ArticleBMC oral health2026
LncRNA FAM30A as a potential biomarker associated with periodontitis and its role in inflammatory responses and osteogenesis.
Article in BMC oral health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study investigated the expression patterns of lncRNA FAM30A in periodontitis, evaluated its diagnostic value, and elucidated the underlying molecular mechanisms.
methodsOne 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.
resultsThe 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.
conclusionThe 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.