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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.

Author information

1
Department of Microbiology, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA, United States.
2
Division of Pediatric Dentistry, Department of Preventive and Restorative Sciences, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA, United States.
3
Research Center for Advanced Oral Science, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.
4
Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
5
Division of Biodiagnostic Sciences and Technologies, National Center for Scientific Research "Demokritos", Athens, Greece.
6
Amyndas Pharmaceuticals, Glyfada, Greece.
7
Center for Clinical and Translational Research, Forsyth Institute, Cambridge, MA, United States.

Abstract

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.

KEYWORDS:

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

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