Evidence map›Paper›PMID 38817019›Full record

ReviewOral diseases2024

NLRP3 inflammasome activity and periodontal disease pathogenesis-A bidirectional relationship.

Andreea C Didilescu, Sreedevi Chinthamani, Frank A Scannapieco, Ashu Sharma

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Oral diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  16. FOXP3+ T Cells-An Emerging Evidence in Periodontitis Therapeutics.Clinical and experimental dental research · 2025
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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

4 authors.

Andreea C DidilescuDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, Buffalo, New York, USA.ORCID 0000-0002-2915-5124
Sreedevi ChinthamaniDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, Buffalo, New York, USA.
Frank A ScannapiecoDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, Buffalo, New York, USA.ORCID 0000-0002-8804-6593
Ashu SharmaDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, Buffalo, New York, USA.ORCID 0000-0001-9252-0668

Funding

Bacterial sialometabolic activity impacts periodontal immunity and microbiotaR01DE029497 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SHARMA, ASHU · 2021 to 2025
$1.8M
Fulbright Visiting Scholar ProgramNIDCR NIH HHS R01 DE029497
6 · The paper itself

Abstract

objectivePeriodontitis is an inflammatory oral disease that occurs as a result of the damaging effects of the immune response against the subgingival microflora. Among the mechanisms involved, the nucleotide-binding oligomerization domain, leucine-rich repeat-containing proteins family member NLRP3 (NLR family pyrin domain-containing 3), proposed as the key regulator of macrophage-induced inflammation, is strongly associated with periodontal disease due to the bacterial activators. This paper aimed to present key general concepts of NLRP3 inflammasome activation and regulation in periodontal disease.

methodA narrative review was conducted in order to depict the current knowledge on the relationship between NLRP3 inflammasome activity and periodontal disease. In vitro and in situ studies were retrieved and commented based on their relevance in the field.

resultsThe NLRP3 inflammasome activity stimulated by periodontal microbiota drive periodontal disease pathogenesis and progression. This occurs through the release of proinflammatory cytokines IL-1β, IL-18, and DAMPs (damage-associated molecular pattern molecules) following inflammasome activation. Moreover, the tissue expression of NLRP3 is dysregulated by oral microbiota, further exacerbating periodontal inflammation.

conclusionThe review provides new insights into the relationship between the NLRP3 inflammasome activity and periodontal disease pathogenesis, highlighting the roles and regulatory mechanism of inflammatory molecules involved in the disease process.

Indexed as

InflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinHumansInterleukin-18Interleukin-1betaMicrobiotaPeriodontal DiseasesPeriodontitisInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanbacteriainflammasomelipopolysaccharidemacrophageperiodontal disease

Identifiers

PMID38817019
PMCPMC11480888

What OpenQuestion holds

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Registered trials

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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.