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1.
目的探讨围手术期使用抗生素对伴高脂血症(hyperlipidemia,HL)或糖尿病(diabetes mellitus,DM)慢性牙周炎(chronic periodontitis,CP)大鼠颈动脉血管及血清白介素-6(interlenkim-6,IL-6)水平的影响。方法分两批次建立HL+CP及DM+CP大鼠模型。分组如下,A和A′组:均为正常对照组,每组各7只;B(HL)和B′(DM)组:每组各7只;C(HL+CP)和C′(DM+CP)组,每组各21只。模型建成后将C和C′组分别分为C1和C1′组(均为自然进程组),C2和C2′组(均为单纯拔牙组),C3和C3′组(均为拔牙+抗生素组),每组各7只。C2、C2′、C3、C3′组分2次分别拔除左右实验牙(双侧上颌第一、二磨牙)。拔牙前后分5个时间点(T1~T5)采集血清(第1次拔牙前为T1,第1次拔牙后1周为T2,第2次拔牙后1、3、5周分别为T3、T4和T5),酶联免疫吸附测定(enzyme-linked immunosorbent assay,ELISA)法检测血清IL-6的绝对含量,实验组IL-6绝对含量与同批次对照组绝对含量...  相似文献   

2.
目的:探讨外源性碱性成纤维细胞生长因子(bFGF)对2型糖尿病(T2DM)大鼠钛种植体骨结合的影响及机制.方法:取SPF级雄性SD大鼠40只,随机分为对照组、T2DM组、bFGF-T2DM组、氯化锂(LiCl)-T2DM组.对照组正常饲料喂养,其余大鼠以高脂高糖喂养+腹腔注射链脲佐菌素(STZ)30 mg/kg建立T2...  相似文献   

3.
目的:研究慢性牙周炎对2型糖尿病(type 2 diabetes mellitus,T2DM)大鼠肾脏功能的影响。方法选用4周龄雄性自发性T2DM OLETF大鼠30只,同种系同周龄糖耐量正常LETO大鼠(L组)20只作为实验对象。36周龄时,将到达糖耐量受损期26只OLETF大鼠(O组),按照是否复合慢性牙周炎模型随机分为糖尿病合并慢性牙周炎组[O CP(+)组]和糖尿病组[O CP(-)组];LETO大鼠也随机分为慢性牙周炎组[L CP(+)组]和正常组[L CP(-)组]。O CP(+)组和L CP(+)组采取丝线结扎联合涂菌建立慢性牙周炎模型,建模20周后处死所有大鼠,收集血清,全自动生化分析仪检测反映肾脏功能的生化指标,包括血清白蛋白、总蛋白、尿素和肌酐4个指标。结果血清白蛋白(t=11.131,P=0.002)、总蛋白水平(t=21.696,P<0.001)O组显著低于L组,O CP(+)组白蛋白(t=2.155,P=0.049)、总蛋白水平(t=2.554,P=0.023)也较O CP(-)组显著下降,而L CP(+)组与L CP(-)组比较差异均无统计学意义。血清肌酐水平O组显著高于L组(t=9.099,P=0.005),O CP(+)组也明显高于O CP (-)组(t=4.443,P<0.001),而L CP(+)组与L CP(-)组比较,差异无统计学意义。血清尿素水平O组比L组显著升高(t=5.684,P=0.024),而O CP(+)组与O CP(-)组比较(t=1.484,P=0.160)、L CP(+)组与L CP(-)组比较(t=0.075,P=0.932)差异无统计学意义。结论慢性牙周炎未对正常大鼠肾脏功能产生明显影响;但在T2DM大鼠肾脏已有损害的情况下,慢性牙周炎恶化了肾脏功能,并且T2DM和牙周炎在肾脏病变发生中有交互、协同作用。  相似文献   

4.
聂莹  张志宏  袁晟  鲍军燕 《口腔医学》2011,31(1):26-28,32
目的 观察糖尿病(diabetes mellitus,DM)对实验性大鼠牙槽骨缺损修复过程中不同时期骨形态发生蛋白-2(bonemorphogenetic protein-2,BMP-2)表达的影响。方法 将48只雄性SD大鼠随机分为DM组和对照组,每组24只,DM组大鼠经腹腔注射链脲佐菌素造成DM大鼠模型,建模成功后行大鼠牙槽骨骨缺损制备,2组均分别于骨缺损制备后1、2、4、8周各取6只大鼠处死,取术区组织。苏木精-伊红染色(hematoxylin-eosin staining,HE染色)镜下观察缺损区内新生骨样组织形成情况;用免疫组化法检测术后1、2、4、8周缺损区内BMP-2的表达情况,比较各组的平均光密度。结果 HE染色观察显示DM组成骨较对照组减少。术后1周、2周免疫组化观察对照组新骨BMP-2的表达强于DM组,二者之间差异有统计学意义(P<0.05),术后4周、8周对照组BMP-2表达较之前弱,但与DM组二者之间差异无统计学意义(P>0.05)。结论 DM影响了大鼠牙槽骨缺损的修复,可能是DM使BMP-2形成减少,从而抑制了未分化间充质向成骨细胞的转化,从而影响种植体骨结合,降低种植初期稳定性。?  相似文献   

