# Platelet-rich plasma promotes cellular recovery from nicotine-induced toxicity via autophagy modulation

**Authors:** Julie Vérièpe-Salerno, José Antonio Cancela, Solange Vischer, Antoine Turzi, Muriel Cuendet, Catherine Giannopoulou, Sarah Berndt

PMC · DOI: 10.1038/s41598-026-38188-1 · Scientific Reports · 2026-02-09

## TL;DR

Platelet-rich plasma (PRP) can reverse nicotine's harmful effects on gum cells by modulating autophagy, offering a potential treatment for periodontitis in smokers.

## Contribution

This study demonstrates PRP's ability to counteract nicotine-induced cellular damage via autophagy modulation in gingival fibroblasts.

## Key findings

- PRP reversed nicotine-induced cellular senescence and autophagy in gingival fibroblasts.
- PRP reduced nicotine-induced autophagy in Caenorhabditis elegans.
- PRP modulated autophagy-related cytokines in the fibroblast secretome.

## Abstract

Chronic exposure to nicotine significantly exacerbates periodontitis, a prevalent inflammatory disease, by inducing cellular processes such as autophagy and inflammation in gingival fibroblasts. Current therapies often fail to fully address these cellular alterations in smokers, highlighting a need for innovative therapeutic and regenerative approaches. This study explores the therapeutic potential of Platelet-Rich Plasma (PRP), a blood-derived product, to modulate nicotine-induced biological activities in primary gingival fibroblasts, particularly in the case of periodontitis in smokers. Gingival fibroblasts were treated with increasing concentrations of nicotine, which led to senescence and autophagy. Nicotine at high concentrations triggered cellular vacuolization, and a decrease in metabolism, viability and proliferation. Concomitant cell treatment with 10% PRP reversed nicotine effects and significantly increased cell migration potential. In Caenorhabditis elegans, PRP reduced the nicotine-induced autophagic activity. A screening of the gingival fibroblast secretome revealed a modulation of autophagy-related cytokines in response to nicotine and/or PRP. The findings demonstrate that PRP could effectively inhibit nicotine-induced autophagy in gingival fibroblasts, offering insights into its possible use as a therapeutic tool for managing periodontitis in smokers. The study underscores the potential of PRP in altering disease progression by modulating key cellular processes affected by smoking.

## Linked entities

- **Chemicals:** nicotine (PubChem CID 942)
- **Diseases:** periodontitis (MONDO:0005076)
- **Species:** Caenorhabditis elegans (taxon 6239)

## Full-text entities

- **Diseases:** periodontitis (MESH:D010518), toxicity (MESH:D064420), inflammation (MESH:D007249)
- **Chemicals:** Nicotine (MESH:D009538)
- **Species:** Caenorhabditis elegans (species) [taxon 6239]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12957464/full.md

## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12957464/full.md

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Source: https://tomesphere.com/paper/PMC12957464