Evidence map›Paper›PMID 28327602›Full record

ArticleScientific reports2017

Glucocorticoid suppression of osteocyte perilacunar remodeling is associated with subchondral bone degeneration in osteonecrosis.

Tristan W Fowler, Claire Acevedo, Courtney M Mazur, Faith Hall-Glenn, Aaron J Fields, Hrishikesh A Bale, Robert O Ritchie, Jeffrey C Lotz, Thomas P Vail, Tamara Alliston

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Article
  5. Regional and Sexual Dimorphism in Murine Skeletal Responses to Osteocytic HIF Pathway Modulation.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026
    Article
  6. Review
  7. Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. SP7: from Bone Development to Skeletal Disease.Current osteoporosis reports · 2023
    Review
  20. Healthy and Osteoarthritis-Affected Joints Facing the Cellular Crosstalk.International journal of molecular sciences · 2023
    Review

2 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Tristan W FowlerDepartment of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA.
Claire AcevedoDepartment of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA.
Courtney M MazurDepartment of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA.
Faith Hall-GlennDepartment of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA.
Aaron J FieldsDepartment of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA.
Hrishikesh A BaleMaterials Science Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.
Robert O RitchieMaterials Science Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.
Jeffrey C LotzDepartment of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA.
Thomas P VailDepartment of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA.
Tamara AllistonDepartment of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA.
University of California, San Francisco · USLawrence Berkeley National Laboratory · USUniversity of California, Berkeley · US

Funding

UCSF/UCB Joint Graduate Group in BIoengineeringT32GM008155 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DESAI, TEJAL A. · 1985 to 2020
$12.2M
The mechanistic control of bone quality and joint crosstalk by osteocytesR01DE019284 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HERNANDEZ, CHRISTOPHER JOHN · 2009 to 2024
$7.6M
UCSF Core Center for Musculoskeletal Biology and MedicineP30AR066262 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOTZ, JEFFREY C. · 2014 to 2018
$3.0M
ROLE OF OSTEOCYTE TbetaRII IN PERILACUNAR REMODELING AND BONE METASTASESF32CA203402 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FOWLER, TRISTAN WILLIAM · 2016 to 2016
$16k
NCI NIH HHS F32 CA203402NIAMS NIH HHS P30 AR066262NIDCR NIH HHS R01 DE019284NIGMS NIH HHS T32 GM008155
6 · The paper itself

Abstract

Through a process called perilacunar remodeling, bone-embedded osteocytes dynamically resorb and replace the surrounding perilacunar bone matrix to maintain mineral homeostasis. The vital canalicular networks required for osteocyte nourishment and communication, as well as the exquisitely organized bone extracellular matrix, also depend upon perilacunar remodeling. Nonetheless, many questions remain about the regulation of perilacunar remodeling and its role in skeletal disease. Here, we find that suppression of osteocyte-driven perilacunar remodeling, a fundamental cellular mechanism, plays a critical role in the glucocorticoid-induced osteonecrosis. In glucocorticoid-treated mice, we find that glucocorticoids coordinately suppress expression of several proteases required for perilacunar remodeling while causing degeneration of the osteocyte lacunocanalicular network, collagen disorganization, and matrix hypermineralization; all of which are apparent in human osteonecrotic lesions. Thus, osteocyte-mediated perilacunar remodeling maintains bone homeostasis, is dysregulated in skeletal disease, and may represent an attractive therapeutic target for the treatment of osteonecrosis.

Indexed as

AnimalsBone MatrixBone RemodelingCathepsin KDelayed-Action PreparationsGene Expression RegulationGlucocorticoidsHumansMaleMatrix Metalloproteinase 13Matrix Metalloproteinase 14Matrix Metalloproteinase 2MiceOsteocytesOsteonecrosisOsteoprotegerinACP5 protein, humanCathepsin KCTSK protein, humanDelayed-Action PreparationsGlucocorticoidsMatrix Metalloproteinase 13Matrix Metalloproteinase 14Matrix Metalloproteinase 2MMP13 protein, humanMMP14 protein, humanMMP2 protein, humanOsteoprotegerinPrednisoloneRANK LigandTartrate-Resistant Acid PhosphataseTNFSF11 protein, humanTranscription FactorsTSC22D3 protein, human

Identifiers

PMID28327602
PMCPMC5361115
OpenAlexW2598649675

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.