Evidence map›Paper›PMID 28987285›Full record

ReviewBone2018

Heterotopic ossification and the elucidation of pathologic differentiation.

David Cholok, Michael T Chung, Kavitha Ranganathan, Serra Ucer, Devaveena Day, Thomas A Davis, Yuji Mishina, Benjamin Levi

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Bone, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

43 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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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.

David CholokDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, USA.
Michael T ChungDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, USA.
Kavitha RanganathanDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, USA.
Serra UcerDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, USA.
Devaveena DayRegenerative Medicine Department, Naval Medical Research Center, Silver Spring, MD, USA.
Thomas A DavisRegenerative Medicine Department, Naval Medical Research Center, Silver Spring, MD, USA; Department of Surgery, Uniformed Services University of the Health Sciences & the Walter Reed National Military Medical Center, Bethesda, MD, USA.
Yuji MishinaSchool of Dentistry, University of Michigan, Ann Arbor, MI, USA.
Benjamin LeviDepartment of Surgery, University of Michigan Health System, Ann Arbor, MI, USA. Electronic address: blevi@med.umich.edu.

Funding

TRAINING PROGRAM IN ORGANOGENESIST32HD007505 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PASCA DI MAGLIANO, MARINA, SPENCE, JASON · 1997 to 2021
$6.9M
Molecular pathogenesis of craniosynostosis caused by enhanced BMP signalingR01DE020843 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MISHINA, YUJI · 2010 to 2019
$4.9M
Targeting Molecular and Cellular Mediators of Inflammation to Prevent Pathologic Cell Differentiation and Heterotopic OssificationR01AR071379 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI LEVI, BENJAMIN · 2017 to 2021
$1.5M
Developing New Diagnostic and Timed, TAK1 Specific Treatment Strategies for Trauma Induced Heterotopic OssificationR01GM123069 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI LEVI, BENJAMIN · 2017 to 2020
$1.2M
Novel Pathway and Prevention Strategy for Heterotopic OssificationK08GM109105 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LEVI, BENJAMIN · 2014 to 2017
$785k
NIAMS NIH HHS R01 AR071379NICHD NIH HHS T32 HD007505NIDCR NIH HHS R01 DE020843NIGMS NIH HHS K08 GM109105NIGMS NIH HHS R01 GM123069
6 · The paper itself

Abstract

Tissue regeneration following acute or persistent inflammation can manifest a spectrum of phenotypes ranging from the adaptive to the pathologic. Heterotopic Ossification (HO), the endochondral formation of bone within soft-tissue structures following severe injury serves as a prominent example of pathologic differentiation; and remains a persistent clinical issue incurring significant patient morbidity and expense to adequately diagnose and treat. The pathogenesis of HO provides an intriguing opportunity to better characterize the cellular and cell-signaling contributors to aberrant differentiation. Indeed, recent work has continued to resolve the unique cellular lineages, and causative pathways responsible for ectopic bone development yielding promising avenues for the development of novel therapeutic strategies shown to be successful in analogous animal models of HO development. This review details advances in the understanding of HO in the context of inciting inflammation, and explains how these advances inform the current standards of diagnosis and treatment.

Indexed as

AnimalsCell DifferentiationDisease Models, AnimalHumansInflammationModels, BiologicalOssification, HeterotopicWounds and InjuriesBone morphogenetic protein receptorsEctopic boneInflammation

Identifiers

PMID28987285
PMCPMC6585944

What OpenQuestion holds

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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.