ReviewFrontiers in immunology2025
Adipose tissue: an inflammatory organ that can not be ignored in periodontal disease related to obesity.
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.
What it found
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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.
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.
Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Age-Related Differences in Oral Microbiota Among Obese Patients with Periodontitis: A Systematic Review.Nutrients · 2026Pooled it
- Insights into taurine therapy for periodontitis: Targeting osteocyte ferroptosis to mitigate obesity-exacerbated bone damage.Redox biology · 2026Article
- Association Between Glyco-Lipid Seven-Factor Index, a Novel Composite Glyco-Lipid Index, and Periodontitis: A Cross-Sectional Study.International dental journal · 2026Article
- Longitudinal trends in general, central, and visceral adiposity indices among women with endometriosis: a population-based study.Journal of endocrinological investigation · 2026Article
- Predictors of Peripheral Neuropathy in Metabolic Disease: A Multivariable Analysis Incorporating the Toronto Clinical Scoring System and Sudomotor Assessment.Medicina (Kaunas, Lithuania) · 2026Article
- Gut Microbiota Has the Potential to Improve Sarcopenic Obesity in Menopausal Women by Regulating Estrogen.International journal of women's health · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
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
Identifiers
What Socratic holds
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 Socratic graph.