 14, 3rd section of Renmin South Road, Chengdu, 610041, China.
Peipei DuanState Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China School & Hospital of Stomatology, Sichuan University, No. 14, 3rd section of Renmin South Road, Chengdu, 610041, China. duanp@scu.edu.cn.ORCID http://orcid.org/0000-0003-4111-8112
Sichuan University · CNAviation General Hospital · CN

Funding

Department of Science and Technology of Sichuan Province 2018JY0139National Natural Science Foundation of China 81701005
6 · The paper itself

Abstract

objectivesThe aim of this study was to investigate cementocyte mechanotransduction during excessive orthodontic intrusive force-induced root resorption and the role of S1P signaling in this process. MATERIALS AND

methodsFifty-four 12-week-old male Wistar rats were randomly divided into 3 groups: control group (Control), intrusive stress application group (Stress), and intrusive stress together with S1PR2-specific antagonist injection group (Stress + JTE). A rat molar intrusion model was established on animals in the Stress and the Stress + JTE groups. The animals in the Stress + JTE group received daily intraperitoneal (i.p.) injection of S1PR2 antagonist JTE-013, while the Control and Stress groups received only the vehicle. Histomorphometric, immunohistochemical, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analyses were performed after euthanizing of the rats.

resultsRoot resorption was promoted in the Stress group with increased volumes of resorption pits and amounts of molar intrusion compared with the Control group. The expression levels of cementogenic- and cementoclastic-related factors were affected under excessive intrusive force. Immunohistochemical staining and qRT-PCR analysis showed promoted S1P signaling activities during molar intrusion. Western blot analysis indicated decreased nuclear translocation of β-catenin under excessive intrusive force. Through the administration of JTE-013, S1P signaling activity was suppressed and excessive intrusive force-induced root resorption was reversed. The regulation of S1P signaling could also influence the nuclear translocation of β-catenin and the expressions of cementogenic- and cementoclastic-related factors.

conclusionsRoot resorption was promoted under excessive orthodontic intrusive force due to the disruption of cementum homeostasis. S1P signaling pathway might play an important role in cementocyte mechanotransduction in this process. CLINICAL RELEVANCE: The S1P signaling might be a promising therapeutic target for novel therapeutic approaches to prevent external root resorption caused by excessive orthodontic intrusive force.

Indexed as

Root ResorptionAnimalsLysophospholipidsMaleMechanotransduction, CellularMolarRatsRats, WistarSignal TransductionSphingosineTooth Movement TechniquesLysophospholipidsSphingosinesphingosine 1-phosphateCementocyteCementum homeostasisMechanotransductionOrthodontic molar intrusionS1P signaling

Identifiers

PMID34363103
OpenAlexW3192140538

What Socratic holds

Textmetadata
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 Socratic graph.