Evidence map›Paper›PMID 35708472›Full record

ReviewJournal of dental research2022

Neuroinflammation: A Distal Consequence of Periodontitis.

X Li, M Kiprowska, T Kansara, P Kansara, P Li

Open access · greenAbstract readReview
In one paragraph

Review 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 80 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 6 pooled it
12.6field-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.

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

80 citing papers in PubMed, 6 syntheses or guidelines pooled it, 94 citations in OpenAlex.

  1. Pooled it
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  7. Determinants of post-stroke cognitive impairment in patients with periodontal disease.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2025
    Trial
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20 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

X LiDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY, USA.ORCID 0000-0002-7414-5734
M KiprowskaDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY, USA.
T KansaraCleveland Clinic- Union hospital, Dover, OH, USA.
P KansaraDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY, USA.ORCID 0000-0002-9268-2402
P LiDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY, USA.
New York University · USCleveland Clinic · USNYU Langone Health · US

Funding

Succinate signaling in periodontitis induced neuroinflammation and dementiaR01AG080696 · NIA · UNIVERSITY OF VIRGINIA · PI Xin Li · 2023 to 2026
$2.5M
Succinate triggers gut dysbiosis and activates SUCNR1 to enhance inflammagingR01AG068857 · NIA · UNIVERSITY OF VIRGINIA · PI LI, XIN, SAXENA, DEEPAK · 2020 to 2024
$2.4M
NIA NIH HHS R01 AG068857NIA NIH HHS R01 AG080696
6 · The paper itself

Abstract

Periodontitis, a chronic, inflammatory disease, induces systemic inflammation and contributes to the development of neurodegenerative diseases. The precise etiology of the most common neurodegenerative disorders, such as sporadic Alzheimer's, Parkinson's diseases and multiple sclerosis (AD, PD, and MS, respectively), remains to be revealed. Chronic neuroinflammation is a well-recognized component of these disorders, and evidence suggests that systemic inflammation is a possible stimulus for neuroinflammation development. Systemic inflammation can lead to deleterious consequences on the brain if the inflammation is sufficiently severe or if the brain shows vulnerabilities due to genetic predisposition, aging, or neurodegenerative diseases. It has been proposed that periodontal disease can initiate or contribute to the AD pathogenesis through multiple pathways, including key periodontal pathogens. Dysbiotic oral bacteria can release bacterial products into the bloodstream and eventually cross the brain-blood barrier; these bacteria can also cause alterations to gut microbiota that enhance inflammation and potentially affect brain function via the gut-brain axis. The trigeminal nerve has been suggested as another route for connecting oral bacterial products to the brain. PD and MS are often preceded by gastrointestinal symptoms or aberrant gut microbiome composition, and alterations in the enteric nervous system accompany the disease. Clinical evidence has suggested that patients with periodontitis are at a higher risk of developing PD and MS. This nexus among the brain, periodontal disease, and systemic inflammation heralds new ways in which microglial cells, the main innate immune cells, and astrocytes, the crucial regulators of innate and adaptive immune responses in the brain, contribute to brain pathology. Currently, the lack of understanding of the pathogenesis of neurodegeneration is hindering treatment development. However, we may prevent this pathogenesis by tackling one of its possible contributors (periodontitis) for systemic inflammation through simple preventive oral hygiene measures.

Indexed as

Neurodegenerative DiseasesPeriodontitisBacteriaBrainDysbiosisHumansInflammationNeuroinflammatory Diseasesdysbiosisinflammationneurodegenerationoral hygieneoral microbiomeperiodontal disease

Identifiers

PMID35708472
PMCPMC9608094
OpenAlexW4282982148

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.