Evidence map›Paper›PMID 31463433›Full record

ArticleJOR spine2018

Autologous chondrocyte grafting promotes bone formation in the posterolateral spine.

J Alex Sielatycki, Masanori Saito, Masato Yuasa, Stephanie N Moore-Lotridge, Sasidhar Uppuganti, Juan M Colazo, Alexander A Hysong, J Patton Robinette, Atsushi Okawa, Toshitaka Yoshii and 3 more

Open access · goldAbstract read
In one paragraph

Article in JOR spine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Revision strategies for failed adult spinal deformity surgery.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
    Article
  4. Article
  5. Review
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

13 authors at 3 institutions in 2 countries.

J Alex SielatyckiDepartment of Orthopaedics and Rehabilitation Vanderbilt University Medical Center Nashville Tennessee.
Masanori SaitoDepartment of Orthopaedics and Rehabilitation Vanderbilt University Medical Center Nashville Tennessee.
Masato YuasaDepartment of Orthopaedics and Rehabilitation Vanderbilt University Medical Center Nashville Tennessee.
Stephanie N Moore-LotridgeDepartment of Orthopaedics and Rehabilitation Vanderbilt University Medical Center Nashville Tennessee.ORCID 0000-0002-3045-4199
Sasidhar UppugantiDepartment of Orthopaedics and Rehabilitation Vanderbilt University Medical Center Nashville Tennessee.
Juan M ColazoVanderbilt University School of Medicine Nashville Tennessee.
Alexander A HysongVanderbilt University School of Medicine Nashville Tennessee.
J Patton RobinetteVanderbilt University School of Medicine Nashville Tennessee.
Atsushi OkawaDepartment of Orthopaedic Surgery Tokyo Medical and Dental University Tokyo Japan.
Toshitaka YoshiiDepartment of Orthopaedic Surgery Tokyo Medical and Dental University Tokyo Japan.
Herbert S SchwartzDepartment of Orthopaedics and Rehabilitation Vanderbilt University Medical Center Nashville Tennessee.
Jeffry S NymanDepartment of Orthopaedics and Rehabilitation Vanderbilt University Medical Center Nashville Tennessee.ORCID 0000-0001-7403-7605
Jonathan G SchoeneckerDepartment of Orthopaedics and Rehabilitation Vanderbilt University Medical Center Nashville Tennessee.ORCID 0000-0002-3097-5496
Vanderbilt University · USTokyo Medical and Dental University · JPVanderbilt University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background contextPseudarthrosis following spinal fusion remains problematic despite modern surgical and grafting techniques. In surgical spinal fusion, new bone forms via intramembranous and endochondral ossification, with endochondral ossification occurring in the hypoxic zones of the fusion bed. During bone development and fracture healing, the key cellular mediator of endochondral ossification is the hypertrophic chondrocyte given its ability to function in hypoxia and induce neovascularization and ossification. We therefore hypothesize that hypertrophic chondrocytes may be an effective bone graft alternative. PURPOSE: Spinal fusion procedures have increased substantially; yet 5% to 35% of all spinal fusions may result in pseudoarthrosis. Pseudoarthrosis may occur because of implant failure, infection, or biological failure, among other reasons. Advances in surgical techniques and bone grafting have improved fusion; however pseudarthrosis rates remain unacceptably high. Thus, the goal of this study is to investigate hypertrophic chondrocytes as a potential biological graft alternative.

methodsUsing a validated murine fracture model, hypertrophic chondrocytes were harvested from fracture calluses and transplanted into the posterolateral spines of identical mice. New bone formation was assessed by X-ray, microcomputed tomography (μCT), and

resultsRadiography, μCT, and

conclusionsThis proof-of-concept study indicates that hypertrophic chondrocytes can promote bone formation comparable to iliac crest bone graft. These findings provide the foundation for future studies to investigate the potential therapeutic use of hypertrophic chondrocytes in spinal fusion.

Indexed as

bone formationbone‐morphogenic proteinfracture callushypertrophic chondrocytesiliac crest bone graftossificationposterolateral spinal fusionvascular endothelia growth factor

Identifiers

PMID31463433
PMCPMC6686810
OpenAlexW2794370084

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.