Evidence map›Paper›PMID 35327515›Full record

ArticleBiomedicines2022

Periodontal Disease Augments Cardiovascular Disease Risk Biomarkers in Rheumatoid Arthritis.

Jeneen Panezai, Ambereen Ghaffar, Mohammad Altamash, Mikael Åberg, Thomas E Van Dyke, Anders Larsson, Per-Erik Engström

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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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 at 6 institutions in 3 countries.

Jeneen PanezaiSection of Oral Health and Periodontology, Division of Oral Diseases, Department of Dental Medicine, Karolinska Institutet, 14104 Huddinge, Sweden.ORCID 0000-0001-5417-9788
Ambereen GhaffarRheumatology Clinic, Habib Medical Centre, Karachi 75950, Pakistan.
Mohammad AltamashDepartment of Periodontology, Altamash Institute of Dental Medicine, Karachi 75500, Pakistan.
Mikael ÅbergClinical Chemistry, Department of Medical Sciences, Uppsala University, 75236 Uppsala, Sweden.
Thomas E Van DykeDepartment of Applied Oral Sciences, The Forsyth Institute, Cambridge, MA 02142, USA.
Anders LarssonClinical Chemistry, Department of Medical Sciences, Uppsala University, 75236 Uppsala, Sweden.ORCID 0000-0003-3161-0402
Per-Erik EngströmSection of Oral Health and Periodontology, Division of Oral Diseases, Department of Dental Medicine, Karolinska Institutet, 14104 Huddinge, Sweden.
Uppsala University · SEBalochistan University of Information Technology, Engineering and Management Sciences · PKHabib University · PKHarvard University · USKarachi Medical and Dental College · PKKarolinska Institutet · SE

Funding

Mechanisms of Resolvin E1 in Periodontal RegenerationR01DE025020 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI GUASTALDI, FERNANDO, VAN DYKE, THOMAS ELLIOTT · 2015 to 2023
$4.9M
NIDCR NIH HHS R01 DE025020
6 · The paper itself

Abstract

Objectives: Periodontal disease (PD) and rheumatoid arthritis (RA) are known chronic conditions with sustained inflammation leading to osteolysis. Cardiovascular diseases (CVD) are frequent comorbidities that may arise from sustained inflammation associated with both PD and RA. In order to determine CVD risk, alterations at the molecular level need to be identified. The objective of this study, therefore, was to assess the relationship of CVD associated biomarkers in RA patients and how it is influenced by PD. Methods: The study consisted of patient (26 RA with PD, 21 RA without PD, 51 patients with PD only) and systemically and periodontally healthy control (n = 20) groups. Periodontal parameters bleeding on probing, probing pocket depth, and marginal bone loss were determined to characterize the patient groups. Proteomic analysis of 92 CVD-related protein biomarkers was performed using a multiplex proximity extension assay. Biomarkers were clustered using the search tool for retrieval of interacting genes (STRING) to determine protein−protein interaction (PPI) networks. Results: RA patients with PD had higher detection levels for 47% of the measured markers (ANGPT1, BOC, CCL17, CCL3, CD4, CD84, CTRC, FGF-21, FGF-23, GLO1, HAOX1, HB-EGF, hOSCAR, HSP 27, IL16, IL-17D, IL18, IL-27, IL6, LEP, LPL, MERTK, MMP12, MMP7, NEMO, PAPPA, PAR-1, PARP-1, PD-L2, PGF, PIgR, PRELP, RAGE, SCF, SLAMF7, SRC, THBS2, THPO, TNFRSF13B, TRAIL-R2, VEGFD, VSIG2, and XCL1) as compared to RA without PD. Furthermore, a strong biological network was identified amongst these proteins (clustering coefficient = 0.52, PPI enrichment p-value < 0.0001). Coefficients for protein clusters involved in CVD (0.59), metabolic (0.53), and skeletal (0.51) diseases were strongest in the PD group. Conclusion: Periodontal disease augments CVD-related biomarkers in RA through shared pathological clusters, concurrently enhancing metabolic and skeletal disease protein interactions, independent of autoimmune status.

Indexed as

cardiovascular diseaseinflammationperiodontal diseaseproteinsproteomicsrheumatoid arthritis

Identifiers

PMID35327515
PMCPMC8945365
OpenAlexW4220846911

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.