脂联素对Ⅱ型糖尿病患者伴牙周炎的影响

脂联素是目前发现的对人体有保护作用的脂肪细胞特异分泌的激素蛋白,具有降糖、增加胰岛素敏感性、抗炎、抗动脉粥样硬化和调节骨代谢的作用,是Ⅱ型糖尿病的保护性因子.牙周炎被认为是糖尿病的第六并发症,两者相互影响.脂联素与牙周炎的相互作用尚不明了,本文就脂联素与Ⅱ型糖尿病合并牙周炎的相关性研究现状进行综述,以期为今后的治疗及研...     

脂联素对骨髓间充质干细胞的作用及其 调控机制

骨髓间充质干细胞(BMSCs)是治疗颅颌面骨疾病的研究热点,BMSCs在增殖、分化、迁徙方面的功能以及在组织环境中的存活能力决定了其骨质修复重建的质量和速度。脂联素(APN)是一种主要由脂肪组织分泌的脂肪因子,除了与脂代谢密切相关,近年来研究发现其还能通过多种途径调控BMSCs而影响成骨作用的进程,对骨—脂代谢平衡具有重要的调节作用。本文对APN的生物学特性、APN调控BMSCs增殖、成骨分化、迁徙和存活能力的作用以及相关信号通路的研究进展作一综述,为骨质疏松等骨相关疾病的预防和治疗提供新思路。     

脂联素对人牙周膜成纤维细胞的作用

目的:原代培养人牙周膜成纤维细胞(human periodontal ligament cell,hPDLC),研究脂联素受体(adiponectinreceptor,Adipo R)在hPDLC中的表达情况,以及脂联素(adiponectin,ADP)对hPDLC增殖的作用。方法:收集因正畸需要而拔除的健康前磨牙10颗,玻片覆盖组织块法原代培养hPDLC,RT-PCR法检测分析AdipoR1和AdipoR2在hPDLC中的表达。使用不同浓度ADP(0,5,10,20ng/μL)刺激体外培养的hPDLC,采用四甲基偶氮唑盐(MTT)法,分别测定第1、4、7天的细胞增殖活性。采用SSPS16.0软件包对数据进行统计学分析。结果:免疫组化显示,培养的细胞波形丝蛋白染色阳性,角蛋白染色阴性,证明体外原代培养细胞及传代细胞均为中胚层组织来源的hPDLC,且无上皮来源细胞混杂。琼脂糖凝胶电泳检测显示,Adipo R2在人牙周膜成纤维细胞中表达阳性。MTT法检测的生长曲线显示,随着ADP浓度的增加,细胞增殖活性增加。培养24h后,C、D组与对照组相比差异显著(P相似文献   

罗格列酮对牙周炎大鼠牙龈脂联素受体表达的影响

目的:探讨罗格列酮(ROS)对牙周炎大鼠牙龈脂联素受体1(AdipoRl) mRNA、脂联素受体2(AdipoR2) mRNA和TNF-α等炎症因子表达的影响及在牙周炎中对牙槽骨保护的潜能.方法:50只SD大鼠随机分为5组(n=10),大鼠不干预处理作为空白对照,40只大鼠用于制作牙周炎模型后分别用蒸馏水(牙周炎组)、1、3、10 mg/kg ROS(低、中、高剂量组)灌胃1次/d,持续4周.然后取样,RT-PCR测定牙龈组织AdipoR1和AdipoR2 mRNA表达水平,ELISA测牙龈组织TNF-α、MMP-9和血浆脂联素浓度,标准化的数码摄影测量釉牙骨质界到牙槽骨嵴顶(CEJ-A)距离.结果:牙周炎组和空白对照组相比,牙龈组织AdipoR1和AdipoR2的mRNA表达水平显著降低(P＜0.01),血浆脂联素水平无差异(P＞0.05),TNF-α和MMP-9浓度显著上升(P＜0.01).和牙周炎组相比,低、中、高剂量治疗组牙龈组织AdipoRl mRNA表达均升高(P＜0.05),TNF-α浓度显著降低(P＜0.01);中、高剂量治疗组牙龈组织AdipoR2 mRNA表达显著升高(P＜0.01),MMP-9浓度显著降低(P＜0.01),血浆脂联素浓度升高(P＜0.05),牙槽骨吸收量显著降低(P＜0.01).结论:ROS可能通过上调牙龈组织中AdipoR1和AdipoR2 mRNA表达水平,降低TNF-α、MMP-9浓度,缓解牙周组织炎症,降低牙槽骨吸收.     

