Evidence map›Paper›PMID 33101657›Full record

ArticleBone & joint research2020

Parathyroid hormone (1-34) ameliorates cartilage degeneration and subchondral bone deterioration in collagenase-induced osteoarthritis model in mice.

Li-Tao Shao, Yu Gou, Jia-Kang Fang, Yun-Peng Hu, Qiang-Qiang Lian, Yu-Ying Zhang, Yu-Dan Wang, Fa-Ming Tian, Liu Zhang

Open access · goldAbstract read
In one paragraph

Article in Bone & joint research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  13. Latest insights in disease-modifying osteoarthritis drugs development.Therapeutic advances in musculoskeletal disease · 2023
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  20. Diabetes - osteoarthritis and joint pain.Bone & joint research · 2021
    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

9 authors at 3 institutions in 1 country.

Li-Tao ShaoDepartment of Orthopedic Surgery, Hebei Medical University, Shijiazhuang, China.ORCID 0000-0002-1123-166X
Yu GouDepartment of Orthopaedic Surgery, Tianjin Hospital, Tianjin University, Tianjin, China.
Jia-Kang FangMedical Research Center, Hebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, China.
Yun-Peng HuMedical Research Center, Hebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, China.
Qiang-Qiang LianMedical Research Center, Hebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, China.
Yu-Ying ZhangMedical Research Center, Hebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, China.
Yu-Dan WangMedical Research Center, Hebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, China.
Fa-Ming TianMedical Research Center, Hebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, China.
Liu ZhangDepartment of Orthopedic Surgery, Hebei Medical University, Shijiazhuang, China.
North China University of Science and Technology · CNHebei Medical University · CNTianjin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsParathyroid hormone (PTH) (1-34) exhibits potential in preventing degeneration in both cartilage and subchondral bone in osteoarthritis (OA) development. We assessed the effects of PTH (1-34) at different concentrations on bone and cartilage metabolism in a collagenase-induced mouse model of OA and examined whether PTH (1-34) affects the JAK2/STAT3 signalling pathway in this process.

methodsCollagenase-induced OA was established in C57Bl/6 mice. Therapy with PTH (1-34) (10 μg/kg/day or 40 μg/kg/day) was initiated immediately after surgery and continued for six weeks. Cartilage pathology was evaluated by gross visual, histology, and immunohistochemical assessments. Cell apoptosis was analyzed by TUNEL staining. Microcomputed tomography (micro-CT) was used to evaluate the bone mass and the microarchitecture in subchondral bone.

resultsEnhanced matrix catabolism, increased apoptosis of chondrocytes in cartilage, and overexpressed JAK2/STAT3 and p-JAK2/p-STAT3 were observed in cartilage in this model. All of these changes were prevented by PTH (1-34) treatment, with no significant difference between the low-dose and high-dose groups. Micro-CT analysis indicated that bone mineral density (BMD), bone volume/trabecular volume (BV/TV), and trabecular thickness (Tb.Th) levels were significantly lower in the OA group than those in the Sham, PTH 10 μg, and PTH 40 μg groups, but these parameters were significantly higher in the PTH 40 μg group than in the PTH 10 μg group.

conclusionIntermittent administration of PTH (1-34) exhibits protective effects on both cartilage and subchondral bone in a dose-dependent manner on the latter in a collagenase-induced OA mouse model, which may be involved in regulating the JAK2/STAT3 signalling pathway.Cite this article:

Indexed as

CartilageOsteoarthritis

Identifiers

PMID33101657
PMCPMC7563035
OpenAlexW3094070548

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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 OpenQuestion graph.