Evidence map›Paper›PMID 20599785›Full record

ReviewBiochemical pharmacology2010

Complement and periodontitis.

George Hajishengallis

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% of its field
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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. The Molecular Comorbidity Network of Periodontal Disease.International journal of molecular sciences · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Mechanism of resistance to phagocytosis and pulmonary persistence in mucoidFrontiers in cellular and infection microbiology · 2023
    Article
  20. Article
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

1 author at 1 institution in 1 country.

George HajishengallisDepartment of Microbiology and Immunology, University of Louisville School of Dentistry, Loueisville, KY 40292, USA. g0haji01@louisville.edu
University of Louisville · US

Funding

P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Oral Pathogen Exploitation of Innate Recognition as a Function of AgeR01DE018292 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2007 to 2011
$1.6M
NIDCR NIH HHS DE015254NIDCR NIH HHS DE018292NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE018292
6 · The paper itself

Abstract

Although the complement system is centrally involved in host defense, its overactivation or deregulation (e.g., due to inherent host genetic defects or due to pathogen subversion) may excessively amplify inflammation and contribute to immunopathology. Periodontitis is an oral infection-driven chronic inflammatory disease which exerts a systemic impact on health. This paper reviews evidence linking complement to periodontal inflammation and pathogenesis. Clinical and histological observations show a correlation between periodontal inflammatory activity and local complement activation. Certain genetic polymorphisms or deficiencies in specific complement components appear to predispose to increased susceptibility to periodontitis. Animal model studies and in vitro experiments indicate that periodontal bacteria can either inhibit or activate distinct components of the complement cascade. Porphyromonas gingivalis, a keystone species in periodontitis, subverts complement receptor 3 and C5a anaphylatoxin receptor signaling in ways that promote its adaptive fitness in the presence of non-productive inflammation. Overall, available evidence suggests that complement activation or subversion contributes to periodontal pathogenesis, although not all complement pathways or functions are necessarily destructive. Effective complement-targeted therapeutic intervention in periodontitis would require determining the precise roles of the various inductive or effector complement pathways. This information is essential as it may reveal which specific pathways need to be blocked to counteract microbial evasion and inflammatory pathology or, conversely, kept intact to promote host immunity.

Indexed as

AnimalsComplement ActivationComplement C5aComplement Inactivating AgentsComplement System ProteinsGenetic Predisposition to DiseaseHost-Pathogen InteractionsHumansImmunity, InnateMacrophage-1 AntigenMolecular Targeted TherapyPeriodontitisPorphyromonas gingivalisReceptor, Anaphylatoxin C5aSignal TransductionComplement C5aComplement Inactivating AgentsComplement System ProteinsMacrophage-1 AntigenReceptor, Anaphylatoxin C5a

Identifiers

PMID20599785
PMCPMC2955993
OpenAlexW1971558491

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.