Effects of P38 MAPK Pathway Inhibition on the Metabolism of Periodontal Ligament Fibroblasts During Inflammation.

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.