Abstract

Objective To investigate the diagnostic value and regulatory role of FAM30A in patients with chronic periodontitis (CP). Methods The study included 104 CP patients. Saliva and periodontal ligament tissue samples were stored at -80°C. Logistic regression predicted risk factors for CP. Periodontal ligament stem cells (PDLSCs) were stimulated with 100 ng/mL LPS to establish an in vitro model. RT-qPCR assessed gene expression. CCK-8 and flow cytometry evaluated cell proliferation and apoptosis. ELISA measured inflammatory cytokine expression, while kits quantified oxidative stress products. Dual luciferase reporter assays and RNA immunoprecipitation examined gene-target relationships. Results FAM30A was upregulated in saliva and periodontal ligament tissue from CP patients. FAM30A demonstrated diagnostic value in both sample types and was identified as a risk factor for CP. LPS stimulation increased FAM30A expression in cells. si-FAM30A promoted cell proliferation, reduced apoptosis, and suppressed inflammatory and oxidative stress levels. miR-424-5p was downregulated in CP patients. Furthermore, FAM30A competitively binds miR-424-5p to modulate PDLSCs' function. Transfection with miR inhibitor counteracts si- FAM30A-induced cellular dysfunction and inflammatory responses. Conclusion FAM30A induces CP by targeting miR-424-5p to inhibit PDLSCs proliferation, promote apoptosis, and increase inflammatory and oxidative stress levels.