Cross-sectional study demonstrates STAT3 pathway activation in peri-implantitis tissues, highlighting a bacterial mechanism driving mucosal inflammation.
Key Points
To assess STAT3 pathway activation in peri-implantitis tissues and determine how peri-implantitis-associated bacteria affect STAT3 signaling in oral epithelial cells.
Analyzed gingival biopsies from patients with healthy gingiva, periodontitis, and peri-implantitis for pSTAT3/STAT3 ratios, pathway-dependent mRNA, and immunofluorescence-positive cells.
Stimulated oral epithelial cells in vitro with S. sanguinis, P. gingivalis, F. nucleatum, and patient-derived microbial communities, evaluating mRNA expression and the effect of pSTAT3 inhibition.
Peri-implantitis tissues displayed higher pSTAT3/STAT3 ratios, elevated IL6 and SOCS3 mRNA expression, and an increased proportion of pSTAT3-positive epithelial cells relative to healthy and periodontitis tissues.
Stimulation with P. gingivalis and F. nucleatum increased mRNA levels of STAT3-related (IL6, IL23A, SOCS3), chemoattractant (CXCL8, IL36G), and inflammatory (IL1B, TNFA) mediators.
Inhibition of pSTAT3 decreased the mRNA expression of downstream cytokines as well as the neutrophil chemoattractants CXCL8 and IL36G.