ArticleClinical rheumatology2026
The diagnostic value and pathological application of TREM2 in patients with osteoarthritis.
Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOsteoarthritis (OA) is a prevalent degenerative joint disease with limited diagnostic biomarkers. Triggering receptor expressed on myeloid cells 2 (TREM2) is a key regulator of inflammation and bone metabolism, but its role in OA remains unclear.
methodsPlasma and synovial fluid samples were collected from patients with OA and patients with joint trauma serving as controls. Levels of TREM2 and IL-6 were measured using RT-qPCR and ELISA. Correlation analyses were conducted to assess relationships among TREM2, IL-6, and clinical parameters. The diagnostic value of TREM2 was evaluated via receiver operating characteristic (ROC) curve analysis. Additionally, the role and regulatory mechanism of TREM2 were investigated in lipopolysaccharide (LPS)-induced chondrocytes.
resultsTREM2 levels were significantly elevated in both plasma and synovial fluid of patients with OA and showed positive correlations with IL-6, Kellgren-Lawrence score and body mass index (BMI). ROC analysis revealed AUCs of 0.880 for plasma TREM2 and 0.869 for synovial fluid TREM2, with superior performance compared to IL-6 in the same cohort. Multivariate logistic regression confirmed that TREM2 remained independently associated with OA after adjusting for confounders (OR = 28.29, P = 0.006). In vitro, LPS treatment upregulated TREM2 expression in chondrocytes, which was associated with changes in cell proliferation, apoptosis, inflammatory cytokine release and oxidative stress, with preliminary evidence suggesting involvement of the NLRP3-mediated pyroptosis-associated pathway.
conclusionElevated TREM2 in plasma and synovial fluid represents a promising exploratory biomarker for OA. In vitro findings suggest that TREM2 may modulate chondrocyte functions in association with NLRP3 inflammasome-associated molecular pathways.
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