Evidence map›Paper›PMID 42167887›Full record

ArticleRMD open2026

Gut microbiota dysbiosis and metabolic alterations in rheumatoid arthritis: a barrier to periodontal repair.

Di Cui, Yingying Zhou, Yibing Zhou, Ruiyang Ge, Haowei Mao, Motilal Mathesh, Lei Han, Wenrong Yang, Fuhua Yan

Abstract read
In one paragraph

Article in RMD open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Di Cui *Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China yanfh@nju.edu.cn d.cui@deakin.edu.au pinedream@163.com.ORCID 0000-0003-1086-2192
Yingying Zhou *Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Yibing ZhouNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Ruiyang GeNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Haowei MaoNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Motilal MatheshSchool of Life and Environmental Sciences, Centre for Sustainable Bioproducts, Deakin University, Melbourne, Victoria, Australia.
Lei HanNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China yanfh@nju.edu.cn d.cui@deakin.edu.au pinedream@163.com.
Wenrong YangSchool of Life and Environmental Sciences, Centre for Sustainable Bioproducts, Deakin University, Melbourne, Victoria, Australia.
Fuhua YanNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China yanfh@nju.edu.cn d.cui@deakin.edu.au pinedream@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the impact of rheumatoid arthritis (RA) on periodontal healing and the underlying mechanisms.

methodsMandibular periodontal bone defect (PBD) and collagen-induced arthritis (CIA) models were established in male Sprague-Dawley rats aged 6 weeks, assigned to four groups: control (CON), CIA, PBD and CIA+PBD. Periodontal repair was evaluated at 1, 3 and 6 weeks. To examine the contribution of gut microbiota, pseudo-germ-free rats with PBD received 3-week faecal microbiota transplantation (FMT) from either healthy or CIA donors. Arthritis severity was assessed by paw thickness and arthritis index, while bone microarchitecture was examined by micro-CT and histology. Gut microbiota and metabolites were analysed using 16S ribosomal RNA high-throughput sequencing and untargeted metabolomics.

resultsCIA was found to significantly impair periodontal bone healing and suppress osteogenesis-related markers, including runt-related transcription factor 2 and alkaline phosphatase. Compared with CON rats, CIA and PBD, CIA+PBD groups exhibited gut microbial dysbiosis and metabolic alterations, particularly in arachidonic acid and tryptophan pathways. FMT from CIA donors further increased osteoclast numbers and delayed bone regeneration. Furthermore, gut-derived factors from CIA animals were associated with increased macrophage expression of pro-inflammatory cytokines, including tumour necrosis factor-alpha and interleukin-1 beta.

conclusionOverall, RA-related gut microbiota dysbiosis and metabolic disturbances are linked to impaired periodontal healing, potentially through enhanced inflammatory responses. This study highlights a microbiome-immune-metabolic axis that may influence periodontal regeneration in RA.

Indexed as

Arthritis, RheumatoidDysbiosisGastrointestinal MicrobiomeAnimalsArthritis, ExperimentalBiomarkersBone RegenerationCytokinesDisease Models, AnimalFecal Microbiota TransplantationHumansMaleMetabolomicsRatsRats, Sprague-DawleyRNA, Ribosomal, 16SBiomarkersCytokinesRNA, Ribosomal, 16SBone DensityInflammationRheumatoid ArthritisRisk Factors

Identifiers

PMID42167887
PMCPMC13202092

What Socratic 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 Socratic graph.