Evidence map›Paper›PMID 24796520›Full record

ReviewHistology and histopathology2014

Molecular and cellular mechanisms of heterotopic ossification.

Diana M Ramirez, Melissa R Ramirez, Anthony M Reginato, Damian Medici

Abstract readReview
In one paragraph

Review in Histology and histopathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
5.9field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
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  18. Mkx-Deficient Mice Exhibit Hedgehog Signaling-Dependent Ectopic Ossification in the Achilles Tendons.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
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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

4 authors at 1 institution in 1 country.

Diana M RamirezDepartment of Orthopaedics, Warren Alpert Medical School of Brown University, and Cardiovascular Research Center, Rhode Island Hospital, Providence, RI, USA.
Melissa R RamirezDepartment of Orthopaedics, and Division of Rheumatology, Department of Medicine, Warren Alpert Medical School of Brown University, Providence, RI, USA.
Anthony M ReginatoDivision of Rheumatology, Department of Medicine, Warren Alpert Medical School of Brown University, Providence, RI, USA.
Damian MediciDepartment of Orthopaedics, Warren Alpert Medical School of Brown University, and Cardiovascular Research Center, Rhode Island Hospital, Providence, RI, USA. damian_medici@brown.edu.
Brown University · US

Funding

COBRE for Skeletal Health and RepairP20GM104937 · NIGMS · RHODE ISLAND HOSPITAL · PI CHEN, QIAN · 2012 to 2016
$10.8M
Endothelial Plasticity in Human DiseaseR01HL112860 · NHLBI · RHODE ISLAND HOSPITAL · PI LIANG, OLIN D. · 2012 to 2017
$2.0M
NHLBI NIH HHS R01 HL112860NHLBI NIH HHS R01HL112860NIGMS NIH HHS P20 GM104937NIGMS NIH HHS P20GM104937
6 · The paper itself

Abstract

Heterotopic ossification (HO) is a debilitating condition in which cartilage and bone forms in soft tissues such as muscle, tendon, and ligament causing immobility. This process is induced by inflammation associated with traumatic injury. In an extremely rare genetic disorder called fibrodysplasia ossificans progessiva (FOP), a combination of inflammation associated with minor soft tissue injuries and a hereditary genetic mutation causes massive HO that progressively worsens throughout the patients' lifetime leading to the formation of an ectopic skeleton. An activating mutation in the BMP type I receptor ALK2 has been shown to contribute to the heterotopic lesions in FOP patients, yet recent studies have shown that other events are required to stimulate HO including activation of sensory neurons, mast cell degranulation, lymphocyte infiltration, skeletal myocyte cell death, and endothelial-mesenchymal transition (EndMT). In this review, we discuss the recent evidence and mechanistic data that describe the cellular and molecular mechanisms that give rise to heterotopic bone.

Indexed as

AnimalsHumansOssification, Heterotopic

Identifiers

PMID24796520
PMCPMC4372050
OpenAlexW136290339

What OpenQuestion holds

Textmetadata
LicenceTDM
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.