牙周基础治疗对慢性牙周炎伴肥胖患者的治疗效果及对脂联素和代谢水平的影响

目的:探讨牙周基础治疗对慢性牙周炎伴肥胖患者治疗效果及对脂联素和代谢水平的影响.方法:选取2018年10月～2019年5月我院收治的慢性牙周炎伴肥胖患者64例,随机数字表法随机分成对照组(32例)和观察组(32例).对照组患者予以常规口腔卫生指导,观察组口腔卫生指导基础上联合予以牙周基础治疗.治疗后6个月,比较两组治疗...     

牙周干预对伴冠心病牙周炎患者血清炎性因子和脂联素的影响

目的分析冠心病伴牙周炎患者牙周干预治疗前、后血清中炎性因子和脂联素水平的变化,探讨慢性牙周炎与冠心病的关系及牙周干预治疗对冠心病伴牙周炎患者的重要性。方法本研究包括冠心病伴牙周炎患者56例和单纯冠心病不伴牙周炎患者42例。冠心病伴牙周炎患者给予牙周干预治疗,对冠心病组及冠心病伴牙周炎组干预前、后的牙周临床指标及血清炎性因子（CRP、TNF-α、IL-6）和脂联素水平进行比较分析。结果冠心病伴牙周炎组牙周干预后牙周临床指数比干预前明显好转。冠心病伴牙周炎组干预前与冠心病组相比,所有血清炎性因子（CRP、TNF-α、IL-6）水平升高;干预3个月后明显降低（P〈0.05）。冠心病伴牙周炎组干预前水平有所降低的脂联素在干预3个月后明显升高（P〈0.05）。结论慢性牙周炎可增加冠心病的发病风险,牙周干预治疗可降低血清中炎性因子水平,提高血管保护因子水平,对冠心病病程的发展有改善作用。     

内源性大麻素系统与骨代谢

内源性大麻素系统是包括了内源性大麻素、大麻素受体(CB)以及相关酶的一个复杂的生理系统。近年来内源性大麻素系统与骨代谢的关系被一步步证实。大量研究发现CB-1受体及CB-2受体存在于骨细胞中，并在骨代谢的过程中起到不同的作用。其余受体包括TPRV1、GPR55、GPR119、TPRV4等，亦参与了骨代谢的过程。以anandamide和2-arachidonoylglycerol为代表的内源性大麻素以及其激动剂和拮抗剂可以通过大麻素受体的介导影响成骨细胞与破骨细胞的增殖分化及骨重塑。可见内源性大麻素系统可作为骨再生治疗的新靶点，然而目前尚无足够数量的相关临床数据，因此大麻素与骨代谢的关系值得进一步研究。     

慢性牙周炎伴2型糖尿病患者龈沟液中脂联素水平的检测及意义

目的：探究牙周炎伴2型糖尿病患者龈沟液中脂联素水平及意义。方法：纳入慢性牙周炎伴糖尿病患者（DM&CP）、慢性牙周炎患者（CP）、健康对照者（H）各20例,记录其临床指标（SBI、PLI、PD 和 AL）,并收集龈沟液（GCF）样本,用龈沟液测量仪 periotron8000对 GCF 进行定量,用脂联素 ELISA 试剂盒检测样本中脂联素含量,比较组间检测指标的差异以及临床指标与 GCF 中脂联素水平的相关性。结果：DM&CP 组 GCF 中脂联素水平显著低于其他2组（P ＜0．05）,CP 患者龈沟液脂联素水平与牙周健康组相比无统计学差异（P ＞0．05）。GCF 中脂联素水平与临床指标 PD 值、AL 值有负相关性（P ＜0．05）,与 SBI、PLI 无明显相关（P ＞0．05）。结论：龈沟液中脂联素水平降低可能与 DM&CP 发生发展有关。     

