ArticleScientific reports2015
The peptidylarginine deiminase gene is a conserved feature of Porphyromonas gingivalis.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Higher odds of periodontitis in systemic lupus erythematosus compared to controls and rheumatoid arthritis: a systematic review, meta-analysis and network meta-analysis.Frontiers in immunology · 2024Pooled it
- Pathogenicity ofFrontiers in cellular and infection microbiology · 2026Article
- Immunomodulatory effects of oral microbiota in the pathogenesis of rheumatoid arthritis.Frontiers in immunology · 2026Review
- Virulence diversity amongJournal of oral microbiology · 2026Review
- Epidemiology and pathogenesis of the link between rheumatoid arthritis and periodontitis.Journal of Zhejiang University. Science. B · 2025Review
- Polymorphic Variants of Peptidylarginine Deiminase Gene fromInternational journal of molecular sciences · 2025Article
- Potential roles and mechanisms of bacterial peptidylarginine deiminase in dental biofilm mediated byJournal of oral microbiology · 2025Review
- Review
- Oral microbiome in human health and diseases.mLife · 2024Review
- Microbial Mechanisms of Rheumatoid Arthritis Pathogenesis.Current rheumatology reports · 2024Review
- The Role of Citrullination Modification in CD4Biomolecules · 2024Review
- Identification of a new genetic variant (G231N, E232T, N235D) of peptidylarginine deiminase fromFrontiers in immunology · 2024Article
- Periodontitis and periodontopathic bacteria as risk factors for rheumatoid arthritis: A review of the last 10 years.The Japanese dental science review · 2023Review
- Article
- Porphyromonas gulae and PPAD antibodies are not related to citrullination in rheumatoid arthritis.Clinical oral investigations · 2023Article
- Phylogenomic analysis of theFrontiers in microbiology · 2023Article
- The impact of the human microbiome in tumorigenesis, cancer progression, and biotherapeutic development.BMC microbiology · 2022Review
- Bacteria derived extracellular vesicles in the pathogenesis and treatment of gastrointestinal tumours.Frontiers in oncology · 2022Review
- Influence of Oral Microbiota on the Presence of IgA Anti-Citrullinated Protein Antibodies in Gingival Crevicular Fluid.Frontiers in oral health · 2022Article
- Should We Be Screening for and Treating Periodontal Disease in Individuals Who Are at Risk of Rheumatoid Arthritis?Healthcare (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periodontitis is an infective process that ultimately leads to destruction of the soft and hard tissues that support the teeth (the periodontium). Periodontitis has been proposed as a candidate risk factor for development of the autoimmune disease rheumatoid arthritis (RA). Porphyromonas gingivalis, a major periodontal pathogen, is the only known prokaryote expressing a peptidyl arginine deiminase (PAD) enzyme necessary for protein citrullination. Antibodies to citrullinated proteins (anti-citrullinated protein antibodies, ACPA) are highly specific for RA and precede disease onset. Objective of this study was to assess P. gingivalis PAD (PPAD) gene expression and citrullination patterns in representative samples of P. gingivalis clinical isolates derived from periodontitis patients with and without RA and in related microbes of the Porphyromonas genus. Our findings indicate that PPAD is omnipresent in P. gingivalis, but absent in related species. No significant differences were found in the composition and expression of the PPAD gene of P. gingivalis regardless of the presence of RA or periodontal disease phenotypes. From this study it can be concluded that if P. gingivalis plays a role in RA, it is unlikely to originate from a variation in PPAD gene expression.
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