# Therapeutic Efficacy of Floating Electrode–Dielectric Barrier Discharge Plasma in Experimental Periodontitis: A Pilot Study

**Authors:** Ruixue Wang, Yesi Xie, Chenhe Liu, Yanan Jing, Xuan Yang, Qiang Sun

PMC · DOI: 10.3390/bioengineering13020211 · Bioengineering · 2026-02-12

## TL;DR

This study shows that a new plasma treatment can reduce inflammation and harmful bacteria in a rat model of periodontitis, improving gum and bone health.

## Contribution

A novel FE-DBD plasma probe is introduced as a potential multifaceted therapy for periodontitis.

## Key findings

- FE-DBD reduced harmful bacteria like Bacteroidota and increased beneficial taxa such as Proteobacteria.
- The treatment suppressed pro-inflammatory genes and increased anti-inflammatory IL-10 expression.
- FE-DBD modulated bone remodeling by altering key gene ratios and reducing osteoclast activity.

## Abstract

Periodontitis is a chronic inflammatory disease characterized by dysbiotic biofilms and host-mediated destruction of periodontal tissues. This study evaluated the efficacy of a novel needle-shaped floating electrode–dielectric barrier discharge (FE-DBD) plasma probe in treating experimental periodontitis. Using a split-mouth design in a rat model of ligature-induced periodontitis, subgingival microbiome changes were analyzed via 16S rRNA sequencing, while gene expression of inflammatory mediators and osteoclastogenic factors was quantified by qRT-PCR. Histopathological evaluation and osteoclast activity were assessed through H&E and TRAP staining, respectively. FE-DBD treatment significantly shifted the subgingival microbiome by reducing pathobionts such as Bacteroidota and Fusobacteriota and increasing health-associated taxa including Proteobacteria and Actinobacteriota. The therapy also exerted immunomodulatory effects by suppressing pro-inflammatory genes (TNF-α, ICAM-1, CCL2) and elevating anti-inflammatory IL-10 expression. Moreover, FE-DBD favorably modulated bone remodeling by downregulating RANK and RANKL, upregulating OPG, and raising the OPG/RANKL ratio 3.72-fold, accompanied by reduced inflammatory infiltration and osteoclast numbers. These findings demonstrate that FE-DBD plasma effectively ameliorates periodontitis by simultaneously targeting pathogenic biofilms, host inflammation, and osteoclastogenesis, highlighting its potential as a multifaceted adjunctive therapy for periodontal disease.

## Linked entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124], ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383], CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347], IL10 (interleukin 10) [NCBI Gene 3586], TNFRSF11A (TNF receptor superfamily member 11a) [NCBI Gene 8792], TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600], BTF3P11 (basic transcription factor 3 pseudogene 11) [NCBI Gene 690]
- **Diseases:** periodontitis (MONDO:0005076)
- **Species:** Bacteroidota (taxon 976), Fusobacteriota (taxon 32066)

## Full-text entities

- **Genes:** Tdrd7 (tudor domain containing 7) [NCBI Gene 85425] {aka Pctaire2bp}, GTF2E1 (general transcription factor IIE subunit 1) [NCBI Gene 2960] {aka FE, TF2E1, TFIIE-A}, Actb (actin, beta) [NCBI Gene 81822] {aka Actx}, Tnfsf11 (TNF superfamily member 11) [NCBI Gene 117516] {aka ODF, OPGL, RANKL, TRANCE}, Tnfrsf11b (TNF receptor superfamily member 11B) [NCBI Gene 25341] {aka Opg}, Ccl2 (C-C motif chemokine ligand 2) [NCBI Gene 24770] {aka MCP-1, MCP1, Scya2, Sigje}, Il10 (interleukin 10) [NCBI Gene 25325] {aka IL10X, If2a}, Acp5 (acid phosphatase 5, tartrate resistant) [NCBI Gene 25732] {aka TTRRAP, Trap}, Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Icam1 (intercellular adhesion molecule 1) [NCBI Gene 25464] {aka CD54, ICAM, RICAM-I}, Il1b (interleukin 1 beta) [NCBI Gene 24494] {aka IL-1F2}
- **Diseases:** periodontal disease (MESH:D010510), hyperplasia (MESH:D006965), infection (MESH:D007239), CAP (MESH:D000067390), health (OMIM:603663), gingival epithelial hyperplasia (MESH:D017573), alveolar bone loss (MESH:D016301), bone loss (MESH:D001847), oral dysbiosis (MESH:D064806), Inflammatory (MESH:D007249), Periodontitis (MESH:D010518), injury to (MESH:D014947)
- **Chemicals:** eosin (MESH:D004801), argon (MESH:D001128), formalin (MESH:D005557), SYBR Green (MESH:C098022), agarose (MESH:D012685), OH (MESH:C031356), LPS (MESH:D008070), chloroform (MESH:D002725), epoxy resin (MESH:D004853), H&amp;E (MESH:D006371), CAP (-), hematoxylin (MESH:D006416), PCB (MESH:D011078), hydroxyl radical (MESH:D017665), nitric oxide (MESH:D009569), chloral hydrate (MESH:D002697), water (MESH:D014867), TRIzol (MESH:C411644), FE (MESH:D007501), N2 (MESH:D009584), EDTA (MESH:D004492), DBD (MESH:C036010), paraffin (MESH:D010232), sulfate (MESH:D013431), O2 (MESH:D010100)
- **Species:** Bacillota (clostridial firmicutes, phylum) [taxon 1239], Fusobacterium nucleatum (species) [taxon 851], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], Desulfovibrionaceae (family) [taxon 194924], Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606], Porphyromonas gingivalis (species) [taxon 837], Fusobacteriota (phylum) [taxon 32066], Actinomycetota (actinobacteria, phylum) [taxon 201174], Pseudomonadota (proteobacteria, phylum) [taxon 1224], Mus musculus (house mouse, species) [taxon 10090], Aggregatibacter actinomycetemcomitans (species) [taxon 714]
- **Cell lines:** AP221-02 — Homo sapiens (Human), Finite cell line (CVCL_ZY23)

## Full text

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## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12938390/full.md

## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938390/full.md

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Source: https://tomesphere.com/paper/PMC12938390