Evidence map›Paper›PMID 34636272›Full record

ArticleJournal of dental research2022

Novel Preosteoclast Populations in Obesity-Associated Periodontal Disease.

K H Kwack, L Zhang, J Sohn, V Maglaras, R Thiyagarajan, K L Kirkwood

Open access · greenAbstract read
In one paragraph

Article in Journal of dental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Role of regulatory immune cells in pathogenesis and therapy of periodontitis.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Tristetraprolin regulates the skeletal phenotype and osteoclastogenic potential through monocytic myeloid-derived suppressor cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  15. Review
  16. Article
  17. Review
  18. Osteoclast biology in the single-cell era.Inflammation and regeneration · 2022
    Review
  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

6 authors at 3 institutions in 1 country.

K H KwackDepartment of Oral Biology, University at Buffalo, Buffalo, NY, USA.
L ZhangDepartment of Oral Biology, University at Buffalo, Buffalo, NY, USA.
J SohnDepartment of Oral Biology, University at Buffalo, Buffalo, NY, USA.
V MaglarasDepartment of Oral Biology, University at Buffalo, Buffalo, NY, USA.
R ThiyagarajanDepartment of Medicine, University at Buffalo, Buffalo, NY, USA.
K L KirkwoodDepartment of Oral Biology, University at Buffalo, Buffalo, NY, USA.ORCID 0000-0003-4519-8973
University at Buffalo, State University of New York · USRoswell Park Comprehensive Cancer Center · USVA Western New York Healthcare System · US

Funding

Bioinformatic Approaches for Understanding Macrophage Plasticity and Microbiome in Oral DiseasesK18DE029526 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI KIRKWOOD, KEITH L · 2020 to 2020
$94k
NIDCR NIH HHS K18 DE029526
6 · The paper itself

Abstract

Although there is a clear relationship between the degree of obesity and periodontal disease incidence, the mechanisms that underpin the links between these conditions are not completely understood. Understanding that myeloid-derived suppressor cells (MDSCs) are expanded during obesity and operate in a context-defined manner, we addressed the potential role of MDSCs to contribute toward obesity-associated periodontal disease. Flow cytometry revealed that in the spleen of mice fed a high-fat diet (HFD), expansion in monocytic MDSCs (M-MDSCs) significantly increased when compared with mice fed a low-fat diet (LFD). In the osteoclast differentiation assay, M-MDSCs isolated from the bone marrow of HFD-fed mice showed a larger number and area of osteoclasts with a greater number of nuclei. In the M-MDSCs of HFD-fed mice, several osteoclast-related genes were significantly elevated when compared with LFD-fed mice according to a focused transcriptomic platform. In experimental periodontitis, the number and percentage of M-MDSCs were greater, with a significantly larger increase in HFD-fed mice versus LFD-fed mice. In the spleen, the percentage of M-MDSCs was significantly higher in HFD-fed periodontitis-induced (PI) mice than in LFD-PI mice. Alveolar bone volume fraction was significantly reduced in experimental periodontitis and was further decreased in HFD-PI mice as compared with LFD-PI mice. The inflammation score was significantly higher in HFD-PI mice versus LFD-PI mice, with a concomitant increase in TRAP staining for osteoclast number and area in HFD-PI mice over LFD-PI mice. These data support the concept that M-MDSC expansion during obesity to become osteoclasts during periodontitis is related to increased alveolar bone destruction, providing a more detailed mechanistic appreciation of the interconnection between obesity and periodontitis.

Indexed as

Diet, High-FatPeriodontal DiseasesAnimalsMiceMice, Inbred C57BLObesityOsteoclastsboneinflammationmyeloid-derived suppressor cellsosteoclasts, metabolic diseasesperiodontitis

Identifiers

PMID34636272
PMCPMC8982008
OpenAlexW3207757752

What OpenQuestion 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 OpenQuestion graph.