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Updated: Jun 3, 2026
Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
Published on: February 17, 2023
Effects of P38 MAPK Pathway Inhibition on the Metabolism of Periodontal Ligament Fibroblasts During Inflammation
Cheng Qian1, Yifan Gu2, Feiyan Gao3
1Department of Stomatology, Shaoxing Central Hospital, Zhejiang, China.
Abstract:
During the development of periodontitis, osteoclast function is activated by the MAPK pathway. MMPs are able to participate in cross-activation and self-activation cascades, thereby modulating gene expression for osteoclast differentiation. Among the MAPK family, the p38 family has a particularly significant impact on the development of chronic inflammation in periodontal tissue. Activation of p38 MAPK signalling directly or indirectly mediates the expression of inflammatory cytokines, thereby synergistically stimulating MMP production. This experiment aims to understand how p38 MAPK affects inflammatory hPDLFs treated with Pseudomonas gingivalis. Compared with the control group, secretion of MMP-2, -1, and -3 of hPDLFs treated with P. gingivalis-LPS was significantly increased and was closely related to the concentration of P. gingivalis-LPS. Cell scratching and CCK-8 experiments revealed that MMP-1, -2, and -3 inhibited cell proliferation and motility. To explore the signalling pathways involved in p38 MAPK regulation, hPDLFs were treated with P. gingivalis-LPS alone or in combination with a p38 MAPK kinase inhibitor. The results suggest that MMP-1, -2, and -3 can serve as salivary biomarkers for the chronic inflammatory disease periodontitis and regulate inflammation through the p38 MAP kinase pathway.
Insights
Matrix metalloproteinases (MMPs) are linked to periodontitis inflammation via the p38 MAP kinase pathway. Increased MMP-1, -2, and -3 levels in human periodontal ligament fibroblasts (hPDLFs) correlate with disease severity and inhibit cell function.
Area of Science:
- Periodontology
- Molecular Biology
- Immunology
Background:
- Periodontitis involves osteoclast activation via the MAPK pathway.
- Matrix metalloproteinases (MMPs) modulate osteoclast differentiation and inflammation.
- The p38 MAPK pathway significantly impacts chronic periodontal inflammation.
Purpose of the Study:
- To investigate the role of p38 MAPK in regulating MMP expression in human periodontal ligament fibroblasts (hPDLFs) stimulated by Pseudomonas gingivalis.
- To determine the effect of MMP-1, -2, and -3 on hPDLF proliferation and motility.
- To explore the signalling mechanisms underlying p38 MAPK-mediated MMP regulation.
Main Methods:
- Stimulation of hPDLFs with P. gingivalis-lipopolysaccharide (LPS) and a p38 MAPK kinase inhibitor.
- Quantification of MMP-2, -1, and -3 secretion using ELISA.
- Assessment of cell proliferation and motility using cell scratching and CCK-8 assays.
Main Results:
- P. gingivalis-LPS significantly increased MMP-2, -1, and -3 secretion in hPDLFs in a dose-dependent manner.
- MMP-1, -2, and -3 were found to inhibit hPDLF proliferation and motility.
- p38 MAPK signalling was confirmed to be involved in the regulation of MMP expression.
Conclusions:
- MMP-1, -2, and -3 are upregulated in periodontitis via the p38 MAP kinase pathway.
- These MMPs may play a role in modulating periodontal inflammation and cell function.
- MMP-1, -2, and -3 show potential as salivary biomarkers for periodontitis.
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