Evidence map›Paper›PMID 27335224›Full record

ArticleJournal of the Royal Society, Interface2016

Thermally induced osteocyte damage initiates pro-osteoclastogenic gene expression in vivo.

Eimear B Dolan, David Tallon, Wing-Yee Cheung, Mitchell B Schaffler, Oran D Kennedy, Laoise M McNamara

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the Royal Society, Interface, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 31% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Osteolysis after cervical disc arthroplasty.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2020
    Pooled it
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

6 authors at 4 institutions in 2 countries.

Eimear B DolanBiomechanics Research Centre (BMEC), Biomedical Engineering, College of Engineering and Informatics, National University of Ireland, Galway, Republic of Ireland.
David TallonStryker Instruments, Cork, Republic of Ireland.
Wing-Yee CheungDepartment of Biomedical Engineering, The City College of New York, New York, NY, USA.
Mitchell B SchafflerDepartment of Biomedical Engineering, The City College of New York, New York, NY, USA.
Oran D KennedyDepartment of Orthopaedics, New York University School of Medicine, New York, NY, USA.
Laoise M McNamaraBiomechanics Research Centre (BMEC), Biomedical Engineering, College of Engineering and Informatics, National University of Ireland, Galway, Republic of Ireland laoise.mcnamara@nuigalway.ie.
City College of New York · USOllscoil na Gaillimhe – University of Galway · IENew York University · USStryker (Ireland) · IE

Funding

Osteocyte Integrity and Bone RemodelingR01AR041210 · NIAMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI SCHAFFLER, MITCHELL B · 1997 to 2019
$5.8M
NIAMS NIH HHS L30 AR051739NIAMS NIH HHS R01 AR041210
6 · The paper itself

Abstract

Bone is often subject to harsh temperatures during orthopaedic procedures resulting in thermally induced bone damage, which may affect the healing response. Postsurgical healing of bone is essential to the success of surgery, therefore, an understanding of the thermally induced responses of bone cells to clinically relevant temperatures in vivo is required. Osteocytes have been shown to be integrally involved in the bone remodelling cascade, via apoptosis, in micro-damage systems. However, it is unknown whether this relationship is similar following thermal damage. Sprague-Dawley rat tibia were exposed to clinically relevant temperatures (47°C or 60°C) to investigate the role of osteocytes in modulating remodelling related factors. Immunohistochemistry was used to quantify osteocyte thermal damage (activated caspase-3). Thermally induced pro-osteoclastogenic genes (Rankl, Opg and M-csf), in addition to genes known to mediate osteoblast and osteoclast differentiation via prostaglandin production (Cox2), vascularization (Vegf) and inflammatory (Il1a) responses, were investigated using gene expression analysis. The results demonstrate that heat-treatment induced significant bone tissue and cellular damage. Pro-osteoclastogenic genes were upregulated depending on the amount of temperature elevation compared with the control. Taken together, the results of this study demonstrate the in vivo effect of thermally induced osteocyte damage on the gene expression profile.

Indexed as

Gene Expression RegulationHot TemperatureAnimalsBone RemodelingCaspase 3Cyclooxygenase 2Interleukin-1alphaMacrophage Colony-Stimulating FactorOsteocytesOsteoprotegerinRANK LigandRatsRats, Sprague-DawleyTibiaVascular Endothelial Growth Factor ACasp3 protein, ratCaspase 3Cyclooxygenase 2Interleukin-1alphaMacrophage Colony-Stimulating FactorOsteoprotegerinPtgs2 protein, ratRANK LigandTnfrsf11b protein, ratVascular Endothelial Growth Factor Avascular endothelial growth factor A, ratapoptosisosteocyteremodellingthermal damage

Identifiers

PMID27335224
PMCPMC4938095
OpenAlexW2469113988

What OpenQuestion 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 OpenQuestion graph.