Abstract
OBJECTIVE: Peri-implantitis (PI) is the primary cause of implant failure. Long noncoding RNA MIR31HG is highly expressed in PI. This study aims to investigate the clinical value and potential regulatory mechanisms of MIR31HG in PI. METHODS: The study included 112 patients with PI. RT-qPCR assessed MIR31HG and miR-641 expression levels in patients and cells; it also evaluated the mRNA expression of inflammatory factors TNF-α, IL-6, IL-1β and osteogenic markers ALP, OCN and OPN in cells. Cell proliferation capacity was evaluated using the CCK-8 assay. Apoptosis was detected via flow cytometry. The DLR assay examined the binding relationship between MIR31HG and miR-641. Logistic regression analysed independent factors influencing PI prognosis. GO and KEGG analyses identified potential signaling pathways involving miR-641 target genes. RESULTS: MIR31HG expression was significantly upregulated in PI patients, while miR-641 was downregulated. MIR31HG also serves as a risk factor for poor prognosis in PI patients. MIR31HG negatively regulates miR-641 expression. Following MIR31HG knockdown, miR-641 expression increased, leading to reduced apoptosis, enhanced proliferation, decreased inflammatory factor levels and markedly elevated levels of osteogenic differentiation biomarkers. Inversely, inhibition of miR-641 significantly reversed these changes. miR-641 target genes may participate in mTOR and Ras signaling pathways to influence PI progression. CONCLUSION: MIR31HG modulates gingival mesenchymal stem cells (GMSC) inflammation and osteogenic differentiation by regulating miR-641 levels, thereby participating in the pathogenesis and progression of PI. MIR31HG holds promise as a clinical diagnostic and prognostic biomarker for PI patients and may serve as a molecular-level therapeutic target for PI management.