脂联素对不同培养条件下成骨细胞与间充质干细胞中SDF-1/CXCR4表达影响的实验研究

目的研究不同培养条件下,脂联素对成骨细胞的基质细胞衍生因子(SDF-1)以及间充质干细胞CXCR4表达的影响。方法提取重组的脂联素蛋白,将10μg/m L脂联素作用于单独培养的MC3T3-E1以及C3H10T1/2细胞,Real-time定量PCR方法检测SDF-1/CXCR4表达变化;设计MC3T3-E1及C3H10T1/2细胞共培养体系,比较共培养对MC3T3-E1及C3H10T1/2细胞的SDF-1/CXCR4表达变化;将脂联素加入共培养体系,比较脂联素对共培养体系中MC3T3-E1及C3H10T1/2细胞SDF-1/CXCR4 mRNA表达变化。结果 Real-time定量PCR结果显示:单独培养条件下,脂联素促进了MC3T3-E1细胞SDF-1mRNA的表达;而在共培养体系中,脂联素则下调了MC3T3-E1细胞SDF-1mRNA的表达。无论单独培养还是共同培养,脂联素对C3H10T1/2细胞的CXCR4表达均起下调作用。结论脂联素对成骨细胞SDF-1的表达呈双向调节作用,而对间充质干细胞CXCR4则起下调作用。脂联素通过调节SDF-1/CXCR4影响间充质干细胞和成骨细胞的微环境。     

促红细胞生成素肝细胞激酶受体及其膜结合配体相关因子在口腔疾病中的表达及作用机制的研究进展

促红细胞生成素肝细胞激酶受体及其膜结合配体（Eph/ephrin）可以通过细胞与细胞间短距离的信号传导,参与调节生长发育,促进疾病发生发展的各个过程。研究Eph/ephrin与口腔相关疾病的机制可以为口腔疾病的治疗提供新的思路。近年来,针对Eph/ephrin通路调控口腔相关疾病,尤其是在牙周疾病防治、正畸骨改建以及口腔肿瘤的生物学治疗领域的研究逐渐深入,本文即对这3个方面的研究进展进行综述。     

病毒转染技术在骨组织细胞研究中的应用

［摘要］随着病毒转染技术的发展,运用病毒转染骨组织细胞的方法来研究骨组织代谢及其相关的基因治疗已经越来越热门。本文总结了近年来运用病毒在体内外转染骨组织细胞的研究进展,为选择最合适的病毒载体及最佳的转染方式提供有价值的参考,为研究骨组织细胞的调控机制及代谢提供更有效的研究手段。     

The relationship between periodontal condition and serum levels of resistin and adiponectin in elderly Japanese

Background and Objective:  Diabetes and periodontitis are associated with each other. Adipokines, specifically adiponectin and resistin, are secreted from adipocytes and are thought to cause insulin resistance in rodents. Additionally, adiponectin and resistin may play a role in inflammation and immune responses. The aim of this study was to clarify the relationship between serum levels of adipokines and periodontal conditions in elderly Japanese people with and without periodontitis.
Material and Methods:  A total of 158 Japanese men and women (76 years old) with or without periodontitis were selected for the study. Serum adiponectin, resistin, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) concentrations were compared between subjects with and without periodontitis.
Results:  Serum resistin levels and total leukocyte counts in subjects with periodontitis were higher than in control subjects. No significant differences were observed in adiponectin, IL-6 and TNF-α levels between subjects with and without periodontitis. Logistic regression analysis showed that periodontitis with at least one tooth that displayed a probing pocket depth of ≥6 mm was significantly associated with higher serum resistin levels (odds ratio, 2.0; 95% confidence interval, 1.0–4.0). When excluding periodontitis subjects with ≤10% of bleeding on probing and excluding control subjects with >10% bleeding on probing, differences between groups and odds ratio increased. Serum adiponectin tended to decrease in patients with periodontitis, albeit not significantly.
Conclusion:  Increased serum resistin levels were significantly associated with periodontal condition, especially when considering bleeding on probing, in elderly Japanese people. There was also a trend, though non-significant, toward decreased levels of adiponectin in subjects with periodontitis.     

Dickkopf 1与骨破坏性疾病的关系

Dickkopf（DKK）1是一种分泌型糖蛋白,为无翅型小鼠乳房肿瘤病毒整合位点家族（WNT）信号转导通路的重要抑制因子之一,可通过与低密度脂蛋白受体相关蛋白5/6等WNT受体复合体的结合来抑制WNT信号转导通路的信号转导。DKK1既在骨质疏松症、类风湿关节炎、多发性骨髓瘤和牙周炎等疾病中都存在着异常表达,亦在骨代谢中发挥重要的作用。本文就近年来DKK1与骨破坏性疾病的关系等研究进展作一综述,以抑制骨破坏和修复骨损失为最终研究目的,为治疗牙周炎和获得牙槽骨再生寻找新的途径。     

Effects of Scaling and Root Planing on Clinical Response and Serum Levels of Adipocytokines in Patients With Obesity and Chronic Periodontitis

