Porphyromonas gingivalis lipopolysaccharide promotes peri-implant inflammation through neutrophil activation

Peri-implant diseases pose significant challenges to the longevity of titanium-based implants, despite their high survival rates. This study investigated how lipopolysaccharide (LPS) from Porphyromonas gingivalis (P. gingivalis) (P. gingivalis-LPS) as a virulence factor affects neutrophil recruitment and activation surrounding titanium implants to elucidate its potential role in the development of peri-implant inflammation.

Using rat and murine models of titanium implantation, we conducted transcriptomic analysis of peri-implant gingival tissues to identify pathways linked neutrophil activity, particularly in the presence of P. gingivalis-LPS. Flow cytometry was used to validate neutrophil recruitment to the peri-implant mucosa in mice. Human neutrophils were also isolated and stimulated with titanium discs and/or P. gingivalis-LPS to assess their activation and apoptosis.

Transcriptomic data revealed significant upregulation of genes associated with neutrophil chemotaxis and activation in peri-implant tissues treated with P. gingivalis-LPS relative to those in the controls (P < 0.05). Flow cytometry data confirmed increased neutrophil infiltration of the peri-implant tissues in mice (P < 0.01). In vitro assays demonstrated that P. gingivalis-LPS significantly enhanced neutrophil CD11b expression and reactive oxygen species production in human neutrophils exposed to titanium (P < 0.01) but inhibited apoptosis (P < 0.001).

P. gingivalis-derived LPS amplified neutrophil recruitment and prolonged neutrophil activation in the presence of titanium, suggesting a potential mechanism underlying peri-implant inflammation. This highlights the need for targeted strategies to mitigate neutrophil-induced tissue damage in peri-implant diseases.