Evidence map›Paper›PMID 32758110›Full record

ReviewJournal of dental research2020

IL-1 Superfamily Members and Periodontal Diseases.

E Papathanasiou, P Conti, F Carinci, D Lauritano, T C Theoharides

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of dental research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 6 pooled it
3.8field-weighted citation impact, top 5% 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

60 citing papers in PubMed, 6 syntheses or guidelines pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Effect of xylitol on Porphyromonas gingivalis: A systematic review.Clinical and experimental dental research · 2023
    Pooled it
  7. Article
  8. Association of Interleukin 1 Receptor Antagonist (International journal of molecular sciences · 2026
    Article
  9. Review
  10. Review
  11. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Inflammasomes in Oral Pathologies: From Periodontal Disease to Oral Cancer.Advances in experimental medicine and biology · 2026
    Review
  17. Review
  18. Article
  19. Article
  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

5 authors at 5 institutions in 2 countries.

E PapathanasiouDepartment of Periodontology, Tufts University School of Dental Medicine, Boston, MA, USA.
P ContiImmunology Division, Postgraduate Medical School, University of Chieti, Pescara, Italy.
F CarinciDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
D LauritanoDepartment of Medicine and Surgery, Centre of Neuroscience of Milan, University of Milano-Bicocca, Milan, Italy.
T C TheoharidesDepartment of Immunology, Tufts University School of Medicine, Boston, MA, USA.
Tufts Medical Center · USTufts University · USUniversity of Chieti-Pescara · ITUniversity of Ferrara · ITUniversity of Milano-Bicocca · IT

Funding

Specialized Pro-resolving Mediators (SPMs) & scar tissue formation after cleft-lip surgical repairK08DE027119 · NIDCR · TUFTS UNIVERSITY BOSTON · PI PAPATHANASIOU, EVANGELOS · 2018 to 2023
$794k
NIDCR NIH HHS K08 DE027119
6 · The paper itself

Abstract

Periodontitis is a complex, multifactorial chronic disease involving continuous interactions among bacteria, host immune/inflammatory responses, and modifying genetic and environmental factors. More than any other cytokine family, the interleukin (IL)-1 family includes key signaling molecules that trigger and perpetuate periodontal inflammation. Over the years, the IL-1 family expanded to include 11 members of cytokines, some with agonist activity (IL-1α, IL-1β, IL-18, IL-33, IL-36α, IL-36β, and IL-36γ), receptor antagonists (IL-1Ra, IL-36Ra), and 2 anti-inflammatory cytokines (IL-37, IL-38). The IL-1 receptor antagonist (IL-1Ra) has emerged as a pivotal player in the defense against periodontitis. IL-33 primarily induces the production of Th2-associated cytokines but acts as an "alarmin" via stimulation of mast cells. The IL-36 subclass of cytokines may be important in regulating mucosal inflammation and homeostasis. IL-37 suppresses innate and acquired immune responses. IL-38 is the most recent member of the IL-1 superfamily and has anti-inflammatory properties similar to those of IL-37 but through different receptors. However, limited evidence exists regarding the role of IL-37 and IL-38 in periodontitis. Despite the development of IL-1 blocking agents, therapeutic blockade of select IL-1 family members for periodontitis has only been partially investigated in preclinical and clinical research, while the development of IL-37 and IL-38 as novel anti-inflammatory drugs has not been considered adequately. Here, we review the key properties of the IL-1 family members and provide insights into targeting or promoting select cytokines as new therapeutic agents.

Indexed as

CytokinesInflammationAdaptive ImmunityHumansInterleukin-18Interleukin 1 Receptor Antagonist ProteinInterleukinsCytokinesIL-38 protein, humanInterleukin-18Interleukin 1 Receptor Antagonist ProteinInterleukinscytokinesIL-18IL-33inflammationinterleukin 1periodontitis

Identifiers

PMID32758110
PMCPMC7684837
OpenAlexW3047193582

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.