ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Local complement-targeted intervention in periodontitis: proof-of-concept using a C5a receptor (CD88) antagonist.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 2 of them syntheses that pooled it.
What it found
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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
85 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.
- Using genetics to explore complement C5 as a druggable protein in periodontitis.Frontiers in immunology · 2024Pooled it
- Therapeutic Targeting of the Complement System: From Rare Diseases to Pandemics.Pharmacological reviews · 2021Pooled it
- Platelet-derived concentrates in the immunological management of periodontitis: from dysbiosis to personalized approaches.Odontology · 2026Review
- Mass Spectrometry-Based Oral Meta-Omics Analysis-What We Know and What We Don't.Advances in experimental medicine and biology · 2026Review
- AMY-101 as complement C3 inhibitor for periodontitis therapy: mechanisms, efficacy, and clinical translation.Frontiers in immunology · 2025Review
- Review
- Elucidating allergic reaction mechanisms in response to SARS-CoV-2 mRNA vaccination in adults.Allergy · 2024Article
- The Complement-Targeted Inhibitor Mini-FH Protects against Experimental Periodontitis via Both C3-Dependent and C3-Independent Mechanisms.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Temporal changes of periodontal tissue pathology in a periodontitis animal model.Journal of periodontal & implant science · 2023Article
- Stiffness-tuned and ROS-sensitive hydrogel incorporating complement C5a receptor antagonist modulates antibacterial activity of macrophages for periodontitis treatment.Bioactive materials · 2023Article
- Illuminating the oral microbiome and its host interactions: animal models of disease.FEMS microbiology reviews · 2023Review
- Determination of the optimal concentration and duration of C5aR antagonist application in an inflammatory model of human dental pulp cells.FEBS open bio · 2023Article
- Molecular systems architecture of host-microbiome interactions in periodontitis.JADA foundational science · 2023Review
- Complement Is Required for Microbe-Driven Induction of Th17 and Periodontitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Pros and cons of causative association between periodontitis and rheumatoid arthritis.Periodontology 2000 · 2022Review
- Porphyromonas gingivalis outside the oral cavity.Odontology · 2022Review
- Transcriptome Analysis of Monocytes and Fibroblasts Provides Insights Into the Molecular Features of Periodontal Ehlers-Danlos Syndrome.Frontiers in genetics · 2022Article
- C3-targeted therapy in periodontal disease: moving closer to the clinic.Trends in immunology · 2021Review
- Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease.International journal of molecular sciences · 2021Review
- The C5a/C5a receptor 1 axis controls tissue neovascularization through CXCL4 release from platelets.Nature communications · 2021Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
When excessively activated or deregulated, complement becomes a major link between infection and inflammatory pathology including periodontitis. This oral inflammatory disease is associated with a dysbiotic microbiota, leads to the destruction of bone and other tooth-supporting structures, and exerts an adverse impact on systemic health. We have previously shown that mice deficient either in complement C5a receptor (C5aR; CD88) or TLR2 are highly and similarly resistant to periodontitis, suggesting that a cross-talk between the two receptors may be involved in the disease process. In this paper, we show that C5aR and TLR2 indeed synergize for maximal inflammatory responses in the periodontal tissue and uncover a novel pharmacological target to abrogate periodontitis. Using two different mouse models of periodontitis, we show that local treatments with a C5aR antagonist inhibited periodontal inflammation through downregulation of TNF, IL-1β, IL-6, and IL-17 and further protected against bone loss, regardless of the presence of TLR2. These findings not only reveal a crucial cooperation between C5aR and TLR2 in periodontal inflammation but also provide proof-of-concept for local targeting of C5aR as a powerful candidate for the treatment of human periodontitis.
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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.