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Updated: Jun 11, 2026
Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Complement and periodontitis
1Department of Microbiology and Immunology, University of Louisville School of Dentistry, Loueisville, KY 40292, USA. g0haji01@louisville.edu
Insights
The complement system plays a key role in host defense but can worsen periodontitis when overactivated. Understanding complement pathways is crucial for developing targeted therapies against this inflammatory oral disease.
Area of Science:
- Immunology
- Oral Biology
- Pathogenesis
Background:
- The complement system is vital for host defense but its dysregulation can cause immunopathology.
- Periodontitis is a chronic inflammatory oral disease with systemic health implications.
- Evidence suggests a link between complement system activity and periodontal disease development.
Purpose of the Study:
- To review the evidence connecting the complement system to periodontal inflammation and pathogenesis.
- To explore how complement activation or subversion by bacteria influences periodontitis.
- To identify the precise roles of different complement pathways in periodontitis for therapeutic targeting.
Main Methods:
- Review of clinical and histological observations correlating periodontal inflammation with complement activation.
- Analysis of studies on genetic polymorphisms and deficiencies in complement components related to periodontitis susceptibility.
- Examination of in vitro and animal model data on periodontal bacteria's interaction with the complement cascade.
- Investigation of specific bacterial mechanisms, like those of Porphyromonas gingivalis, in subverting complement signaling.
Main Results:
- A correlation exists between periodontal inflammatory activity and local complement activation.
- Certain genetic variations in complement components are linked to increased periodontitis susceptibility.
- Periodontal bacteria, including Porphyromonas gingivalis, can modulate complement pathways to their advantage.
- P. gingivalis subverts complement receptor 3 and C5a receptor signaling, promoting its survival in inflammatory environments.
Conclusions:
- Complement activation and subversion contribute to periodontal pathogenesis, though not all pathways are detrimental.
- Targeting the complement system for periodontitis therapy requires precise understanding of individual pathway roles.
- Distinguishing between destructive and protective complement functions is essential for effective therapeutic strategies.
Abstract:
Although the complement system is centrally involved in host defense, its overactivation or deregulation (e.g., due to inherent host genetic defects or due to pathogen subversion) may excessively amplify inflammation and contribute to immunopathology. Periodontitis is an oral infection-driven chronic inflammatory disease which exerts a systemic impact on health. This paper reviews evidence linking complement to periodontal inflammation and pathogenesis. Clinical and histological observations show a correlation between periodontal inflammatory activity and local complement activation. Certain genetic polymorphisms or deficiencies in specific complement components appear to predispose to increased susceptibility to periodontitis. Animal model studies and in vitro experiments indicate that periodontal bacteria can either inhibit or activate distinct components of the complement cascade. Porphyromonas gingivalis, a keystone species in periodontitis, subverts complement receptor 3 and C5a anaphylatoxin receptor signaling in ways that promote its adaptive fitness in the presence of non-productive inflammation. Overall, available evidence suggests that complement activation or subversion contributes to periodontal pathogenesis, although not all complement pathways or functions are necessarily destructive. Effective complement-targeted therapeutic intervention in periodontitis would require determining the precise roles of the various inductive or effector complement pathways. This information is essential as it may reveal which specific pathways need to be blocked to counteract microbial evasion and inflammatory pathology or, conversely, kept intact to promote host immunity.
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