Periodontitis is a highly prevalent disease. As it progresses, it causes serious morbidity in the form of periodontal abscesses and tooth loss and, in the latter stages, pain. It is also now known that periodontitis is strongly associated with several nonoral diseases. Thus, patients with periodontitis are at greater risk for the development and/or exacerbation of diabetes, chronic obstructive pulmonary disease, and cardiovascular diseases, among other conditions. Although it is without question that specific groups of oral bacteria which populate dental plaque play a causative role in the development of periodontitis, it is now thought that once this disease has been triggered, other factors play an equal, and possibly more important, role in its progression, particularly in severe cases or in cases that prove difficult to treat. In this regard, we allude to the host response, specifically the notion that the host, once infected with oral periodontal pathogenic bacteria, will mount a defense response mediated largely through the innate immune system. The most abundant cell type of the innate immune system – polymorphonuclear neutrophils – can, when protecting the host from microbial invasion, mount a response that includes upregulation of proinflammatory cytokines, matrix metalloproteinases, and reactive oxygen species, all of which then contribute to the tissue damage and loss of teeth commonly associated with periodontitis. Of the mechanisms referred to here, we suggest that upregulation of reactive oxygen species might play one of the most important roles in the establishment and progression of periodontitis (as well as in other diseases of inflammation) through the development of oxidative stress. In this overview, we discuss both innate and epigenetic factors (eg, diabetes, smoking) that lead to the development of oxidative stress. This oxidative stress then provides an environment conducive to the destructive processes observed in periodontitis. Therefore, we shall describe some of the fundamental characteristics of oxidative stress and its effects on the periodontium, discuss the diseases and other factors that cause oxidative stress, and, finally, review potentially novel therapeutic approaches for the management (and possibly even the reversal) of periodontitis, which rely on the use of therapies, such as resveratrol and other antioxidants, that provide increased antioxidant activity in the host.

中文翻译：

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牙周炎是一种氧化应激的炎性疾病：我们应该这样治疗。

牙周炎是一种高度流行的疾病。随着疾病的发展，它会以牙周脓肿和牙齿脱落的形式引起严重的发病，并在随后的阶段引起疼痛。现在还知道，牙周炎与几种非口腔疾病密切相关。因此，患有牙周炎的患者更有可能患上糖尿病，慢性阻塞性肺疾病和心血管疾病等疾病，并/或加重病情。尽管毫无疑问，牙菌斑中特定的口腔细菌群在牙周炎的发展中起着致病作用，但现在人们认为，一旦引发这种疾病，其他因素就在牙周炎中起着同等甚至更重要的作用。其进展，特别是在严重病例或证明难以治疗的病例中。在这方面，我们提到宿主反应，特别是这样的观念，即宿主一旦感染了口腔牙周病原菌，就会发出主要通过先天免疫系统介导的防御反应。当保护宿主免受微生物侵袭时，先天性免疫系统中最丰富的细胞类型-多形核中性粒细胞-可以引起包括促炎性细胞因子，基质金属蛋白酶和活性氧物种上调的应答，所有这些都有助于组织通常与牙周炎有关的牙齿损伤和脱落。在这里提到的机制中，我们建议，通过氧化应激的发展，活性氧的上调可能在牙周炎（以及其他炎症疾病）的建立和发展中起着最重要的作用。在本概述中，我们讨论了导致氧化应激发展的先天和表观遗传因素（例如糖尿病，吸烟）。然后，该氧化应激提供了有利于在牙周炎中观察到的破坏性过程的环境。因此，我们将描述氧化应激的一些基本特征及其对牙周膜的影响，讨论引起氧化应激的疾病和其他因素，最后，回顾潜在的新颖治疗方法（甚至可能逆转）牙周炎