Ⅱ型糖尿病牙周炎及牙周基础治疗对其影响的现状研究

Ⅱ型糖尿病是引起慢性牙周炎的主要危险因素之一,慢性牙周炎增加了Ⅱ型糖尿病的患病风险,但至今为止糖尿病牙周炎的发病机制尚未明确。牙周基础治疗不仅可以改善牙周炎患者的牙周状况,而且在一定程度上改善了糖尿病牙周炎患者的血糖状况。随着分子生物学技术的不断发展,研究人员对糖尿病牙周炎疾病在微生物、免疫及炎症因子方面的研究不断深入,该文对糖尿病牙周炎的微生物指标,免疫、炎症因子指标,临床指标及牙周基础治疗对疾病的影响做一综述。     

牙周基础治疗对2型糖尿病伴慢性牙周炎患者龈沟液丝氨酸蛋白酶抑制剂和肿瘤坏死因子-α水平的影响

目的 观察牙周基础治疗对2型糖尿病伴发或不伴发慢性牙周炎患者龈沟液(gingival crevicular flu-id,GCF)丝氨酸蛋白酶抑制剂(vaspin)和肿瘤坏死因子-α(TNF-α)水平的影响.方法 本研究包含60个研究对象,分为4组:15例2型糖尿病伴发慢性牙周炎患者为DM-CP组;15例慢性牙周炎不伴发2型糖尿病患者为CP组;15例牙周健康的2型糖尿病患者为DM组;15例牙周及全身系统均健康的个体为CTRL组.治疗前与牙周基础治疗8周后取样GCF并检测牙周临床指标.通过ELISA法检测GCF样本中vaspin和TNF-α的水平.结果 治疗前慢性牙周炎组GCF中vaspin和TNF-α水平显著高于牙周健康组(P<0.05),治疗后慢性牙周炎组GCF中vaspin和TNF-α水平显著降低(P<0.05).各组vaspin总量与TNF-α总量、糖化血红蛋白水平、牙龈指数以及探诊深度在统计学上存在正相关关系(P<0.05).结论 牙周基础治疗能明显降低慢性牙周炎患者GCF中vaspin和TNF-α的水平.提示GCF中vaspin和TNF-α可作为糖尿病、牙周炎诊断及其预后的炎性标志物.     

糖尿病患者牙周非手术治疗对血糖水平的影响

目的　探讨牙周非手术治疗对糖尿病患者牙周炎症控制及血糖水平的影响。方法　从83例胰岛素非依赖性糖尿病牙周炎患者中选出代谢控制不良的 31例 ,行牙周非手术治疗 ,测量并比较术前、术后 4、8周的探诊出血、探诊深度及糖化血红蛋白水平。结果　所有患者治疗后探诊出血、探诊深度明显减少。重度牙周炎患者糖化血红蛋白从 ( 9 86± 2 1 0 ) %降低为 ( 8 77± 1 62 ) % ,差异有显著性 (P <0 0 1 ) ;中轻度牙周炎患者糖化血红蛋白的变化差异无显著性 (P >0 0 5)。结论　糖尿病患者牙周炎症控制能在一定程度上改善代谢水平 ,但改善的效果可能与治疗前血糖水平和牙周状况有关     

牙周基础治疗对糖尿病患者血糖控制的影响

目的:研究依赖胰岛素治疗的糖尿病伴牙周炎患者经牙周基础治疗后,对患者空腹血糖、血脂和TNF- α的影响.方法:选择依赖胰岛素治疗的糖尿病伴牙周炎患者40 例,随机分为牙周基础治疗组和对照组,分析治疗前及治疗后4 周、3、6 个月的牙周临床指标、空腹血糖、血脂以及糖化血红蛋白(HbA1c)、肿瘤坏死因子(TNF- α)的水平.结果:牙周基础治疗组经治疗后患者的HbA1c、TNF- α、总胆固醇、甘油三脂及空腹血糖水平较治疗前均有明显降低,与对照组比较相差显著.结论:糖尿病伴牙周炎患者行牙周基础治疗有助于其血糖控制.     

