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.
Front Immunol. 2019 Mar 12;10:406. doi: 10.3389/fimmu.2019.00406. eCollection 2019.
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.
牙周炎是一种常见的炎症性疾病，可导致牙齿支持组织的破坏。目前的治疗方法并非对所有患者都有效，这种口腔疾病仍然是一个重大的公共卫生和经济负担。牙周病发病机制的核心是微生物失调和破坏性炎症之间的相互增强的相互作用，这表明宿主调节疗法具有潜在的相关性。本综述总结和讨论了临床观察和临床前干预研究，这些研究共同表明，补体在牙周炎中过度激活，抑制补体可提供治疗益处。具体来说，使用局部给予的小肽化合物（Cp40/AMY-101）阻断补体级联反应的中心成分 C3，可保护非人类灵长类动物免受诱导或自然发生的牙周炎的侵害。这些研究表明，C3 靶向干预值得作为人类牙周病的辅助治疗进行研究。
