Evidence map›Paper›PMID 32154622›Full record

ArticleCell proliferation2020

Parathyroid hormone ameliorates temporomandibular joint osteoarthritic-like changes related to age.

Chen Cui, Liwei Zheng, Yi Fan, Jun Zhang, Ruoshi Xu, Jing Xie, Xuedong Zhou

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  19. PTHrP promotes subchondral bone formation in TMJ-OA.International journal of oral science · 2022
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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

7 authors at 1 institution in 1 country.

Chen CuiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Sichuan, China.ORCID https://orcid.org/0000-0002-9972-7343
Liwei ZhengState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Yi FanState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Jun ZhangState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Ruoshi XuState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Jing XieState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Sichuan, China.ORCID https://orcid.org/0000-0001-8156-0322
Xuedong ZhouState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Sichuan University · CN

Funding

China Association for Science and Technology 2018QNRC001Department of Science and Technology of Sichuan Province 2016JQ0054National Natural Science Foundation of China 81771033National Natural Science Foundation of China 81800928
6 · The paper itself

Abstract

objectivesAgeing could be a contributing factor to the progression of temporomandibular joint osteoarthritis (TMJ OA), whereas its pathogenesis and potential therapeutic strategy have not been comprehensively investigated. MATERIALS AND

methodsWe generated ageing mouse models (45-week and 60-week; 12-week mice as control) and intermittently injected 45-week mice with parathyroid hormone (PTH(1-34)) or vehicle for 4 weeks. Cartilage and subchondral bone of TMJ were analysed by microCT, histological and immunostaining. Western blot, qRT-PCR, ChIP, ELISA and immunohistochemical analysis were utilized to examination the mechanism of PTH(1-34)'s function.

resultsWe showed apparent OA-like phenotypes in ageing mice. PTH treatment could ameliorate the degenerative changes and improve bone microarchitecture in the subchondral bone by activating bone remodelling. Moreover, PTH inhibited phosphorylation level of Smad3, which can combine with p16

conclusionsIn summary, PTH may reduce the accumulation of senescent cells in subchondral bone by inhibiting p16

Indexed as

AgingAnimalsCalcium-Regulating Hormones and AgentsCells, CulturedDisease Models, AnimalMaleMiceMice, Inbred C57BLOsteoarthritisOsteogenesisParathyroid HormoneTemporomandibular JointCalcium-Regulating Hormones and AgentsParathyroid Hormonecellular senescencecyclin-dependent kinase inhibitor P16INK4Amarrow mesenchymal stem cellsosteoarthritistemporomandibular joint disorders

Identifiers

PMID32154622
PMCPMC7162802
OpenAlexW3011156830

What OpenQuestion holds

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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.