牙周基础治疗对动脉硬化患者血清炎症因子和血脂水平的影响

目的 比较颈动脉粥样硬化合并牙周炎的患者牙周基础治疗前、后血清炎症因子和血脂水平的变化,探讨牙周炎与动脉粥样硬化乃至冠心病间的关系,及牙周干预治疗对动脉粥样硬化患者病情发展的影响.方法 纳入体检中心彩超检查有颈动脉粥样硬化合并牙周炎患者32例,选取单纯牙周炎患者31例,实施牙周基础治疗.治疗前和治疗后3个月,分别对2组患者的血清c反应蛋白、总胆固醇、低密度脂蛋白水平进行检测、比较.结果 动脉粥样硬化伴牙周炎患者治疗前后血清炎症因子、脂质水平改变有显著差异(P<0.05),单纯牙周病组治疗前、后血清炎症因子水平改变有显著差异(P<0.05),血脂水平无明显改变.2组各自治疗前、后的牙周指标对照有明显改善.结论 慢性牙周炎基础治疗可改善牙龈、牙周局部炎症状态,降低血清炎症及动脉硬化患者血脂水平,有利于动脉粥样硬化的预防和改善.     

牙周基础治疗对Ⅱ型糖尿病伴慢性牙周炎患者糖脂代谢的影响

许多研究已经证实糖尿病与牙周炎有双向影响关系[1-2],通过牙周基础治疗不仅可以改善Ⅱ型糖尿病患者的牙周状况,在一定程度上还能改善患者糖代谢的控制水平[3],甚至对其脂代谢水平的控制也有一定帮助.但也有学者并不承认其降低血脂的意义[4].本实验旨在观察牙周基础治疗对Ⅱ型糖尿病合并慢性牙周炎患者的牙周状况及糖脂代谢的影响.     

2型糖尿病伴慢性牙周炎患者HbAlc含量及血清炎性细胞因子的变化

目的：分析2型糖尿病伴慢性牙周炎患者牙周基础治疗后糖化血红蛋白含量及血清炎性细胞因子的变化。方法：60例2型糖尿病伴慢性牙周炎患者作为研究组,选取同期体检的60例牙周健康者作为对照组。观察并检测两组患者的牙周状况、HbAlc含量及血清炎性细胞因子情况。结果：牙周基础治疗前,研究组患者的白细胞介素?6、肿瘤坏死因子?α、C反应蛋白含量以及HbAlc含量显著高于对照组,差异有统计学意义（ P＜0?05）。牙周基础治疗后,研究组患者的白细胞介素?6、肿瘤坏死因子?α、C反应蛋白含量以及HbAlc含量明显下降,与对照组相比,差异无统计学意义（P＞0?05）。结论：2型糖尿病伴慢性牙周炎患者牙周基础治疗后,可降低糖化血红蛋白含量及血清炎性细胞因子可避免其他并发症的发生及发展。     

糖尿病与牙周炎的关系

糖尿病与牙周炎关系密切,糖尿病患者伴发重度牙周炎的风险比非糖尿病患者增高2～3倍,而牙周慢性炎症又会促进患者血糖升高。二者有共同的遗传学基础,糖尿病还通过对牙周菌群、中性粒细胞功能、炎症反应强度、胶原代谢及组织愈合能力的影响促进牙周炎的发生。本文探讨了糖尿病和牙周炎的相互影响及糖尿病患者的牙周治疗有关注意事项。     

激光在糖尿病患者牙周炎非手术治疗中的应用

与糖尿病相伴随的牙周炎是一种易造成牙周支持组织显著破坏的疾病,在中老年人群具有较高发病率,常规治疗效果欠佳。激光是一种单光子的人造光,具有杀菌消毒、降低促炎症因子水平以及减少牙槽骨吸收的作用,对以炎症为联系基础的糖尿病伴牙周炎患者的治疗效果较显著。因此,本文主要从糖尿病患者牙周炎的诊疗特点,激光治疗在其中应用的原理、类型、疗效以及存在的问题和发展方向等作一综述。     

