LncRNA FAM30A as a potential biomarker associated with periodontitis and its role in inflammatory responses and osteogenesis

lncRNA FAM30A 作为牙周炎的潜在生物标志物及其在炎症反应和成骨作用中的作用

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Abstract

BACKGROUND: This study investigated the expression patterns of lncRNA FAM30A in periodontitis, evaluated its diagnostic value, and elucidated the underlying molecular mechanisms. METHODS: One hundred eight patients with periodontitis and 100 controls were enrolled. An in vitro model was established by stimulating human periodontal ligament cells (hPDLCs) with Porphyromonas gingivalis (P. g)-LPS. The expression levels of FAM30A in gingival crevicular fluid (GCF) and hPDLCs were quantified by RT-qPCR. ROC analysis assessed diagnostic accuracy, logistic regression pinpointed risk factors for stage III/IV periodontitis, and ELISA measured levels of inflammatory cytokines and MMP-1/MMP-3Cell viability and apoptosis were assessed by CCK-8 and flow cytometry. Osteogenic marker expression was quantified by RT-qPCR. The interaction among FAM30A, miR-28-5p, and KAT6A was confirmed using RIP and DLR assays. RESULTS: The FAM30A levels rose significantly in GCF of periodontitis patients and in P.g-LPS-stimulated hPDLCs, while miR-28-5p expression dropped markedly. Elevated FAM30A improves periodontitis diagnosis (sensitivity 82.41%, specificity 96.00%). Its levels are higher in Stage III/IV periodontitis and independently predict periodontitis progression. Functionally, FAM30A knockdown attenuated P.g-LPS-induced inflammatory cytokine release, increased hPDLC apoptosis, suppressed osteogenic markers, and elevated MMP-1/MMP-3 secretion. These effects were partially reversed by miR-28-5p inhibition. Mechanistically, miR-28-5p targets FAM30A and KAT6A. CONCLUSION: The present study first demonstrates that FAM30A is a promising diagnostic biomarker, which is strongly linked to periodontitis staging (Stage I/II vs. Stage III/IV) and thus offers a new approach for clinical diagnosis. Additionally, silencing FAM30A may alleviate the progression of periodontitis by regulating the miR-28-5p/KAT6A axis, reducing inflammation, and promoting bone formation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12903-026-08033-y.

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