Evidence map›Paper›PMID 26375893›Full record

ReviewMicrobial pathogenesis2016

Role of bacteria in leukocyte adhesion deficiency-associated periodontitis.

George Hajishengallis, Niki M Moutsopoulos

Open access · greenAbstract readReview
In one paragraph

Review in Microbial pathogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. β2 Integrins-Multi-Functional Leukocyte Receptors in Health and Disease.International journal of molecular sciences · 2020
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
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  20. Review
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

2 authors at 2 institutions in 1 country.

George HajishengallisDepartment of Microbiology, University of Pennsylvania Penn Dental Medicine, Philadelphia, PA 19104, USA. Electronic address: geoh@upenn.edu.
Niki M MoutsopoulosOral Immunity and Inflammation Unit, National Institute of Dental and Craniofacial Research, NIH, Bethesda, MD 20892, USA. Electronic address: nmoutsopoulos@dir.nidr.nih.gov.
National Institute of Dental and Craniofacial Research · USUniversity of Pennsylvania · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
Oral Microbial and Immunological Characterization of Patients with Immune DysfunZIADE000732 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI MOUTSOPOULOS, NIKI · 2010 to 2024
$13.2M
P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Del-1: Molecular and Cellular Targets in PeriodontitisR01DE024716 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2015 to 2019
$2.0M
Novel mechanisms and 'complement-ary' therapy in periodontitisR01DE021685 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2012 to 2016
$2.0M
NIAID NIH HHS P01 AI068730NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE021685NIDCR NIH HHS R01 DE024716
6 · The paper itself

Abstract

Leukocyte adhesion deficiency Type I (LAD-I)-associated periodontitis is an aggressive form of inflammatory bone loss that has been historically attributed to lack of neutrophil surveillance of the periodontal infection. However, this form of periodontitis has proven unresponsive to antibiotics and/or mechanical removal of the tooth-associated biofilm. Recent studies in LAD-I patients and relevant animal models have shown that the fundamental cause of LAD-I periodontitis involves dysregulation of a granulopoietic cytokine cascade. This cascade includes interleukin IL-23 (IL-23) and IL-17 that drive inflammatory bone loss in LAD-I patients and animal models and, moreover, foster a nutritionally favorable environment for bacterial growth and development of a compositionally unique microbiome. Although the lack of neutrophil surveillance in the periodontal pockets might be expected to lead to uncontrolled bacterial invasion of the underlying connective tissue, microbiological analyses of gingival biopsies from LAD-I patients did not reveal tissue-invasive infection. However, bacterial lipopolysaccharide was shown to translocate into the lesions of LAD-I periodontitis. It is concluded that the bacteria serve as initial triggers for local immunopathology through translocation of bacterial products into the underlying tissues where they unleash the dysregulated IL-23-IL-17 axis. Subsequently, the IL-23/IL-17 inflammatory response sustains and shapes a unique local microbiome which, in turn, can further exacerbate inflammation and bone loss in the susceptible host.

Indexed as

Bacterial Physiological PhenomenaAlveolar Bone LossAnimalsGingivaHumansInterleukin-17Interleukin-23Leukocyte-Adhesion Deficiency SyndromeLipopolysaccharidesNeutrophilsPeriodontitisRadiography, PanoramicIL17A protein, humanInterleukin-17Interleukin-23LipopolysaccharidesIL-17IL-23InflammationLeukocyte adhesion deficiencyMicrobiotaPeriodontitis

Identifiers

PMID26375893
PMCPMC4791199
OpenAlexW1650441004

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.