Evidence mapPaperPMID 41246338Full record

ReviewFrontiers in immunology2025

Adipose tissue: an inflammatory organ that can not be ignored in periodontal disease related to obesity.

Qiqi Wang, Hongyan Li, Yu Huan, Tianyu Zhou, Jingdan Zhang, Rongkaixuan Fang, Yue Sun, Lan A, Wenzhou Xu

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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

9 authors.

Qiqi Wang *Department of Periodontology, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
Hongyan Li *Department of Periodontology, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
Yu HuanDepartment of Periodontology, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
Tianyu ZhouJilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
Jingdan ZhangDepartment of Periodontology, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
Rongkaixuan FangJilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
Yue SunDepartment of Oral Implantology, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
Lan ADepartment of Oral Implantology, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
Wenzhou XuDepartment of Periodontology, Hospital of Stomatology, Jilin University, Changchun, Jilin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In obesity, the pathological remodeling of adipose tissue characterized by hyperplasia and hypertrophy serves as a critical hub driving chronic inflammation. This process triggers adipose microenvironment disruption, manifesting as reduced angiogenesis, excessive extracellular matrix deposition, dysregulated adipokine secretion, and enhanced immune cell infiltration, ultimately leading to a systemic low-grade inflammatory state. Functioning as an active inflammatory organ, dysfunctional adipose tissue specifically exacerbates periodontitis progression through multiple mechanisms: including glucose/lipid metabolic imbalance, dysregulated bone metabolism with imbalanced osteoclast-osteoblast activity, immunometabolic disturbances, microcirculatory impairment, degradation of periodontal extracellular matrix and dysfunction of epithelial barrier and gut microbiota dysbiosis. This review systematically elucidates the interactive mechanisms between adipose tissue-derived inflammatory signaling and periodontal pathology, emphasizing its central role in obesity-associated periodontal diseases. Based on these mechanisms, we propose targeted intervention strategies: modulating adipokine secretion, suppressing immune cell infiltration in adipose tissue or restoring adipose tissue metabolic homeostasis may emerge as novel approaches to disrupt the obesity-periodontitis vicious cycle. Future studies might enhance the clinical translation of multi-organ treatment approaches that target the adipose tissue-periodontium axis while continuing to explore the regulatory effects of immune pathways specific to adipose tissue on the periodontal microenvironment.

Indexed as

Adipose TissueObesityPeriodontal DiseasesAdipokinesAnimalsHumansInflammationPeriodontitisAdipokinesadipose tissuechronic inflammationimmune metabolic disorderobesityperiodontitis

Identifiers

PMID41246338
PMCPMC12615176

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.