糖尿病与牙周炎治疗效果的相互影响

目的:探讨2型糖尿病与牙周炎治疗的相互影响。方法:随机选择患2型糖尿病伴中、重度慢性牙周炎的患者66名,其中联合治疗组(n=34)进行降糖和牙周基础治疗;糖尿病治疗组(n=32)进行单纯降糖治疗。观察比较两组治疗8周后牙周炎及糖尿病各相关指标。结果:治疗8周后,联合治疗组牙周炎症状明显改善,白细胞介素-1β降低,糖尿病症状也有明显改善,较治疗前相比均有显著性差异(P<0.05);糖尿病治疗组糖尿病与牙周炎症状均明显改善(P<0.05);联合治疗组牙周指标的改善明显优于糖尿病治疗组(P<0.05),但两组糖尿病指标的改善无显著差异(P>0.05)。结论:对于糖尿病伴慢性牙周炎的患者,糖尿病的有效控制有利于牙周炎症状的改善,糖尿病牙周联合治疗更有利于患者牙周炎症状的改善。     

牙周炎和前列腺疾病相关性研究现状

牙周炎是常见的口腔炎症性疾病,有大量文献报告牙周炎与全身系统性疾病存在密切联系,如心血管疾病、2型糖尿病、早产低出生体重儿等.牙周炎与前列腺疾病有相似的风险因素,年龄、吸烟、肥胖和糖尿病以及炎症的刺激对疾病有显著影响.该文主要对牙周炎和前列腺疾病的相关性的研究情况,共同的影响因素,以及相关的生物学机制等进行综述.     

The role of adipokines in periodontal infection and healing

Periodontitis is a chronic inflammatory disease of the periodontium, which is caused by pathogenic bacteria in combination with other risk factors. The bacteria induce an immunoinflammatory host response, which can lead to irreversible matrix degradation and bone resorption. Periodontitis can be successfully treated. To achieve regenerative periodontal healing, bioactive molecules, such as enamel matrix derivative (EMD), are applied during periodontal surgery. Recently, it has been shown that obesity is associated with periodontitis and compromised healing after periodontal therapy. The mechanisms underlying these associations are not well understood so far, but adipokines may be a pathomechanistic link. Adipokines are bioactive molecules that are secreted by the adipose tissue, and that regulate insulin sensitivity and energy expenditure, but also inflammatory and healing processes. It has also been demonstrated that visfatin and leptin increase the synthesis of proinflammatory and proteolytic molecules, whereas adiponectin downregulates the production of such mediators in periodontal cells. In addition, visfatin and leptin counteract the beneficial effects of EMD, whereas adiponectin enhances the actions of EMD on periodontal cells. Since visfatin and leptin levels are increased and adiponectin levels are reduced in obesity, these adipokines could be a pathomechanistic link whereby obesity and obesity‐related diseases enhance the risk for periodontitis and compromised periodontal healing. Recent studies have also revealed that adipokines, such as visfatin, leptin and adiponectin, are produced in periodontal cells and regulated by periodontopathogenic bacteria. Therefore, adipokines may also represent a mechanism whereby periodontal infections can impact on systemic diseases.     

Periodontitis as a Novel Contributor of Adipose Tissue Inflammation Promotes Insulin Resistance in a Rat Model

