miR-671-5p as a diagnostic biomarker and therapeutic target in periodontitis via THBS1 regulation.

Background: Early diagnosis and therapeutic targeting of periodontitis remain challenging. This study aimed to investigate the clinical relevance and mechanistic role of miR-671-5p in pathogenesis of periodontitis.

Methods: Clinical data and gingival crevicular fluid (GCF) samples were collected from 78 periodontitis patients and 79 healthy controls. miR-671-5p expression in GCF was quantified via quantitative reverse transcription polymerase chain reaction (qRT-PCR), and the diagnostic efficacy was evaluated by receiver operating characteristic (ROC) analysis. To model inflammation, lipopolysaccharide (LPS)-stimulated human periodontal ligament fibroblasts (hPDLFs) were employed. Subsequently, miR-671-5p mimics or inhibitors were transfected to assess effects on cell viability assessed by CCK-8, cellular migration measured via Transwell assays, and cytokine secretion analyzed using enzyme-linked immunosorbent assay (ELISA). THBS1 targeting by miR-671-5p was validated via dual-luciferase assays.

Results: miR-671-5p expression was significantly reduced in GCF of periodontitis patients, and a strongly correlation was observed with clinical severity indices. ROC analysis revealed high diagnostic accuracy. Furthermore, miR-671-5p levels exhibited an inverse correlation with TNF-α, IL-6, and IL-1β. In LPS-treated hPDLFs, miR-671-5p was associated with a dose-dependent reduction in cell viability and migration, as well as an increase in the production of inflammatory cytokines. miR-671-5p was found to directly target THBS1 mRNA, inhibiting its expression. miR-671-5p overexpression reversed LPS-induced functional impairment and inflammation; these beneficial effects were partially counteracted by THBS1 upregulation.

Conclusions: miR-671-5p holds promise as a potential diagnostic biomarker and therapeutic target in periodontitis by regulating THBS1-mediated inflammatory responses and dysfunction of hPDLFs.