氧化应激在糖尿病相关性牙周炎发病中的作用

在糖尿病相关性牙周炎发病机制的研究中,糖尿病患者中长期慢性的高糖状态可能通过多个途径诱发氧化应激,局部产生大量的活性氧族(ROS),而ROS可改变信号传导通路引起炎症反应因子的基因和蛋白质表达异常,导致机体炎症应答大大增强,促使牙周炎症发生.本文就高血糖诱发氧化应激的可能途径、氧化应激作用机制、抗氧化物在糖尿病相关性牙...     

氧化应激诱发糖尿病性牙周炎作用及机制

糖尿病和牙周炎有双向关系,二者间作用机制尚不清楚。糖尿病长期高糖状态可诱发氧化应激(oxidative stress,OS)反应,产生大量活性氧族(ROS),可通过改变信号传导通路等途径引起炎症因子基因和蛋白质表达异常,导致炎症反应增强,破坏牙周组织。该文从OS诱发糖尿病性牙周炎作用、OS诱发糖尿病性牙周炎机制、抗氧化物治疗及前景等方面进行研究,为糖尿病性牙周炎治疗和研究提供依据。     

透明质酸在慢性牙周炎治疗中的作用

目的　观察局部应用外源性透明质酸(HA)对慢性牙周炎的临床疗效。方法　采用口内自身对照的研究方法。选择20例慢性牙周炎患者的患牙306颗,其中150颗患牙为对照组,156颗为实验组。对照组患牙仅作洁刮治和根面平整(SRP)。实验组患牙在行SRP后,龈下辅助给予0·2%透明质酸凝胶。观察两组患牙的菌斑指数、龈沟液流速、龈沟出血指数、牙周探诊深度和临床附着水平等临床指标的动态变化。结果　对照组和实验组患牙的各临床指标在治疗后均显著改善,实验组患牙龈沟液流速的下降显著快于对照组(P=0·001),但其余临床指标两组间的差异无显著性。结论　本研究未发现HA结合SRP对治疗慢性牙周炎在牙周组织修复再生中有促进作用; HA能迅速减轻牙周组织的炎症反应。     

氧化应激及抗氧化剂辅助治疗牙周炎的研究进展

牙周炎是由菌斑微生物引起的牙周组织慢性炎症,氧化应激作为机体在有害刺激下产生的氧化还原失衡,能够促进牙周组织破坏,已被证实与牙周炎的发生发展密切相关。使用抗氧化剂作为恢复机体氧化/抗氧化状态平衡的辅助治疗已成为近年来研究热点,本文将对氧化应激及抗氧化剂辅助治疗牙周炎的研究进展作一综述。     

肥胖伴慢性牙周炎患者龈沟液中活性氧的表达水平研究

目的:分析慢性牙周炎联合肥胖患者龈沟液中分泌的活性氧(reactive oxygen species, ROS)的含量。方法:以我院口腔科2021年1月～10月期间的160例就诊患者为研究对象,按照是否合肥胖症和慢性牙周炎对所有患者进行分组。实验组A患者为慢性牙周炎伴肥胖的患者,实验组B患者为单纯慢性牙周炎患者,对照组A患者为牙周及体重均正常的患者,对照组B患者为单纯肥胖的牙周健康者。对各组患者龈沟液中ROS的水平使用ELISA检测。结果:各组患者龈沟液中ROS水平表达具有显著差异,实验组A患者龈沟液中ROS表达水平最高,其次是实验组B,对照组A患者龈沟液中ROS表达含量最低。结论:慢性牙周炎伴肥胖患者牙周组织产生ROS能力增强,可能是肥胖加重慢性牙周炎患者临床表现的一个可能机制。     

中间普氏菌在慢性牙周炎发病中的作用

对中间普氏菌在慢性牙周炎发病中的作用机制进行了综述.中间普氏菌通过向牙周组织黏附和定植、直接侵袭口腔组织细胞、促进炎性细胞因子的释放、干扰宿主免疫反应、促进骨吸收、抑制骨形成等作用而参与牙周炎的发生发展.     

金水宝胶囊在慢性牙周炎中的辅助治疗作用

目的探讨金水宝胶囊在慢性牙周炎治疗中的临床疗效。方法60例慢性牙周炎患者,随机分为2组,牙周基础治疗后,实验组给予金水宝胶囊治疗;对照组不服药,3个月后复查各项牙周指数的变化。结果2组患者服药前,菌斑指数(PLI)、牙周探诊深度(PPD)、附着水平(PAL)无显著性差异(P>0.05),3个月后复查,2组各项牙周指数有显著性差异(P<0.01),实验组症状有明显改善。结论金水宝胶囊对慢性牙周炎有一定治疗作用。     

糖尿病性牙周炎与氧化应激的研究进展

糖尿病性牙周炎是糖尿病的并发症之一,由于糖尿病的存在,使得牙周炎病人牙周组织的破坏程度和病程进展速度都显著增高。近年来,氧化应激在糖尿病并发症中的作用机制日益得到重视,本文拟通过文献回顾对目前氧化应激在糖尿病性牙周炎中的的研究进展作一综述。     

慢性牙周炎与慢性肾脏病

大量研究证据表明,慢性牙周炎与全身系统性疾病存在密切的相关性,其主要通过牙菌斑中的内毒素、炎性介质、细胞因子等随血运到全身诱导各系统疾病。在慢性肾脏病的病因研究方面,也同样有炎性介质、细胞因子等致病因素,慢性肾脏病与慢性牙周炎之间可能存在联系。现就慢性牙周炎与慢性肾脏病之间的相互关系做一概述。     