Background: Despite several investigations suggesting that obesity is a risk indicator for periodontitis, little is known about the effect of obesity on periodontal treatment response. The aim of this study is to evaluate the effects of scaling and root planing (SRP) on clinical parameters and circulating levels of leptin and adiponectin in patients with obesity with chronic periodontitis (CP). Methods: Twenty‐four patients with obesity and CP and 24 patients without obesity with CP were submitted to SRP. Clinical parameters were assessed at baseline and 3 and 6 months after therapy. Serum levels of leptin and adiponectin were evaluated at all time points, using enzyme‐linked immunosorbent assay. Results: SRP improved the clinical parameters of both groups at 3 and 6 months (P <0.05). Nonetheless, the patients without obesity presented a lower mean probing depth (PD) at 6 months after therapy and a greater reduction in PD from baseline to 6 months in the full‐mouth analysis (primary outcome variable) and in initially deep sites (P <0.05). Leptin serum levels were higher in patients with obesity than in patients without obesity at all time points (P <0.05). No changes in the serum levels of leptin and adiponectin were observed in groups with and without obesity after therapy (P >0.05). Conclusions: Patients with obesity and CP presented lower reductions in PD than patients without obesity with CP at 6 months after SRP. Furthermore, the treatment did not affect the circulating levels of leptin and adiponectin in any group.     

沉默交配型信息调节因子2同源蛋白1与骨和软骨代谢的关系

沉默交配型信息调节因子2同源蛋白（SIRT）1是一种依赖于烟酰胺腺嘌呤二核苷酸的第3类去乙酰化酶,在骨与软骨的代谢中发挥着重要的作用。SIRT1通过促进成骨细胞生成、骨量增长、抑制破骨细胞生成,调节骨的发育和重建。此外,SIRT1还可促进骨髓间质干细胞的成骨向分化。在软骨代谢过程中,SIRT1对于软骨的改建必不可少。SIRT1在骨与软骨过程中的作用与无翅型小鼠乳房肿瘤病毒整合位点家族信号转导通路、核因子-κB信号转导通路、叉头转录因子O和甲状旁腺素密切相关。本文就沉默信息调节因子SIRT1在骨与软骨代谢中的作用、SIRT1调节骨代谢的信号转导通路等研究进展作一综述。     

Bone metabolism and the receptor activator of nuclear factor-κB ligand (RANKL) pathway: a comprehensive review

The main metabolic function of bone is the homeostasis of calcium and phosphate. This is achieved through a balance of bone resorption and formation. To gain an understanding of bone turnover it is important to appreciate the different cells, regulatory steroids and hormones involved and how these have their actions. This article summarizes bone cells, normal bone metabolism, bone turnover, regulatory mechanisms and the clinical applications of these. The receptor activator of nuclear factor-kB, receptor activator of nuclear factor-kB ligand and osteoprotegerin (RANK/RANKL/OPG) cell signalling pathway is discussed in detail. Understanding these topics enhances knowledge of the pathological processes and diseases that result from failures of bone metabolism.     

Sclerostin and its role as a bone modifying agent in periodontal disease

BackgroundPeriodontitis is a highly prevalent inflammatory disease affecting the periodontium that results from an imbalance between periodontopathogens and host mechanisms. Continuous progression of the disease may lead to tissue and bone destruction, eventually resulting in tooth loss. The extent of bone loss depends on the dysregulated host immune response. Various host-elicited molecules play a major role in disease progression. The discovery of the glycoprotein sclerostin and its role as a regulator of bone mass has led to a better understanding of bone metabolism.HighlightSclerostin, which is primarily expressed by osteocytes, is a negative regulator of bone formation. It is a potent antagonist of the canonical Wingless-related integration site (Wnt) pathway, which is actively involved in bone homeostasis. Sclerostin is known to stimulate bone resorption by altering the osteoprotegerin (OPG)/receptor activator of nuclear factor kappa- β ligand (RANKL) balance. Additionally, in periodontitis, activation of the inflammatory cascade also increases the synthesis of sclerostin.ConclusionThe recently discovered sclerostin antibody has emerged as a positive therapeutic tool for the treatment of metabolic bone diseases. It has been reported to improve bone strength, bone formation, osseointegration around implants and lower the risk of bone fractures in various animal and human models. This review describes the properties and action of sclerostin, its role in periodontal diseases, and the advent and efficacy of sclerostin antibodies.