Background: Recent studies have indicated that the chronic low‐grade inflammation induced by periodontitis is related to obesity and type 2 diabetes mellitus. The purpose of this study is to investigate the effects of periodontitis on obesity‐related adipose tissue inflammation and subsequent systemic insulin resistance in a rat model. Methods: Thirty‐two rats were divided into four groups of eight: 1) obese rats with periodontitis (combination group); 2) obese rats without periodontitis (obesity group); 3) normal rats with periodontitis (periodontitis group); and 4) normal rats without periodontitis (control group). Monosodium glutamate was used to induce obesity during the early postnatal period. Periodontitis was induced by ligatures for 8 weeks. Morphologic features of white adipose tissue (WAT) and islets were observed, and fasting plasma glucose and insulin concentrations and homeostasis model assessment for insulin (HOMA‐IR) were measured at 5 months. Differences among groups were compared with the Fisher post hoc least significant difference test. Results: A slight increase of stromal vascular fractions (SVFs) and macrophage infiltration in the WAT of the periodontitis group was observed. Significant proliferation of SVFs and macrophage infiltration were induced in the combination group. HOMA‐IR scores in the combination and periodontitis groups were higher than in the obesity and control groups, respectively. The disturbance of islet architecture was consistent with a high HOMA‐IR score in the combination group. Conclusions: Periodontitis induced initial stages of WAT inflammation and acted as a contributing factor to exacerbate proinflammatory phenotype of WAT and promote the development of insulin resistance in the obese rat model.     

妊娠期糖尿病伴牙周炎治疗研究进展

牙周炎和妊娠期糖尿病（gestational diabetes mellitus,GDM）都是十分常见的慢性病。研究发现,GDM与牙周炎之间可能存在相关性,GDM影响牙周炎发展的严重程度,牙周炎对GDM的发展亦有着推动作用。GDM伴牙周炎的发病机制复杂,可能对正常妊娠及胎儿生长发育产生不良影响,因此,对GDM伴牙周炎患者的综合治疗需持谨慎的态度。迄今为止,对于GDM合并牙周炎的治疗尚存在争议,主要以降血糖、降低炎症反应的治疗为主,但并无统一的治疗方案。文章回顾了近年来国内外相关研究,就GDM伴牙周炎患者的治疗研究进展做一综述,为其临床诊疗及科学研究提供新的思路。     

Periodontitis and diabetes interrelationships: role of inflammation

Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. One of these complications is periodontal disease (periodontitis). Periodontitis is much more than a localized oral infection. Recent data indicate that periodontitis may cause changes in systemic physiology. The interrelationships between periodontitis and diabetes provide an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease. In this case, it may also be possible for the oral infection to predispose to systemic disease. In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. A potential mechanistic link involves the broad axis of inflammation, specifically immune cell phenotype, serum lipid levels, and tissue homeostasis. Diabetes-induced changes in immune cell function produce an inflammatory immune cell phenotype (upregulation of proinflammatory cytokines from monocytes/polymorphonuclear leukocytes and downregulation of growth factors from macrophages). This predisposes to chronic inflammation, progressive tissue breakdown, and diminished tissue repair capacity. Periodontal tissues frequently manifest these changes because they are constantly wounded by substances emanating from bacterial biofilms. Diabetic patients are prone to elevated low density lipoprotein cholesterol and triglycerides (LDL/TRG) even when blood glucose levels are well controlled. This is significant, as recent studies demonstrate that hyperlipidemia may be one of the factors associated with diabetes-induced immune cell alterations. Recent human studies have established a relationship between high serum lipid levels and periodontitis. Some evidence now suggests that periodontitis itself may lead to elevated LDL/TRG. Periodontitis-induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. Within this context, periodontitis may contribute to elevated proinflammatory cytokines/serum lipids and potentially to systemic disease arising from chronic hyperlipidemia and/or increased inflammatory mediators. These cytokines can produce an insulin resistance syndrome similar to that observed in diabetes and initiate destruction of pancreatic beta cells leading to development of diabetes. Thus, there is potential for periodontitis to exacerbate diabetes-induced hyperlipidemia, immune cell alterations, and diminished tissue repair capacity. It may also be possible for chronic periodontitis to induce diabetes.     

