Evidence map›Paper›PMID 33085000›Full record

ReviewCurrent osteoporosis reports2020

When the Nervous System Turns Skeletal Muscles into Bones: How to Solve the Conundrum of Neurogenic Heterotopic Ossification.

Kylie A Alexander, Hsu-Wen Tseng, Marjorie Salga, François Genêt, Jean-Pierre Levesque

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current osteoporosis reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

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  4. Cytokine array analyses and osteogenic potential of plasma from patients with traumatic brain-/spinal cord injury: predictive markers of heterotopic ossification?European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026
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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

5 authors at 2 institutions in 2 countries.

Kylie A AlexanderMater Research Institute, The University of Queensland, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia.
Hsu-Wen TsengMater Research Institute, The University of Queensland, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia.
Marjorie SalgaDepartment of Physical Medicine and Rehabilitation, CIC 1429, Raymond Poincaré Hospital, APHP, Garches, France.
François GenêtDepartment of Physical Medicine and Rehabilitation, CIC 1429, Raymond Poincaré Hospital, APHP, Garches, France.
Jean-Pierre LevesqueMater Research Institute, The University of Queensland, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia. jean-pierre.levesque@mater.uq.edu.au.ORCID 0000-0002-7299-6025
Translational Research Institute · AUInserm · FR

Funding

National Health and Medical Research Council 1136130National Health and Medical Research Council 1181053
6 · The paper itself

Abstract

purpose of reviewNeurogenic heterotopic ossification (NHO) is the abnormal formation of extra-skeletal bones in periarticular muscles after damage to the central nervous system (CNS) such as spinal cord injury (SCI), traumatic brain injury (TBI), stroke, or cerebral anoxia. The purpose of this review is to summarize recent developments in the understanding of NHO pathophysiology and pathogenesis. Recent animal models of NHO and recent findings investigating the communication between CNS injury, tissue inflammation, and upcoming NHO therapeutics are discussed. RECENT

findingsAnimal models of NHO following TBI or SCI have shown that NHO requires the combined effects of a severe CNS injury and soft tissue damage, in particular muscular inflammation and the infiltration of macrophages into damaged muscles plays a key role. In the context of a CNS injury, the inflammatory response to soft tissue damage is exaggerated and persistent with excessive signaling via substance P-, oncostatin M-, and TGF-β1-mediated pathways. This review provides an overview of the known animal models and mechanisms of NHO and current therapeutic interventions for NHO patients. While some of the inflammatory mechanisms leading to NHO are common with other forms of traumatic and genetic heterotopic ossifications (HO), NHOs uniquely involve systemic changes in response to CNS injury. Future research into these CNS-mediated mechanisms is likely to reveal new targetable pathways to prevent NHO development in patients.

Indexed as

AnimalsCentral Nervous SystemDisease Models, AnimalHumansOssification, HeterotopicCentral nervous systemCytokinesInflammationMacrophagesNeurogenic heterotopic ossification

Identifiers

PMID33085000
OpenAlexW3093589188

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.