ArticleArthritis research & therapy2018
The involvement of C5a in the progression of experimental arthritis with Porphyromonas gingivalis infection in SKG mice.
Article in Arthritis research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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.
Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Porphyromonas gingivalis-derived extracellular vesicles aggravate bone destruction in rheumatoid arthritis by promoting Syk-dependent osteoclastogenesis.International journal of oral science · 2026Article
- Investigating the role of complement 5a in systemic bone loss after myocardial infarction.Bone · 2025Article
- miR-708-3p targetedly regulates LSD1 to promote osteoblast differentiation of hPDLSCs in periodontitis.Odontology · 2025Article
- Periodontopathic bacteria in rheumatoid arthritis pathogenesis: bridging clinical associations to molecular mechanisms.Frontiers in immunology · 2025Review
- The heart-bone connection: relationships between myocardial infarction and osteoporotic fracture.American journal of physiology. Heart and circulatory physiology · 2024Review
- Review
- Oral administration ofJournal of oral microbiology · 2024Article
- Identifying Oxidative Stress-Related Genes (OSRGs) as Potential Target for Treating Periodontitis Based on Bioinformatics Analysis.Combinatorial chemistry & high throughput screening · 2024Article
- Periodontitis and periodontopathic bacteria as risk factors for rheumatoid arthritis: A review of the last 10 years.The Japanese dental science review · 2023Review
- SAP deficiency aggravates periodontitis possibly via C5a-C5aR signaling-mediated defective macrophage phagocytosis of Porphyromonas gingivalis.Journal of advanced research · 2023Article
- Periapical lesion following Cnm-positive Streptococcus mutans pulp infection worsens cerebral hemorrhage onset in an SHRSP rat model.Clinical and experimental immunology · 2022Article
- Increased Levels of C5a in Gingival Crevicular Fluid and Saliva of Patients with Periodontal Disease.Pathogens (Basel, Switzerland) · 2022Article
- Pros and cons of causative association between periodontitis and rheumatoid arthritis.Periodontology 2000 · 2022Review
- Multifaceted Impacts of Periodontal Pathogens in Disorders of the Intestinal Barrier.Frontiers in immunology · 2021Review
- Review
- Effect of Porphyromonas gingivalis infection on gut dysbiosis and resultant arthritis exacerbation in mouse model.Arthritis research & therapy · 2020Article
- Rheumatoid Arthritis-Associated Mechanisms ofJournal of clinical medicine · 2019Review
- Distal Consequences of Oral Inflammation.Frontiers in immunology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpidemiological evidence to suggest that periodontal disease (PD) is involved in the progression of rheumatoid arthritis (RA) is increasing. The complement system plays a critical role in immune responses. C5a has been implicated in chronic inflammatory diseases, including PD and RA. Porphyromonas gingivalis is the major causative bacteria of PD and can produce C5a. Therefore, it is hypothesized that P. gingivalis infection is involved in the progression of RA by elevating C5a levels. In the present study, P. gingivalis-infected RA model mice were established to investigate the involvement of C5a.
methodsSKG mice orally infected with P. gingivalis were immunized with intraperitoneal injection of laminarin (LA) to induce arthritis. Arthritis development was assessed by arthritis score (AS), bone destruction on the talus, histology, and serum markers of RA. In order to investigate the effects of serum C5a on bone destruction, osteoclast differentiation of bone marrow mononuclear cells was examined by using serum samples from each group of mice. The relationship between C5a levels and antibody titers to periodontal pathogens in patients with RA was investigated by enzyme-linked immunosorbent assay.
resultsP. gingivalis oral infection increased AS, infiltration of inflammatory cells, bone destruction on the talus, and serum markers of RA in mice immunized with LA. The addition of serum from LA-injected mice with the P. gingivalis oral infection promoted osteoclast differentiation, and the addition of a neutralization antibody against C5a suppressed osteoclast differentiation. C5a levels of serum in RA patients with positive P. gingivalis antibody were elevated compared with those in RA patients with negative P. gingivalis antibody.
conclusionsThese results suggest that P. gingivalis infection enhances the progression of RA via C5a.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.