Evidence map›Paper›PMID 37285008›Full record

ReviewGeroScience2024

Periodontal disease as a model to study chronic inflammation in aging.

Martinna Bertolini, Daniel Clark

Open access · greenAbstract readReview
In one paragraph

Review in GeroScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 4 pooled it
6.3field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 4 syntheses or guidelines pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Review
  7. Article
  8. Article
  9. Integrated transcriptomic profiling combined withFrontiers in aging neuroscience · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Association between periodontal disease and prostate disease: a mini review.Frontiers in cellular and infection microbiology · 2025
    Review
  17. Review
  18. Article
  19. 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

2 authors at 1 institution in 1 country.

Martinna BertoliniDepartment of Periodontics and Preventive Dentistry, University of Pittsburgh School of Dental Medicine, Pittsburgh, PA, USA.
Daniel ClarkDepartment of Periodontics and Preventive Dentistry, University of Pittsburgh School of Dental Medicine, Pittsburgh, PA, USA. Daniel.Clark@pitt.edu.ORCID 0000-0003-3453-6498
University of Pittsburgh · US

Funding

The impact of the aging immune system on periodontal diseaseK08DE029505 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CLARK, DANIEL R. · 2020 to 2024
$913k
NIDCR NIH HHS K08 DE029505NIDCR NIH HHS K08DE029505
6 · The paper itself

Abstract

Periodontal disease is a chronic inflammatory condition that results in the destruction of the teeth supporting tissues, eventually leading to the loss of teeth and reduced quality of life. In severe cases, periodontal disease can limit proper nutritional intake, cause acute pain and infection, and cause a withdrawal from social situations due to esthetic and phonetic concerns. Similar to other chronic inflammatory conditions, periodontal disease increases in prevalence with age. Research into what drives periodontal disease pathogenesis in older adults is contributing to our general understanding of age-related chronic inflammation. This review will present periodontal disease as an age-related chronic inflammatory disease and as an effective geroscience model to study mechanisms of age-related inflammatory dysregulation. The current understanding of the cellular and molecular mechanisms that drive inflammatory dysregulation as a function of age will be discussed with a focus on the major pathogenic immune cells in periodontal disease, which include neutrophils, macrophages, and T cells. Research in the aging biology field has shown that the age-related changes in these immune cells result in the cells becoming less effective in the clearance of microbial pathogens, expansion of pathogenic subpopulations, or an increase in pro-inflammatory cytokine secretions. Such changes can be pathogenic and contribute to inflammatory dysregulation that is associated with a myriad of age-related disease including periodontal disease. An improved understanding is needed to develop better interventions that target the molecules or pathways that are perturbed with age in order to improve treatment of chronic inflammatory conditions, including periodontal disease, in older adult populations.

Indexed as

AgingInflammationPeriodontal DiseasesAgedChronic DiseaseHumansAgingChronic diseaseInflammationPeriodontal disease

Identifiers

PMID37285008
PMCPMC11226587
OpenAlexW4379601057

What Socratic holds

Textmetadata
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 Socratic graph.