LncRNA HOTTIP as a potential biomarker of chronic periodontitis and its role in inflammatory responses.

Abstract

Chronic periodontitis (CP) is a prevalent oral condition that can elicit a broad spectrum of inflammatory responses. This study investigates the impact of lncRNA HOTTIP on inflammatory responses of CP via targeting and regulating miR-205-5p. This study involved 117 CP patients and 101 controls. The expression levels of HOTTIP and miR-101-3p in the gingival crevicular fluid (GCF) of CP patients were quantified using qPCR. The levels of inflammatory factors IL-1β, IL-6, IL-10, and TNF-α, were measured through ELISA. ROC analysis was conducted to evaluate the diagnostic efficacy. The LPS-induced hPDLFs injury model was established to investigate the effects of HOTTIP silencing, as well as the concurrent inhibition of HOTTIP and miR-101-3p expression, on cellular functionality and inflammatory responses. HOTTIP was elevated in the GCF of CP patients, whereas miR-101-3p was reduced (P < 0.001). HOTTIP exhibited a positive correlation with inflammatory markers and periodontal indicators (r > 0, P < 0.01). HOTTIP possessed the potential to serve a specific biomarker for the auxiliary diagnosis of CP (AUC = 0.967, P < 0.001), as well as a critical parameter for assessing the periodontal condition of patients. In LPS-induced hPDLFs model, the silencing of HOTTIP was found to enhance cell proliferation (P < 0.01), reduce apoptosis (P < 0.001), and the release of inflammatory factors (P < 0.05). However, the simultaneous inhibition of both HOTTIP and miR-101-3p, this inhibitory effect on inflammatory response was counteracted (P < 0.05). HOTTIP regulated cellular function and the release of inflammatory factors via miR-101-3p, thereby exacerbating the inflammatory response with CP patients. HOTTIP is anticipated to emerge as a promising biomarker for the diagnosis of CP.