From periodontal inflammation to hepatic immune remodeling: emerging concepts of myeloid reprogramming in stage-dependent MASLD
- 1Department of Stomatology, the First Hospital of Jilin University
Abstract
Periodontitis and metabolic dysfunction-associated steatotic liver disease (MASLD) are common chronic inflammatory disorders. Recent population studies support epidemiological associations between periodontitis and MASLD and related hepatic phenotypes, but substantial heterogeneity remains in their strength and independence, and current evidence is insufficient to establish causality. This review focuses on the periodontal-to-liver direction, using circulating myeloid cells as a central line of inquiry to examine the potential link between periodontitis-associated systemic myeloid reprogramming and intrahepatic myeloid remodeling in MASLD. Direct evidence that periodontitis-conditioned myeloid cells enter the MASLD liver and alter immune remodeling or disease progression is still lacking. Although both processes are independently supported, the cross-organ bridge between them remains unresolved. Evidence is also asymmetric across myeloid pathways: the neutrophil–NET axis has relatively direct functional support at both ends, whereas the monocyte–macrophage axis is supported mainly on the hepatic side. We propose that periodontitis may alter the pre-hepatic functional state of myeloid cells, while their biological effects are expected to depend on the stage and local immune environment of the recipient liver. Testing this model will require lineage-informed cell tracking, stage-specific perturbation, and longitudinal studies integrating periodontal inflammation, circulating myeloid phenotypes, and hepatic phenotypes within the same patients.
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BibTeX
@article{song2026from,
title = {{From periodontal inflammation to hepatic immune remodeling: emerging concepts of myeloid reprogramming in stage-dependent MASLD}},
author = {Xudong Song and Congxiao Zhang},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.2003684},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.2003684/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - From periodontal inflammation to hepatic immune remodeling: emerging concepts of myeloid reprogramming in stage-dependent MASLD
AU - Xudong Song
AU - Congxiao Zhang
PY - 2026
DA - 2026/10/22
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.2003684
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.2003684/full
AB - Periodontitis and metabolic dysfunction-associated steatotic liver disease (MASLD) are common chronic inflammatory disorders. Recent population studies support epidemiological associations between periodontitis and MASLD and related hepatic phenotypes, but substantial heterogeneity remains in their strength and independence, and current evidence is insufficient to establish causality. This review focuses on the periodontal-to-liver direction, using circulating myeloid cells as a central line of inquiry to examine the potential link between periodontitis-associated systemic myeloid reprogramming and intrahepatic myeloid remodeling in MASLD. Direct evidence that periodontitis-conditioned myeloid cells enter the MASLD liver and alter immune remodeling or disease progression is still lacking. Although both processes are independently supported, the cross-organ bridge between them remains unresolved. Evidence is also asymmetric across myeloid pathways: the neutrophil–NET axis has relatively direct functional support at both ends, whereas the monocyte–macrophage axis is supported mainly on the hepatic side. We propose that periodontitis may alter the pre-hepatic functional state of myeloid cells, while their biological effects are expected to depend on the stage and local immune environment of the recipient liver. Testing this model will require lineage-informed cell tracking, stage-specific perturbation, and longitudinal studies integrating periodontal inflammation, circulating myeloid phenotypes, and hepatic phenotypes within the same patients.
SN - 1664-3224
ER -