Wei Pi-Fen, Ho Kun-Yen, Ho Yea-Pyng, Wu Yi-Min, Yang Yi-Hsin, Tsai Chi-Cheng
Department of Periodontics, Graduate Institute of Dental Sciences, College of Dental Medicine, Kaohsiung Medical University, Taiwan.
J Periodontal Res. 2004 Oct;39(5):287-93. doi: 10.1111/j.1600-0765.2004.00744.x.
Human periodontal diseases are inflammatory disorders that are the result of complex interactions between periodontopathogens and the host's immune response. Two important and interrelated factors are involved in the pathophysiological progression of periodontal diseases, i.e. the activation of immune system and the production of oxygen radicals and their related metabolites. Increased production of oxygen radicals may contribute to oxidative stress, which is reported to be involved in many diseases, including periodontal diseases.
The objective of this study was to investigate glutathione peroxidase, lactoferrin and myeloperoxidase, which play an essential role in free radical production and defenses, and the proinflammatory cytokine interleukin-1beta (IL-1beta), which is important in the regulation of immunological and inflammatory reactions in human periodontal diseases.
Gingival crevicular fluid (GCF) samples were collected from 27 subjects, 19 periodontitis patients and eight healthy controls, ranging in ages from 24 to 62 years. Clinical parameters were recorded. GCF glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta were analyzed by enzyme-linked immunosorbent assays (ELISA).
The periodontitis sites exhibited significantly greater total amount of glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta than healthy sites. Total amount of glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta was positively correlated with plaque index, gingival index, probing depth and probing attachment level (p < 0.05).
The imbalance between the levels of myeloperoxidase/IL-1beta and glutathione peroxidase/lactoferrin could result in tissue damage of reactive oxygen species (ROS) in periodontitis which is initiated and perpetuated by the chronic insults of periodontopathogens.
人类牙周疾病是炎症性疾病，是牙周病原体与宿主免疫反应之间复杂相互作用的结果。牙周疾病的病理生理进展涉及两个重要且相互关联的因素，即免疫系统的激活以及氧自由基及其相关代谢产物的产生。氧自由基产生增加可能导致氧化应激，据报道氧化应激与包括牙周疾病在内的许多疾病有关。
本研究的目的是调查在自由基产生和防御中起重要作用的谷胱甘肽过氧化物酶、乳铁蛋白和髓过氧化物酶，以及在人类牙周疾病免疫和炎症反应调节中起重要作用的促炎细胞因子白细胞介素-1β（IL-1β）。
从27名年龄在24至62岁之间的受试者中采集龈沟液（GCF）样本，其中19名牙周炎患者和8名健康对照。记录临床参数。通过酶联免疫吸附测定（ELISA）分析GCF中的谷胱甘肽过氧化物酶、乳铁蛋白、髓过氧化物酶和IL-1β。
牙周炎部位的谷胱甘肽过氧化物酶、乳铁蛋白、髓过氧化物酶和IL-1β总量显著高于健康部位。谷胱甘肽过氧化物酶、乳铁蛋白、髓过氧化物酶和IL-1β总量与菌斑指数、牙龈指数、探诊深度和探诊附着水平呈正相关（p < 0.05）。
髓过氧化物酶/IL-1β与谷胱甘肽过氧化物酶/乳铁蛋白水平之间的失衡可能导致牙周炎中活性氧（ROS）的组织损伤，这种损伤由牙周病原体的慢性刺激引发并持续存在。
