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Front Immunol. 2019 Mar 12;10:406. doi: 10.3389/fimmu.2019.00406. eCollection 2019.

Complement-Dependent Mechanisms and Interventions in Periodontal Disease.

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Department of Microbiology, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Division of Pediatric Dentistry, Department of Preventive and Restorative Sciences, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Research Center for Advanced Oral Science, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.
Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Division of Biodiagnostic Sciences and Technologies, National Center for Scientific Research "Demokritos", Athens, Greece.
Amyndas Pharmaceuticals, Glyfada, Greece.
Center for Clinical and Translational Research, Forsyth Institute, Cambridge, MA, United States.


Periodontitis is a prevalent inflammatory disease that leads to the destruction of the tooth-supporting tissues. Current therapies are not effective for all patients and this oral disease continues to be a significant public health and economic burden. Central to periodontal disease pathogenesis is a reciprocally reinforced interplay between microbial dysbiosis and destructive inflammation, suggesting the potential relevance of host-modulation therapies. This review summarizes and discusses clinical observations and pre-clinical intervention studies that collectively suggest that complement is hyperactivated in periodontitis and that its inhibition provides a therapeutic benefit. Specifically, interception of the complement cascade at its central component, C3, using a locally administered small peptidic compound (Cp40/AMY-101) protected non-human primates from induced or naturally occurring periodontitis. These studies indicate that C3-targeted intervention merits investigation as an adjunctive treatment of periodontal disease in humans.


AMY-101; C3; complement; compstatin Cp40; inflammation; periodontitis; primate models; therapeutics

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