Evidence map›Paper›PMID 41763351›Full record

ArticleOsteoarthritis and cartilage2026

Potential role of bile acids as a microbiome-derived mechanism in synovitis of knee osteoarthritis synovitis.

Jessica D Murillo-Saich, Helena Mannochio-Russo, Marta Sala-Climent, Nathan Argel, Anna Quan, Michal Kalli Hose, Rocio Paz-Gonzalez, Meghana Akkati, Eric Chang, Adnan Cutuk and 5 more

Abstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

15 authors.

Jessica D Murillo-SaichDepartment of Medicine, University of California San Diego, San Diego, CA 92093, USA. Electronic address: jdmurillosaich@health.ucsd.edu.
Helena Mannochio-RussoCollaborative Mass Spectrometry Innovation Center, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, San Diego, CA, USA. Electronic address: hmannochiorusso@health.ucsd.edu.
Marta Sala-ClimentDepartment of Medicine, University of California San Diego, San Diego, CA 92093, USA. Electronic address: msalacliment@health.ucsd.edu.
Nathan ArgelDepartment of Medicine, University of California San Diego, San Diego, CA 92093, USA. Electronic address: nargel@ucsd.edu.
Anna QuanVA San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: anna.quan@va.gov.
Michal Kalli HoseVA San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: michalkalli.hose@va.gov.
Rocio Paz-GonzalezDepartment of Medicine, University of California San Diego, San Diego, CA 92093, USA; Grupo de Investigación de Reumatología (GIR), INIBIC-Hospital Universitario A Coruña, SERGAS, A Coruña, Spain. Electronic address: rpazgonzalez@health.ucsd.edu.
Meghana AkkatiDepartment of Medicine, University of California San Diego, San Diego, CA 92093, USA. Electronic address: makkati@ucsd.edu.
Eric ChangVA San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: e8chang@health.ucsd.edu.
Adnan CutukVA San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: Adnan.Cutuk@va.gov.
Emily GentryCollaborative Mass Spectrometry Innovation Center, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, San Diego, CA, USA; Department of Chemistry, Virginia Tech, Blacksburg, VA 24061, USA. Electronic address: egentry@vt.edu.
Roxana CorasDepartment of Medicine, University of California San Diego, San Diego, CA 92093, USA. Electronic address: roxana.juverdeanu@gmail.com.
Nancy E LaneDepartment of Medicine, U.C. Davis Health, Sacramento, CA 95817, USA. Electronic address: nelane@ucdavis.edu.
Pieter C DorresteinCollaborative Mass Spectrometry Innovation Center, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, San Diego, CA, USA. Electronic address: pdorrestein@health.ucsd.edu.
Monica GumaDepartment of Medicine, University of California San Diego, San Diego, CA 92093, USA; VA San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: mguma@health.ucsd.edu.

Funding

Rheumatic Diseases Research Training GrantT32AR064194 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GARY S FIRESTEIN, Monica Guma · 2013 to 2026
$3.8M
Obesity-Induced Inflammatory Mediators Predict Lack of Response in Patients with Rheumatoid Arthritis Starting Biological TherapiesR01AR083584 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Monica Guma · 2024 to 2026
$1.4M
Can circulating bile acids predict knee OA progression?R21AR082029 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUMA, MONICA, LANE, NANCY E · 2023 to 2024
$378k
NIAMS NIH HHS R01 AR083584NIAMS NIH HHS R21 AR082029NIAMS NIH HHS T32 AR064194
6 · The paper itself

Abstract

objectiveTo evaluate the relationship between bile acids (BAs) and synovitis in knee osteoarthritis (KOA).

methodsRadiographic KOA patients with complete datasets were included. WOMAC total and subscores were calculated. Synovitis was assessed by ultrasound or Krenn score. BAs were profiled in plasma (N=28) or synovial fluid (SF, N=29) using liquid chromatography-tandem mass spectrometry. OA synovial explants, OA fibroblast-like synoviocytes (FLS), and bone marrow-derived macrophages (BMDM) were used for in vitro experiments. Data analysis was performed using R and MetaboAnalyst.

resultsSixteen KOA participants had low-grade (0-1) and twelve had high-grade synovitis (2-3). Glycohyodeoxycholic acid (1.198 ± 0.983 vs. 1.954 ± 0.686, 0.76[95% CI: 0.04-1.89]) and lithocholic acid (0.19 ± 0.53 vs. 0.825 ± 0.866, 0.63[95% CI: 0.00-1.58]) were elevated in subjects with high-grade synovitis. LPS-binding protein (LBP) (rho = 0.58, p = 0.037, [95% CI: -0.807-0.46]) correlated with synovitis but only in obese participants (BMI ≥ 30). LBP, lithocholic acid, and glycohyodeoxycholic acid predicted high synovitis (92% sensitivity, 75% specificity, AUC = 0.875[95% CI: 0.99-1.05], p < 0.001). In SF, taurodeoxycholic and glycohyodeoxycholic acids correlated positively with WOMAC pain and stiffness subscores and the total WOMAC score. The BA receptors, TGR5 and LXR, were present in synovial tissue. In vitro, BAs reduced cytokine secretion in FLS and BMDM.

conclusionDetection of BAs and their receptors in synovial tissue, together with their modulatory effects on synovial cells, supports a potential biological role for BAs in KOA.

Indexed as

Bile Acids and SaltsMicrobiotaOsteoarthritis, KneeSynovitisAgedFemaleHumansMacrophagesMaleMiddle AgedSynovial FluidSynovial MembraneSynoviocytesBile Acids and SaltsBile acidsOsteoarthritisSynovitis

Identifiers

PMID41763351
PMCPMC13327719

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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.