# Possible Involvement of Leptin in Pathogenesis of Periodontal Disease

**Authors:** Małgorzata Kozak, Agata Poniewierska-Baran, Michał Czerewaty, Karolina Łuczkowska, Małgorzata Mazurek-Mochol, Bogusław Machaliński, Andrzej Pawlik

PMC · DOI: 10.3390/biology14101454 · Biology · 2025-10-20

## TL;DR

This study shows that leptin can increase inflammation in periodontal tissues by affecting the production of certain cytokines in ligament cells.

## Contribution

The study reveals a novel role of leptin in modulating pro-inflammatory cytokine expression in periodontal ligament cells.

## Key findings

- Leptin significantly increased IL-6 and IL-8 expression at both mRNA and protein levels.
- Leptin caused a transient increase in IL-1 expression up to 24 hours.
- Leptin decreased IL-10 mRNA expression after 48 hours but not its protein levels.

## Abstract

Periodontitis involves chronic inflammation of the periodontal tissues, primarily caused by a bacterial infection that triggers an immune system response. Recent studies have highlighted the effect of leptin on periodontal tissues, particularly on fibroblasts of the periodontal ligament. Periodontal ligament fibroblasts form the main cell population within the ligament and are responsible for regulating tissue homeostasis as well as activating the immune system. They secrete numerous pro-inflammatory mediators, cytokines, and chemokines involved in the development of inflammation in periodontal tissues. The periodontal ligament itself can be a source of many pro-inflammatory mediators. The aim of this study was to examine the effect of leptin on periodontal ligament cells and their secretion of selected pro-inflammatory mediators that may contribute to the pathogenesis of periodontal disease. The results of this study suggest that leptin may contribute to the pathogenesis of periodontitis by modulating the expression of certain pro-inflammatory cytokines in periodontal ligament cells.

Periodontitis is a chronic inflammatory condition of the periodontal tissues, ultimately leading to their destruction. The periodontal ligament is a key structure that not only secures the teeth within the alveolus but can also act as a source of numerous mediators involved in the development of inflammation in periodontal tissues. The aim of this study was to investigate the effect of leptin on periodontal ligament cells and their secretion of selected pro-inflammatory mediators that may contribute to the pathogenesis of periodontal disease. The study was conducted on cultured periodontal ligament cells stimulated with leptin. The effect of leptin was assessed on the expression of selected cytokines implicated in the pathogenesis of periodontal disease (IL-1, IL-6, IL-8, IL-10, IL-17, IL-18, and tumour necrosis factor-alpha [TNF-α]) at the mRNA level, as well as on the protein concentrations of these cytokines in culture supernatants. Assessments were carried out after 12, 24, and 48 h of leptin stimulation. The results showed a statistically significant effect of leptin on IL-6 and IL-8 expression at both the mRNA and protein levels. For IL-1, a transient increase in mRNA expression and protein concentration was observed, persisting up to 24 h. A decrease in IL-10 mRNA expression was noted after 48 h of leptin stimulation, with no corresponding effect on IL-10 protein concentration. No significant effect of leptin was found on IL-17 or IL-18 protein concentrations in periodontal ligament cell cultures. These findings suggest that leptin may contribute to the pathogenesis of periodontitis by modulating the expression of certain pro-inflammatory cytokines in periodontal ligament cells.

## Linked entities

- **Proteins:** lepa (leptin a), IL1A (interleukin 1 alpha), IL6 (interleukin 6), CXCL8 (C-X-C motif chemokine ligand 8), IL10 (interleukin 10), IL17A (interleukin 17A), IL18 (interleukin 18)
- **Diseases:** periodontitis (MONDO:0005076)

## Full-text entities

- **Genes:** IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, IL18 (interleukin 18) [NCBI Gene 3606] {aka IGIF, IL-18, IL-1g, IL1F4}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** inflammation (MESH:D007249), Periodontal Disease (MESH:D010510), Periodontitis (MESH:D010518)

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12561792/full.md

## References

38 references — full list in the complete paper: https://tomesphere.com/paper/PMC12561792/full.md

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Source: https://tomesphere.com/paper/PMC12561792