MIR31HG Promotes the Onset and Progression of Peri-Implantitis by Regulating the miR-641 Levels

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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