Oxidative stress in oral diseases

Oxidative species, including reactive oxygen species (ROS), are components of normal cellular metabolism and are required for intracellular processes as varied as proliferation, signal transduction, and apoptosis. In the situation of chronic oxidative stress, however, ROS contribute to various pathophysiologies and are involved in multiple stages of carcinogenesis. In head and neck cancers specifically, many common risk factors contribute to carcinogenesis via ROS‐based mechanisms, including tobacco, areca quid, alcohol, and viruses. Given their widespread influence on the process of carcinogenesis, ROS and their related pathways are attractive targets for intervention. The effects of radiation therapy, a central component of treatment for nearly all head and neck cancers, can also be altered via interfering with oxidative pathways. These pathways are also relevant to the development of many benign oral diseases. In this review, we outline how ROS contribute to pathophysiology with a focus toward head and neck cancers and benign oral diseases, describing potential targets and pathways for intervention that exploit the role of oxidative species in these pathologic processes.     

The effects of chronic periodontitis and rheumatoid arthritis on serum and gingival crevicular fluid total antioxidant/oxidant status and oxidative stress index

Background: Chronic periodontitis (CP) and rheumatoid arthritis (RA) appear to share many pathologic features. Oxygen metabolism has an important role in the pathogenesis of both CP and RA. The aim of this study is to evaluate the relationship between these two chronic inflammatory diseases with regard to antioxidant and oxidant status. Methods: A total of 80 participants were divided into four groups of 20 each: group RA–CP (patients with RA and CP), group RA (periodontally healthy patients with RA), group CP (systemically healthy patients with CP), and group C (periodontally and systemically healthy volunteers) were included in the study. After assessment of periodontal measurements, gingival crevicular fluid (GCF) samples were taken at one incisor, premolar, and molar tooth and stored with serum samples at ?80°C for the antioxidant/oxidant assay. Results: Although all clinical measurements in groups RA–CP and CP were statistically higher compared to those of C and RA groups (P <0.001), there were no differences between CP and RA–CP groups (P >0.05). GCF total oxidant status (TOS) values of CP and RA–CP groups were higher than those of the RA group (P <0.05). GCF oxidative stress index (OSI) values of the RA–CP group were higher than those of the RA group (P <0.05). There were no differences among the groups in terms of serum TOS and OSI values (P >0.05). Conclusions: Local OSI values in groups with patients with CP were higher, whereas systemic OSI values showed no difference among the groups. The presence of RA seems not to affect local and systemic OSI values in patients with CP.     

The impact of smoking status on antioxidant enzyme activity and malondialdehyde levels in chronic periodontitis

Background: The aim of this study is to investigate the impact of smoking status on the systemic and local superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and catalase (CAT) activities and malondialdehyde (MDA) levels in subjects with chronic periodontitis (CP). Methods: Sixty‐five CP patients (23 smokers [CP‐S], 23 former smokers [CP‐FS], and 19 non‐smokers [CP‐NS]) and 20 periodontally healthy non‐smoker controls (PH‐NS) were included in the study. After the clinical measurements, serum and gingival tissue samples were collected. SOD, GSH‐Px, and CAT activities and MDA levels in hemolysates and gingival tissue samples were spectrophotometrically assayed. Results: Blood MDA levels in all the periodontitis groups were higher than in the PH‐NS group but only the difference between CP‐FS and PH‐NS groups was significant (P <0.01). Gingival tissue MDA levels in the periodontitis groups were significantly higher than that in the control group (P <0.01). However, the control group had the highest gingival SOD, GSH‐Px, and CAT activities compared with all the periodontitis groups (P <0.01). The CP‐S group had the highest gingival MDA levels and SOD, GSH‐Px, and CAT activities among the periodontitis groups, whereas the lowest values were observed in the CP‐NS group (P <0.01). The blood and gingival MDA levels in the CP‐FS group were similar in the CP‐NS group, whereas they were lower than in the CP‐S group. Conclusions: Systemic and local MDA levels are increased by smoking in addition to the impact of periodontitis. The decreased local SOD, GSH‐Px, and CAT activities observed in periodontitis patients may increase with smoking.     

Effect of priming in subpopulations of peripheral neutrophils from patients with chronic periodontitis

Background: Patients with periodontal disease are reported to generate more reactive oxygen species (ROS) than matched controls, suggesting increased inflammatory defense activity. The purpose of this study is to determine whether there are subpopulations of peripheral neutrophils in patients with chronic periodontitis (CP) that generate different levels of intracellular ROS when primed with tumor necrosis factor‐α (TNF‐α) or the chemokine interleukin‐8 (IL‐8, CXCL8) compared to controls. Methods: Venous blood was collected from 13 patients with CP despite careful maintenance over 2 to 8 years and from 13 healthy age‐ and sex‐matched controls. Neutrophils were separated from whole blood over a Percoll gradient and then activated via the Fcγ receptor with opsonized Staphylococcus aureus after priming with TNF‐α or IL‐8. The samples were analyzed by flow cytometry using the fluorescent probe dihydrorhodamine 123. Generation of ROS was measured as the intensity of fluorescence (IFL). Results: Two subpopulations were found in both patients and controls: one with low and one with high generation of IFL. The subpopulation with high generation of IFL in patients with CP was more responsive to IL‐8 (P <0.05) than the same subpopulation in healthy controls. No other differences in generation of ROS or priming effects were found between patients with CP and controls. Generation of ROS was dependent on nicotinamide adenine dinucleotide phosphate oxidase, and the intracellular ROS was primarily the oxygen anion. Conclusion: Patients with CP had a subpopulation of peripheral neutrophils that were more responsive to IL‐8 priming than controls.