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Background <p>This study investigated the expression patterns of lncRNA FAM30A in periodontitis, evaluated its diagnostic value, and elucidated the underlying molecular mechanisms.</p> Methods <p>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 <i>Porphyromonas gingivalis (P. g)</i>-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.</p> Results <p>The FAM30A levels rose significantly in GCF of periodontitis patients and in <i>P.g</i>-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 <i>P.g</i>-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.</p> Conclusion <p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月13日

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  • Yongbiao Huo,
  • Limin Liu,
  • Cancan Fan,
  • Jieyi Chen,
  • Haijing Gu

摘要

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.