Evidence map›Paper›PMID 29409971›Full record

ReviewBone2018

Stem cells and heterotopic ossification: Lessons from animal models.

John B Lees-Shepard, David J Goldhamer

Abstract readReview
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 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Identification of a Tenochondral Ossification Sequence Producing Heterotopic Ossification in Human Achilles Tendinopathy.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026
    Article
  6. Gut microbiome-dependent IL-1 signaling is a mediator of ACVR1bioRxiv : the preprint server for biology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Myelin protein zero (Genes & diseases · 2023
    Article
  14. Review
  15. Overexpression of Wild-Type ACVR1 in Fibrodysplasia Ossificans Progressiva Mice Rescues Perinatal Lethality and Inhibits Heterotopic Ossification.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

John B Lees-ShepardDepartment of Molecular & Cell Biology, University of Connecticut Stem Cell Institute, University of Connecticut, Storrs, CT 06269, United States.
David J GoldhamerDepartment of Molecular & Cell Biology, University of Connecticut Stem Cell Institute, University of Connecticut, Storrs, CT 06269, United States. Electronic address: david.goldhamer@uconn.edu.
University of Connecticut · US

Funding

Function of Fibro-Adipogenic Progenitors in Heterotopic Ossification of Skeletal MuscleR01AR072052 · NIAMS · UNIVERSITY OF CONNECTICUT STORRS · PI GOLDHAMER, DAVID J · 2017 to 2021
$1.7M
The Cellular Basis of Heterotopic OssificationR01AR057371 · NIAMS · UNIVERSITY OF CONNECTICUT STORRS · PI GOLDHAMER, DAVID J · 2010 to 2014
$1.6M
NIAMS NIH HHS R01 AR057371NIAMS NIH HHS R01 AR072052
6 · The paper itself

Abstract

Put most simply, heterotopic ossification (HO) is the abnormal formation of bone at extraskeletal sites. HO can be classified into two main subtypes, genetic and acquired. Acquired HO is a common complication of major connective tissue injury, traumatic central nervous system injury, and surgical interventions, where it can cause significant pain and postoperative disability. A particularly devastating form of HO is manifested in the rare genetic disorder, fibrodysplasia ossificans progressiva (FOP), in which progressive heterotopic bone formation occurs throughout life, resulting in painful and disabling cumulative immobility. While the central role of stem/progenitor cell populations in HO is firmly established, the identity of the offending cell type(s) remains to be conclusively determined, and little is known of the mechanisms that direct these progenitor cells to initiate cartilage and bone formation. In this review, we summarize current knowledge of the cells responsible for acquired HO and FOP, highlighting the strengths and weaknesses of animal models used to interrogate the cellular origins of HO.

Indexed as

AnimalsDisease Models, AnimalHumansOssification, HeterotopicStem CellsActivinACVR1ALK2Animal modelsBMPEndotheliumFAPsFibro/adipogenic progenitorsFibrodysplasia ossificans progressivaFOPHeterotopic ossificationMx1PDGFRαProgenitor cellsSatellite cellScleraxisSkeletal muscleStem cellsTendonTIE2

Identifiers

PMID29409971
PMCPMC5866227
OpenAlexW2790724263

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.