Güllü Cigdem, Ozmeric Nurdan, Tokman Benay, Elgün Serenay, Balos Köksal
Department of Periodontology, Faculty of Dentistry, Gazi University, Ankara, Turkey.
J Periodontal Res. 2005 Apr;40(2):168-75. doi: 10.1111/j.1600-0765.2005.00784.x.
Nitric oxide (NO) is synthesized from the conversion of L-arginine to L-citrulline by NO synthase (NOS). Arginase, which is an arginine-depleting enzyme, can compete with NOS for the common substrate L-arginine and thus inhibit NO production.
In the present study, we aimed to examine the correlation between the arginase and NOS activity in patients with chronic periodontitis and to compare the effects of scaling and root planing and modified Widman flap procedures on enzyme activity.
The study included 13 patients diagnosed with chronic periodontitis. Using a split-mouth design, the defects showing>or=7 mm of attachment loss were treated either with scaling and root planing or with modified Widman flap. Gingival biopsies from both sites were obtained at baseline and 2 months after periodontal treatment. Immunohistochemical staining was performed for evaluating NOS expression and specific arginase activity was determined spectrophotometrically.
Although inflamed periodontal tissues demonstrated a strong inducible NOS (iNOS) expression at baseline, immunostaining decreased after periodontal treatment. iNOS expression intensity and the number of inflammatory cells showing iNOS expression were found to be higher in the scaling and root planing group compared to the modified Widman flap group. The specific activity of arginase was measured as 0.18+/-0.07 IU/mg protein in the modified Widman flap group and 0.25+/-0.11 IU/mg protein in the scaling and root planing group at baseline. After periodontal therapy, the enzyme level was increased to 0.68+/-0.14 IU/mg protein in the modified Widman flap and to 1.10+/-0.23 IU/mg protein in the scaling and root planing group.
This study was the first report of evaluating the involvement of the arginine-NO pathway in chronic periodontitis and this might be considered to be of value in understanding the periodontal disease mechanisms.
一氧化氮（NO）由一氧化氮合酶（NOS）催化L-精氨酸转化为L-瓜氨酸合成。精氨酸酶是一种消耗精氨酸的酶，它可与NOS竞争共同底物L-精氨酸，从而抑制NO的产生。
在本研究中，我们旨在检测慢性牙周炎患者精氨酸酶与NOS活性之间的相关性，并比较龈下刮治术和改良Widman瓣手术对酶活性的影响。
本研究纳入13例诊断为慢性牙周炎的患者。采用自身对照设计，附着丧失≥7mm的患牙分别接受龈下刮治术或改良Widman瓣手术治疗。在基线及牙周治疗后2个月时，从两处取材进行牙龈活检。采用免疫组织化学染色评估NOS表达，并通过分光光度法测定精氨酸酶的比活性。
虽然炎症牙周组织在基线时显示出强烈的诱导型NOS（iNOS）表达，但牙周治疗后免疫染色减弱。与改良Widman瓣组相比，龈下刮治术组iNOS表达强度及显示iNOS表达的炎症细胞数量更高。基线时，改良Widman瓣组精氨酸酶比活性为0.18±0.07IU/mg蛋白，龈下刮治术组为0.25±0.11IU/mg蛋白。牙周治疗后，改良Widman瓣组酶水平升至0.68±0.14IU/mg蛋白，龈下刮治术组升至1.10±0.23IU/mg蛋白。
本研究首次报道了评估精氨酸-NO途径在慢性牙周炎中的作用，这可能对理解牙周疾病机制具有重要意义。