Diabetes mellitus-associated periodontitis: differences between type 1 and type 2 diabetes mellitus

Aspriello SD, Zizzi A, Tirabassi G, Buldreghini E, Biscotti T, Faloia E, Stramazzotti D, Boscaro M, Piemontese M. Diabetes mellitus‐associated periodontitis: differences between type 1 and type 2 diabetes mellitus. J Periodont Res 2011; 46: 164–169. © 2010 John Wiley & Sons A/S Background and Objective: Although many studies have appeared about diabetes mellitus‐associated periodontitis, few have compared periodontitis inflammatory markers between type 1 (T1DM) and type 2 diabetes mellitus (T2DM), and information regarding this issue is scarce and contradictory. We evaluated the levels of plasma C‐reactive protein and of interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α) in gingival crevicular fluid in two groups of subjects affected by T1DM and T2DM, in order to identify possible differences between the two classes in the inflammatory mechanisms of diabetes mellitus‐associated periodontitis. Material and Methods: Plasma C‐reactive protein and gingival crevicular fluidIL‐1β, IL‐6 and TNF‐α were measured in periodontitis patients affected by type 1 (P‐T1DM, n = 24) and type 2 diabetes mellitus (P‐T2DM, n = 24). Results: Gingival crevicular fluid levels of IL‐1β and TNF‐α in P‐T1DM subjects were significantly higher than in P‐T2DM subjects. In P‐T1DM subjects, we found significant negative correlations between the duration of diabetes mellitus and IL‐1β and between the duration of diabetes mellitus and TNF‐α. Conclusion: This study shows that IL‐1β and TNF‐α levels in periodontitis patients with T1DM are affected by the duration of diabetes mellitus.     

OPG、RANKL在2型糖尿病伴牙周炎大鼠牙槽骨中的表达

目的:探讨骨保护素(OPG)和核因子κB受体活化因子(RANKL)在2型糖尿病伴牙周炎大鼠模型中的表达水平.方法:46只Wistar雄性大鼠,随机分为健康组10只;单纯牙周炎组12只;2型糖尿病组12只;2型糖尿病牙周炎组12只;分别建模,免疫组织化学方法检测牙槽骨OPG、RANKL蛋白表达.结果:与健康组相比,OPG在2型糖尿病组、单纯牙周炎组、2型糖尿病伴牙周炎组表达水平依次降低,RANKL的表达水平依次增强;OPG及RANKL的表达除2型糖尿病牙周炎组与单纯牙周炎组间比较无差异外,其余组间比较有统计学意义(P＜0.05).结论:炎症可能导致破骨细胞及免疫细胞中RANKL的上调和成骨细胞中OPG的下调.     

Periodontal inflamed surface area and C-reactive protein as predictors of HbA1c: a study in Indonesia

Periodontitis may exert an infectious and inflammatory burden, evidenced by increased C-reactive protein (CRP). This burden may impair blood glucose control (HbA1c). The aim of our study was to analyze whether periodontitis severity as measured with the periodontal inflamed surface area (PISA) and CRP predict HbA1c levels in a group of healthy Indonesians and a group of Indonesians treated for type 2 diabetes mellitus (DM2). A full-mouth periodontal examination, including probing pocket depth, gingival recession, clinical attachment loss, plaque index and bleeding on probing, was performed in 132 healthy Indonesians and 101 Indonesians treated for DM2. Using these data, PISA was calculated. In addition, HbA1c and CRP were analyzed. A validated questionnaire was used to assess smoking, body mass index (BMI), education and medical conditions. In regression analyses, it was assessed whether periodontitis severity and CRP predict HbA1c, controlling for confounding and effect modification (i.e., age, sex, BMI, pack years, and education). In healthy Indonesians, PISA and CRP predicted HbA1c as did age, sex, and smoking. In Indonesians treated for DM2, PISA did not predict HbA1c. Periodontitis may impair blood glucose regulation in healthy Indonesians in conjunction with elevated CRP levels. The potential effect of periodontitis on glucose control in DM2 patients may be masked by DM2 treatment. Clinical relevance: periodontitis may impair blood glucose control through exerting an inflammatory and infectious burden evidenced by increased levels of CRP.