Radvar Mehrdad, Tavakkol-Afshari Jalil, Bajestan Mahboobeh N, Naseh Mohammad-Reza, Arab Hamid-Reza
Department of Periodontology, School of Dentistry, Mashhad University of Medical Sciences, Mashhad, Iran.
Iran J Immunol. 2008 Jun;5(2):100-6.
Several cytokines, including IL-6 have been implicated in the pathogenesis of periodontal disease. It is established that monocytes from periodontitis subjects show an increased production of IL-6 as compared to healthy subjects. However, little is known about the effect of periodontal treatment on IL-6 production by monocytes in subsets of periodontitis patients.
The aim of the present study was to evaluate the effect of surgical periodontal treatment on IL-6 production of peripheral blood monocytes (PBM) in aggressive periodontitis patients (AP) and chronic periodontitis patients (CP) before and after stimulation by E.coli LPS.
Fifteen AP patients, 15 CP patients and 15 periodontally healthy subjects (PH) took part in the study. PBM IL-6 pro-duction was measured, using ELISA, before and after stimulation of cultured PBM cells by 0.1 microg/ml LPS of E.coli. Following full-mouth non-surgical and surgical periodontal treatment of the AP and CP groups, the same measurements were repeated for these two groups.
LPS-stimulated IL-6 production was significantly greater than non-stimulated IL-6 for all 3 groups. Before periodontal treatment, LPS-stimulated IL-6 pro-duction of the AP group was significantly greater than the other 2 groups. Periodontal treatment did not result in a significant decrease in unstimulated or LPS-stimulated IL-6 production by PBM cells in AP and CP patients. No correlation was detected between IL-6 levels and baseline clinical parameters or changes in clinical parameters.
PBM cells in AP patients might be hyper-responsive in terms of IL-6 production. This hyper-responsiveness does not seem to return to that of healthy subjects even after a successful periodontal treatment. Moreover, the regulation of host inflammatory mechanisms upon LPS challenge might be different between AP and CP patients.
包括白细胞介素-6(IL-6)在内的多种细胞因子与牙周病的发病机制有关。已证实,与健康受试者相比,牙周炎患者的单核细胞产生IL-6的量增加。然而,关于牙周治疗对不同亚组牙周炎患者单核细胞产生IL-6的影响知之甚少。
本研究旨在评估外科牙周治疗对侵袭性牙周炎患者(AP)和慢性牙周炎患者(CP)外周血单核细胞(PBM)在大肠杆菌脂多糖(LPS)刺激前后产生IL-6的影响。
15名AP患者、15名CP患者和15名牙周健康受试者(PH)参与了本研究。在0.1μg/ml大肠杆菌LPS刺激培养的PBM细胞前后,使用酶联免疫吸附测定法(ELISA)测量PBM产生IL-6的量。在对AP组和CP组进行全口非手术和外科牙周治疗后,对这两组重复相同的测量。
所有3组中,LPS刺激后产生的IL-6均显著高于未刺激时产生的IL-6。在牙周治疗前,AP组LPS刺激后产生的IL-6显著高于其他两组。牙周治疗并未使AP和CP患者的PBM细胞在未刺激或LPS刺激下产生的IL-6显著减少。未检测到IL-6水平与基线临床参数或临床参数变化之间的相关性。
AP患者的PBM细胞在产生IL-6方面可能反应过度。即使经过成功的牙周治疗,这种过度反应似乎也不会恢复到健康受试者的水平。此外,AP和CP患者在LPS刺激下宿主炎症机制的调节可能不同。