@article{Liu2026, 
author = {Maliya Liu and Mengjiao Tao and Yue Hu and Zhenyu Sun and Mengmeng Lu},
title = {TREM-1: a pathogenic hub mediating the link between oral inflammation and systemic diseases},
year = {2026},
journal = {Oral Science and Homeostatic Medicine},
volume = {2},
number = {2},
pages = {9610059},
keywords = {TREM-1 signaling pathway, inflammation, oral-systemic axis, therapeutic target},
url = {https://www.sciopen.com/article/10.26599/OSHM.2026.9610059},
doi = {10.26599/OSHM.2026.9610059},
abstract = {Triggering receptor expressed on myeloid cells 1 (TREM-1) is a critical amplifier of innate immune responses, orchestrating pathophysiology across diverse inflammatory conditions. In the oral cavity, TREM-1 activation promotes the development of periodontitis, peri-implantitis, and oral lichen planus by polarizing myeloid cells toward a pro-inflammatory state, enhancing pro-inflammatory cytokine release, and accelerating tissue degradation and bone resorption. Notably, this TREM-1-driven myeloid dysregulation also underpins severe systemic comorbidities, including atherosclerotic cardiovascular disease (ASCVD), diabetic kidney disease (DKD), and Alzheimer’s disease (AD). This review synthesizes current knowledge to delineate the TREM-1 axis as a pathogenic hub in oral-systemic crosstalk, specifying three dissemination routes: systemic leakage of local mediators after barrier disruption, peripheral migration of epigenetically primed TREM-1+ cells, and synergy with metabolic risks. We further highlight soluble TREM-1 (sTREM-1) as a promising biomarker reflecting cumulative inflammatory burden. Ultimately, combining established oral therapies with emerging TREM-1-targeted strategies offers a mechanistically grounded framework to disrupt the oral-systemic disease continuum, providing novel therapeutic avenues for inflammatory comorbidities.}
}