Evidence map›Paper›PMID 36161341›Full record

ReviewSkeletal radiology2023

Structural phenotypes of knee osteoarthritis: potential clinical and research relevance.

Frank W Roemer, Mohamed Jarraya, Jamie E Collins, C Kent Kwoh, Daichi Hayashi, David J Hunter, Ali Guermazi

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Skeletal radiology, 2023. 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
–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

41 citing papers in PubMed.

  1. Trial
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  6. Observational
  7. Review
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  10. Review
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  12. Advances in cartilage imaging techniques.Nature reviews. Rheumatology · 2026
    Review
  13. Article
  14. Article
  15. Article
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  18. Article
  19. Observational
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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

7 authors.

Frank W RoemerQuantitative Imaging Center, Department of Radiology, Boston University School of Medicine, 820 Harrison Avenue, FGH Building, 4th floor, Boston, MA, 02118, USA. froemer@bu.edu.ORCID http://orcid.org/0000-0001-9238-7350
Mohamed JarrayaDepartment of Radiology, Massachusetts General Hospital, Harvard University, 55 Fruit St, Boston, MA, 02114, USA.
Jamie E CollinsOrthopaedics and Arthritis Center of Outcomes Research, Brigham and Women's Hospital, Harvard Medical, School, 75 Francis Street, BTM Suite 5016, Boston, MA, 02115, USA.
C Kent KwohUniversity of Arizona Arthritis Center, The University of Arizona College of Medicine, 1501 N. Campbell Avenue, Suite, Tucson, AZ, 8303, USA.
Daichi HayashiDepartment of Radiology, Stony Brook University Renaissance School of Medicine, State University of New York, 101 Nicolls Rd, HSc Level 4, Room 120, Stony Brook, NY, 11794-8460, USA.
David J HunterDepartment of Rheumatology, Royal North Shore Hospital and Institute of Bone and Joint Research, Kolling Institute, University of Sydney, Reserve Rd, St. Leonards, 2065, NSW, Australia.
Ali GuermaziQuantitative Imaging Center, Department of Radiology, Boston University School of Medicine, 820 Harrison Avenue, FGH Building, 4th floor, Boston, MA, 02118, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A joint contains many different tissues that can exhibit pathological changes, providing many potential targets for treatment. Researchers are increasingly suggesting that osteoarthritis (OA) comprises several phenotypes or subpopulations. Consequently, a treatment for OA that targets only one pathophysiologic abnormality is unlikely to be similarly efficacious in preventing or delaying the progression of all the different phenotypes of structural OA. Five structural phenotypes have been proposed, namely the inflammatory, meniscus-cartilage, subchondral bone, and atrophic and hypertrophic phenotypes. The inflammatory phenotype is characterized by marked synovitis and/or joint effusion, while the meniscus-cartilage phenotype exhibits severe meniscal and cartilage damage. Large bone marrow lesions characterize the subchondral bone phenotype. The hypertrophic and atrophic OA phenotype are defined based on the presence large osteophytes or absence of any osteophytes, respectively, in the presence of concomitant cartilage damage. Limitations of the concept of structural phenotyping are that they are not mutually exclusive and that more than one phenotype may be present. It must be acknowledged that a wide range of views exist on how best to operationalize the concept of structural OA phenotypes and that the concept of structural phenotypic characterization is still in its infancy. Structural phenotypic stratification, however, may result in more targeted trial populations with successful outcomes and practitioners need to be aware of the heterogeneity of the disease to personalize their treatment recommendations for an individual patient. Radiologists should be able to define a joint at risk for progression based on the predominant phenotype present at different disease stages.

Indexed as

Bone DiseasesCartilage, ArticularCartilage DiseasesOsteoarthritis, KneeOsteophyteHumansHypertrophyKnee JointMagnetic Resonance ImagingPhenotypeClinical trialMRIOsteoarthritisPhenotypesStructure

Identifiers

PMID36161341
PMCPMC10509066

What OpenQuestion holds

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Registered trials

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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.