ReviewMicroorganisms2022
Modulatory Mechanisms of Pathogenicity in
Review in Microorganisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled 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.
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
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.
- Systematic Review: Porphyromonas gingivalis Outer Membrane Vesicles From Pathogenesis to Therapeutic Implications.International dental journal · 2026Pooled it
- Microplastics in the Pathogenesis of Periodontal Diseases: A Narrative Review.Annals of global health · 2025Pooled it
- Testosterone Modulates Virulence-Associated Phenotypes ofPathogens (Basel, Switzerland) · 2026Article
- HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Structural and mechanistic basis of ubiquitous bacterial kinase signaling identifies PorX as a noncanonical substrate in Porphyromonas gingivalis.The Journal of biological chemistry · 2026Article
- A CRISPR array orchestrates virulence and host response inMicrobiology spectrum · 2026Article
- Microbial dysbiosis and host-microbe interactions in proliferative verrucous leukoplakia: insights into carcinogenic potential.Archives of microbiology · 2025Review
- N6-methyladenosine-mediated overexpression of TREM-1 is associated with periodontal disease.Odontology · 2025Article
- Article
- Microbiological and molecular aspects of periodontitis pathogenesis: an infection-induced inflammatory condition.Frontiers in cellular and infection microbiology · 2025Review
- Inhibition of BTK and SYK attenuatesJournal of oral microbiology · 2025Article
- The intriguing strategies ofFrontiers in oral health · 2024Article
- A simple and cost-effective transformation system forFrontiers in microbiology · 2024Article
- Pathogenic mechanisms and potential applications of extracellular vesicles from periodontal pathogens in periodontitis.Frontiers in immunology · 2024Review
- Association between muscle quality index and periodontal disease among American adults aged ≥ 30 years: a cross-sectional study and mediation analysis.BMC oral health · 2023Article
- Exploring the Antibacterial Potential of Konjac Glucomannan in Periodontitis: Animal and In Vitro Studies.Medicina (Kaunas, Lithuania) · 2023Article
- Hispidulin Inhibits the Vascular Inflammation Triggered byMolecules (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of periodontitis depends on a sustained feedback loop where bacterial virulence factors and immune responses both contribute to inflammation and tissue degradation. Periodontitis is a multifactorial disease that is associated with a pathogenic shift in the oral microbiome. Within this shift, low-abundance Gram-negative anaerobic pathobionts transition from harmless colonisers of the subgingival environment to a virulent state that drives evasion and subversion of innate and adaptive immune responses. This, in turn, drives the progression of inflammatory disease and the destruction of tooth-supporting structures. From an evolutionary perspective, bacteria have developed this phenotypic plasticity in order to respond and adapt to environmental stimuli or external stressors. This review summarises the available knowledge of genetic, transcriptional, and post-translational mechanisms which mediate the commensal-pathogen transition of periodontal bacteria. The review will focus primarily on
Indexed as
Identifiers
What Socratic 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 Socratic graph.