Evidence map›Paper›PMID 36078169›Full record

ArticleCells2022

Inhibition of PGE2 in Subchondral Bone Attenuates Osteoarthritis.

Qi Sun, Yuanzhen Zhang, Yilan Ding, Wenqing Xie, Hengzhen Li, Shaohua Li, Yusheng Li, Ming Cai

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  4. Macrophage Derived TGF-β Recruits BMSCs for Initiation of Bone Formation During Fracture Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  11. [Pathology of Cartilage-to-Bone Crosstalk: A New Angle for Animal Experimental Studies on Osteoarthritis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
    Review
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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

8 authors at 4 institutions in 1 country.

Qi SunDepartment of Orthopaedics, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.
Yuanzhen ZhangDepartment of Orthopaedics, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.
Yilan DingDepartment of Orthopedics, Xiangya Hospital, Central South University, Changsha 410008, China.
Wenqing XieDepartment of Orthopedics, Xiangya Hospital, Central South University, Changsha 410008, China.
Hengzhen LiDepartment of Orthopedics, Xiangya Hospital, Central South University, Changsha 410008, China.
Shaohua LiDepartment of Orthopaedics, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.
Yusheng LiDepartment of Orthopedics, Xiangya Hospital, Central South University, Changsha 410008, China.
Ming CaiDepartment of Orthopaedics, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.
Xiangya Hospital Central South University · CNShanghai Tenth People's Hospital · CNTongji University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant subchondral bone architecture is a crucial driver of the pathological progression of osteoarthritis, coupled with increased sensory innervation. The sensory PGE2/EP4 pathway is involved in the regulation of bone mass accrual by the induction of differentiation of mesenchymal stromal cells. This study aimed to clarify whether the sensory PGE2/EP4 pathway induces aberrant structural alteration of subchondral bone in osteoarthritis. Destabilization of the medial meniscus (DMM) using a mouse model was combined with three approaches: the treatment of celecoxib, capsaicin, and sensory nerve-specific prostaglandin E2 receptor 4 (EP4)-knockout mice. Cartilage degeneration, subchondral bone architecture, PGE2 levels, distribution of sensory nerves, the number of osteoprogenitors, and pain-related behavior in DMM mice were assessed. Serum and tissue PGE2 levels and subchondral bone architecture in a human sample were measured. Increased PGE2 is closely related to subchondral bone's abnormal microstructure in humans and mice. Elevated PGE2 concentration in subchondral bone that is mainly derived from osteoblasts occurs in early-stage osteoarthritis, preceding articular cartilage degeneration in mice. The decreased PGE2 levels by the celecoxib or sensory denervation by capsaicin attenuate the aberrant alteration of subchondral bone architecture, joint degeneration, and pain. Selective EP4 receptor knockout of the sensory nerve attenuates the aberrant formation of subchondral bone and facilitates the prevention of cartilage degeneration in DMM mice. Excessive PGE2 in subchondral bone caused a pathological alteration to subchondral bone in osteoarthritis and maintaining the physiological level of PGE2 could potentially be used as an osteoarthritis treatment.

Indexed as

Cartilage, ArticularOsteoarthritisAnimalsCapsaicinCelecoxibDinoprostoneHumansMiceMice, KnockoutPainCapsaicinCelecoxibDinoprostonebone remodelingCOX2osteoarthritisPGE2sensory nervesubchondral bone

Identifiers

PMID36078169
PMCPMC9454853
OpenAlexW4294693494

What OpenQuestion holds

Textmetadata
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.