Gayathri G, Muthukumar S, Joseph Leena Dennis, Suresh R
Department of Periodontics, Sri Ramachandra Medical College, Chennai, Tamil Nadu, India.
Indian J Dent Res. 2014 Sep-Oct;25(5):567-71. doi: 10.4103/0970-9290.147080.
Chronic periodontitis is an inflammatory condition of supporting tissues initiated by organisms in dental plaque. The reactive oxygen species and free radicals mediate connective tissue destruction in periodontitis. In order to counteract the free radical mediated tissue damage, numerous antioxidant mechanisms exist within the host. One such system is heme oxygenase enzymes. Heme oxygenase is the key enzyme involved in catabolism of heme. It cleaves the heme molecule to yield equimolar amounts of biliverdin, carbon monoxide, and iron. These end products act as important scavengers of reactive oxygen metabolites. Increased heme oxygenase expression has been identified in inflammatory condition, such as pancreatitis, diabetes, nephritis, and atherosclerosis. Since chronic periodontitis is one such inflammatory condition, we assessed the expression of heme oxygenase-1, in smokers and periodontitis group using immunohistochemistry technique.
The aim of this study is to compare the expression of heme oxygenase-1 in patients with healthy periodontium, periodontitis and smokers.
Gingival tissue samples were taken from 30 patients, who were divided into three groups healthy controls (n = 10), chronic periodontitis (n = 10), and smokers with chronic periodontitis (n = 10). All the samples were subjected to immunohistochemical staining using the antiheme oxygenase-1 antibody and were tested for efficiency by staining a positive control (prostate cancer tissue sections) and a negative control. The results were tabulated and analyzed.
Our results showed increased expression of heme oxygenase-1 in the gingival tissue samples taken from smokers compared with periodontitis and healthy tissue.
The results of our study is an increasing evidence of involvement of antioxidant enzymes like heme oxygenase-1 in periodontal inflammation and their implication for treatment of chronic periodontitis.
慢性牙周炎是一种由牙菌斑中的微生物引发的支持组织炎症性疾病。活性氧物种和自由基介导牙周炎中的结缔组织破坏。为了对抗自由基介导的组织损伤,宿主体内存在多种抗氧化机制。其中一个系统是血红素加氧酶。血红素加氧酶是血红素分解代谢的关键酶。它裂解血红素分子,产生等摩尔量的胆绿素、一氧化碳和铁。这些终产物作为活性氧代谢物的重要清除剂。在胰腺炎、糖尿病、肾炎和动脉粥样硬化等炎症性疾病中,已发现血红素加氧酶表达增加。由于慢性牙周炎是此类炎症性疾病之一,我们使用免疫组织化学技术评估了吸烟者和牙周炎组中血红素加氧酶-1的表达。
本研究的目的是比较健康牙周组织、牙周炎患者和吸烟者中血红素加氧酶-1的表达。
从30名患者中采集牙龈组织样本,这些患者被分为三组:健康对照组(n = 10)、慢性牙周炎组(n = 10)和患有慢性牙周炎的吸烟者组(n = 10)。所有样本均使用抗血红素加氧酶-1抗体进行免疫组织化学染色,并通过对阳性对照(前列腺癌组织切片)和阴性对照进行染色来检测效率。结果进行列表并分析。
我们的结果显示,与牙周炎组织和健康组织相比,从吸烟者采集的牙龈组织样本中血红素加氧酶-1的表达增加。
我们的研究结果越来越证明抗氧化酶如血红素加氧酶-1参与牙周炎症及其对慢性牙周炎治疗的意义。