# Contrasting biological responses of gingival fibroblasts and keratinocyte to blue and violet light irradiation: implications for photobiomodulation use in the therapeutic management of periodontal disease

**Authors:** Edward Gait-Carr, Monique Stoffels, Matthias Born, Haripriya Ramasamy, Ryan Moseley, Rachel J Waddington

PMC · DOI: 10.1007/s10103-026-04817-4 · Lasers in Medical Science · 2026-02-28

## TL;DR

This study explores how blue and violet light affect oral cells, finding that blue light has minimal harmful effects and may be useful for periodontal disease treatment.

## Contribution

The study provides new insights into the differential biological responses of gingival fibroblasts and keratinocytes to blue and violet light irradiation.

## Key findings

- Blue light irradiation caused minor reductions in fibroblast viability but enhanced keratinocyte activity.
- Blue light induced ROS production, which was inhibited by N-acetylcysteine.
- No significant changes in antioxidant gene or protein levels were observed after blue light treatment.

## Abstract

Blue light is known to possess anti-microbial activity and has subsequently been proposed as a prophylactic treatment for the management of periodontal diseases. This study investigated the effect of blue light on cells from the soft gingival tissues within the oral cavity, with particular focus on its influence on the regulation of intracellular reactive oxygen species (ROS) production. Primary human gingival fibroblasts (pHGFs) and keratinocytes (pHGKs) were irradiated with either 457nm blue light or with 415nm violet light, with fluences 3–90 J/cm2 and cell viability was assessed. The influence of blue light on ROS production was measured using 2’,7’-dichlorodihydrofluorescein diacetate assay, in the presence and absence of ROS scavenger, N-acetylcysteine. Gene expression for a range of antioxidant genes was quantified and expression changes evaluated by western blot analysis. Following irradiation with blue light, pHGFs displayed minor reductions in cell viability across the fluence range, while pHGK proliferation and metabolic activity was enhanced following irradiation. Significant cytotoxic effects were seen in cells irradiated with violet light. Treatment of pHGFs with blue light induced significant ROS generation, which was inhibited by N-acetylcysteine. Only non-significant increases in antioxidant gene expression were identified for NQO1, GSR, GSS and KEAP1, in response to 36 and 60 J/cm2 doses. No corresponding changes in their corresponding protein levels were evident. Irradiation of gingival cells with 457 nm blue light produced negligible detrimental effects. Although ROS increased, this paper discusses how endogenous antioxidant defence mechanisms are sufficient to control any potential detrimental effects.

## Linked entities

- **Genes:** NQO1 (NAD(P)H quinone dehydrogenase 1) [NCBI Gene 1728], GSR (glutathione-disulfide reductase) [NCBI Gene 2936], GSS (glutathione synthetase) [NCBI Gene 2937], KEAP1 (kelch like ECH associated protein 1) [NCBI Gene 9817]
- **Chemicals:** N-acetylcysteine (PubChem CID 12035)
- **Diseases:** periodontal disease (MONDO:0002635)

## Full-text entities

- **Genes:** OPHN1 (oligophrenin 1) [NCBI Gene 4983] {aka ARHGAP41, MRX60, MRXSBL, OPN1}, SOD3 (superoxide dismutase 3) [NCBI Gene 6649] {aka EC-SOD}, NQO1 (NAD(P)H quinone dehydrogenase 1) [NCBI Gene 1728] {aka DHQU, DIA4, DTD, NMOR1, NMORI, QR1}, GSR (glutathione-disulfide reductase) [NCBI Gene 2936] {aka CNSHA10, GR, GSRD, HEL-75, HEL-S-122m}, SOD2 (superoxide dismutase 2) [NCBI Gene 6648] {aka GC1, GClnc1, IPO-B, IPOB, MNSOD, MVCD6}, POTEF (POTE ankyrin domain family member F) [NCBI Gene 728378] {aka A26C1B, POTE2alpha, POTEACTIN}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, CAT (catalase) [NCBI Gene 847], NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, KEAP1 (kelch like ECH associated protein 1) [NCBI Gene 9817] {aka INrf2, KLHL19}, OPN3 (opsin 3) [NCBI Gene 23596] {aka ECPN, PPP1R116}, GSS (glutathione synthetase) [NCBI Gene 2937] {aka CNSHA6, GSHS, HEL-S-64p, HEL-S-88n}
- **Diseases:** actinic keratosis (MESH:D055623), inflammation (MESH:D007249), fibrosis (MESH:D005355), mitochondrial (MESH:D028361), psoriasis (MESH:D011565), cutaneous infections (MESH:D007239), Cytotoxicity (MESH:D064420), acne (MESH:D000152), periodontal disease (MESH:D010510), necrosis (MESH:D009336)
- **Chemicals:** streptomycin sulphate (MESH:D013307), 2',7'-dichlorodihydrofluorescein diacetate (MESH:C110400), flavins (MESH:D005415), metal (MESH:D008670), FAM (MESH:C031179), Sodium Chloride (MESH:D012965), SDS (MESH:D012967), acrylamide (MESH:D020106), nitric oxide (MESH:D009569), penicillin G sodium (MESH:D010400), sulfhydryl (MESH:D013438), amphotericin (MESH:D000666), GSSG (MESH:D019803), porphyrin (MESH:D011166), O2.- (MESH:D013481), 2',7'-dichlrorodihydrofluorescein diacetate (-), aluminium (MESH:D000535), lipofuscin (MESH:D008062), Tween 20 (MESH:D011136), N-acetylcysteine (MESH:D000111), ROS (MESH:D017382), Alamar Blue (MESH:C005843), CO2 (MESH:D002245), GSH (MESH:D005978), lipids (MESH:D008055), cysteine (MESH:D003545)
- **Species:** Homo sapiens (human, species) [taxon 9606], Enterococcus sp. gc (species) [taxon 381636]
- **Mutations:** A 240 V
- **Cell lines:** fibroblasts — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0594)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12948868/full.md

## References

18 references — full list in the complete paper: https://tomesphere.com/paper/PMC12948868/full.md

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Source: https://tomesphere.com/paper/PMC12948868