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Updated: May 18, 2026

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Complement and dysbiosis in periodontal disease
George Hajishengallis1, John D Lambris
1University of Pennsylvania School of Dental Medicine, Department of Microbiology, Philadelphia, PA 19104, USA. geoh@upenn.edu
Abstract:
Signaling crosstalk between complement and Toll-like receptors (TLRs) normally serves to coordinate host immunity. However, the periodontal bacterium Porphyromonas gingivalis expresses C5 convertase-like enzymatic activity and adeptly exploits complement-TLR crosstalk to subvert host defenses and escape elimination. Intriguingly, this defective immune surveillance leads to the remodeling of the periodontal microbiota to a dysbiotic state that causes inflammatory periodontitis. Understanding the mechanisms by which P. gingivalis modulates complement function to cause dysbiosis offers new targets for complement therapeutics.
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