Evidence map›Paper›PMID 36340583›Full record

ReviewThe Japanese dental science review2022

Macrophages in periodontitis: A dynamic shift between tissue destruction and repair.

Linying Yin, Xinzhu Li, Jin Hou

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in The Japanese dental science review, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07508839 (Evaluation of the Safety and Efficacy of SALI-10 Probiotic Lozenges), which is not on this map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 1% 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.

NCT07508839 narecruitingnot on this mapstarted 2026, after this paper: background citation

Evaluation of the Safety and Efficacy of SALI-10 Probiotic Lozenges: A Prospective, Randomized, Double-Blind, Placebo-Controlled Trial

TypeinterventionalSponsorOstia SciencesRan2026 to 2027Enrolled60ConditionsGingivitis, HalitosisArms3B SALI-10 Lozenge, Placebo
3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. Gut microbes · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  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

3 authors at 1 institution in 1 country.

Linying YinDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xinzhu LiDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jin HouDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontitis is a chronic inflammatory disease associated with a dysbiotic bacterial biofilm in the subgingival environment that may disturb the balance between the oral microbiome and its host. The inability of the immune system to eliminate inflammation may result in the progressive destruction of tooth-support tissues. Macrophages are crucial cellular components of the innate immune system and play important roles in diverse physiological and pathological processes. In response to periodontitis-associated bacterial communities, macrophages contribute to inflammation and restoration of tissue homeostasis through pattern recognition receptor-induced signaling cascades; therefore, targeting macrophages can be a feasible strategy to treat patients with periodontitis. Although recent studies indicate that macrophages have a spectrum of activation states, ranging from pro-inflammatory to anti-inflammatory, the regulatory mechanism of the macrophage response to dysbiosis in a tissue-specific manner remains largely unclear. Herein, we attempt to summarize the potential role of macrophage activation in the progression of periodontitis, as well as its relevance to future approaches in the treatment of periodontitis.

Indexed as

AIM2, absent in melanoma-2CCL2, chemokine (C-C motif) ligand 2CCR2, chemokine (C-C motif) receptor 2DAMP, damage-associated molecular patternDysbiosisIFN, interferonIL, interleukinInflammationIRF, interferon regulatory factorLPS, lipopolysaccharideMacrophagesMLKL, mixed lineage kinase-likeMMP, matrix metalloproteinaseMyD88, myeloid differentiation factor 88NLR, nucleotide oligomerization domain-like receptorOral microbiomePAMP, pathogen-associated molecular patternPeriodontitisPRR, pattern recognition receptorRANKL, receptor activator of nuclear factor kappa-B ligandSTAT, signal transducer and activator of transcriptionTGF, transforming growth factorTLR, toll-like receptorTNF, tumor necrosis factorTRIF, Toll/IL-1R domain-containing adapter-inducing IFN-β

Identifiers

PMID36340583
PMCPMC9630779
OpenAlexW4307488648

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 OpenQuestion graph.