Evidence map›Paper›PMID 27111223›Full record

ArticlePloS one2016

Serum Immunoglobulin G Levels to Porphyromonas gingivalis Peptidylarginine Deiminase Affect Clinical Response to Biological Disease-Modifying Antirheumatic Drug in Rheumatoid Arthritis.

Tetsuo Kobayashi, Satoshi Ito, Daisuke Kobayashi, Atsushi Shimada, Ichiei Narita, Akira Murasawa, Kiyoshi Nakazono, Hiromasa Yoshie

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PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Pathogenesis ofFrontiers in cellular and infection microbiology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Rheumatoid Arthritis-Associated Mechanisms ofJournal of clinical medicine · 2019
    Review
  9. Review
  10. Observational
  11. Review
  12. Review
  13. Article
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

8 authors.

Tetsuo KobayashiGeneral Dentistry and Clinical Education Unit, Niigata University Medical and Dental Hospital, Niigata, Japan.
Satoshi ItoDepartment of Rheumatology, Niigata Rheumatic Center, Shibata, Japan.
Daisuke KobayashiDepartment of Rheumatology, Niigata Rheumatic Center, Shibata, Japan.
Atsushi ShimadaDivision of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Ichiei NaritaDivision of Clinical Nephrology and Rheumatology, Department of Homeostatic Regulation Developments, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Akira MurasawaDepartment of Rheumatology, Niigata Rheumatic Center, Shibata, Japan.
Kiyoshi NakazonoDepartment of Rheumatology, Niigata Rheumatic Center, Shibata, Japan.
Hiromasa YoshieDivision of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo determine whether serum immunity to Porphyromonas gingivalis peptidylarginine deiminase (PPAD) affects the clinical response to biological disease-modifying antirheumatic drug (bDMARD) in patients with rheumatoid arthritis (RA).

methodsIn a retrospective study, rheumatologic and periodontal conditions of 60 patients with RA who had been treated with conventional synthetic DMARD were evaluated before (baseline) and after 3 and 6 months of bDMARD therapy. After serum levels of anti-PPAD immunoglobulin G (IgG) were determined at baseline, the patients were respectively divided into two groups for high and low anti-PPAD IgG titers according to the median measurements. Genotypes at 8 functional single nucleotide polymorphisms (SNPs) related to RA were also determined.

resultsAfter 3 and 6 months of therapy, patients with low anti-PPAD IgG titers showed a significantly greater decrease in changes in the Disease Activity Score including 28 joints using C-reactive protein (DAS28-CRP) (P = 0.04 for both) and anti-cyclic citrullinated peptide (CCP) IgG levels (P = 0.03 and P = 0.04) than patients with high anti-PPAD IgG titers, although these parameter values were comparable at baseline. The anti-PPAD IgG titers were significantly positively correlated with changes in the DAS28-CRP (P = 0.01 for both) and the anti-CCP IgG levels (P = 0.02 for both) from baseline to 3 and 6 months later. A multiple regression analysis revealed a significantly positive association between the anti-PPAD IgG titers and changes in the DAS28-CRP after 6 months of bDMARD therapy (P = 0.006), after adjusting for age, gender, smoking, periodontal condition, and RA-related SNPs.

conclusionThe serum IgG levels to PPAD affect the clinical response to bDMARD in patients with RA.

Indexed as

AgedAntibodies, BacterialAntirheumatic AgentsArthritis, RheumatoidAutoantibodiesBacterial ProteinsBiomarkersC-Reactive ProteinFemaleGenetic LociHumansHydrolasesImmunoglobulin GMiddle AgedPeptides, CyclicPeriodontitisAntibodies, BacterialAntirheumatic AgentsAutoantibodiesBacterial ProteinsBiomarkersC-Reactive Proteincyclic citrullinated peptideHydrolasesImmunoglobulin GPeptides, CyclicProtein-Arginine Deiminases

Identifiers

PMID27111223
PMCPMC4844134

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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.