5.
目的:探索2型糖尿病(T2DM)大鼠颅骨极限骨缺损(CSD)的大小。方法:9周龄SD大鼠(体重300~320 g),用高脂高糖饲料+小剂量链脲佐菌素(STZ)腹腔注射诱导2型糖尿病模型,建模成功后,将糖尿病大鼠及正常大鼠各随机分为4组(n=3),分别于颅骨中央制备直径2、3、4、5 mm的骨缺损,术后8周取材,行大体观察、X线检查及组织学检测。结果:T2DM大鼠行颅骨缺损术后8周,直径2 mm的颅骨缺损愈合完全,X线阻射,组织学检测可见新骨生成良好;直径3、4、5 mm的颅骨缺损愈合不完整,X线透射,新骨生成不足。正常大鼠直径2、3、4 mm的缺损愈合完全,X线阻射,组织学检测可见新骨生成良好;直径5 mm的缺损未见愈合,X线透射,新骨生成较少。结论:T2DM大鼠颅骨极限骨缺损参考直径可定义为3 mm。  相似文献   

6.
目的:比较2型糖尿病(T2MD)大鼠和正常SD大鼠脂肪来源干细胞(ASCs)的增殖及多向分化能力。方法:取16只SPF级8周龄SD大鼠,随机分为两组(n=8):糖尿病组,采用高脂高糖饲料构建T2DM大鼠模型;对照组常规饲料喂养,比较两组大鼠的血糖水平。建模成功8周后,分别培养两组大鼠腹股沟处的ASCs,显微镜下观察细胞形态;CCk-8法检测细胞增殖;流式细胞仪检测细胞表面标志物;取第3代细胞行成骨和成脂诱导实验,实时定量PCR检测成骨诱导7 d时成骨相关基因的表达。结果:两组大鼠脂肪组织均可分离获得ASCs,且细胞形态和增殖能力无显著差异(P>0.05);两组细胞均高表达CD44和CD90,低表达CD34和CD45;T2DM大鼠P3代ASCs成脂诱导后油红O染色较正常组强,而成骨诱导后碱性磷酸酶(ALP)染色和茜素红染色较正常组弱;ALP蛋白活性检测较正常组低;ALP、OCN、OPG和RUNX2等成骨相关基因的表达水平较正常组低。结论:T2DM大鼠ASCs体外成骨分化能力较弱。  相似文献   

7.
目的:通过对伴2型糖尿病慢性牙周炎患者、不伴全身系统性疾病的慢性牙周炎患者以及健康对照组中TNF-α基因携带频率的分析,探讨病例组和对照组在该基因携带频率上的差异,并比较各组牙周临床指标和易感等位基因的关系。方法:采用牙周探针,对112例伴2型糖尿病慢性牙周炎患者(DM组)、99例单纯慢性牙周炎患者(CP组)以及健康对照组进行牙周临床指标检查和TNF-α-308基因型(TNF1/2)检测。采用SPSS13.0软件包对数据进行χ2检验和方差分析。结果:在DM组和轻中度CP组之间,轻中度DM组和重度CP组之间,重度DM组和轻中度CP组之间,重度DM组和重度CP组之间,TNF2的阳性基因型分布均有统计学差异(P<0.05)。携带等位基因TNF2的DM组和CP组的牙周探诊深度、临床附着丧失均分别显著高于只携带等位基因TNF1的DM组和CP组患者(P<0.05)。结论:携带TNF-α-308等位基因TNF2可能会增加人群牙周炎的易感性,并且在2型糖尿病和牙周炎协同作用过程中具有重要作用。  相似文献   

8.
《口腔医学》2017,(6):549-553
目的通过检测龈沟液中β-防御素2、β-防御素3的表达水平,探讨其在慢性牙周病与2型糖尿病中的可能作用。方法选取慢性牙周炎伴2型糖尿病组(T2DMCP组)20例,2型糖尿病组(T2DM组)20例,慢性牙周炎组(CP组)20例,健康组(H组)20例作。采用酶联免疫吸附试验(ELISA)检测龈沟液中β-防御素-2和β-防御素-3水平。比较组间龈沟液中β-防御素-2和β-防御素-3水平的差异性,分析β-防御素-2和β-防御素-3之间的相关性与β-防御素-2和β-防御素-3与牙周指标的相关性。结果 CP组、T2DM组、T2DMCP组的临床指标PD、CAL、BI和GCF量均高于H组(P<0.05)。T2DMCP组的PD、CAL、BI和GCF量均高于T2DM组和CP组(P<0.05)。龈沟液中β-防御素-2,β-防御素-3水平在H组高于CP组、T2DM组和T2DMCP组(P<0.05),CP组和T2DM组高于T2DMCP组(P<0.05)。龈沟液中β-防御素-2水平与β-防御素-3水平呈正相关(P<0.05)。结论慢性牙周炎和2型糖尿病可降低龈沟液β-防御素-2和β-防御素-3的水平,提示β-防御素-2、β-防御素-3对牙周组织起保护作用。  相似文献   

9.
目的:应用SD大鼠建立慢性牙周炎(chronic periodontitis,CP)和慢性阻塞性肺疾病(chronic obstructive pulmonarydiseases,COPD)动物模型,探讨CP在COPD发生发展过程中对肺损伤的作用。方法:将40只SD大鼠雌雄各半随机分成4组:正常对照组,CP组,COPD组,COPD伴CP组,每组10只。各组按照实验设计施加相应建模因素,实验10周末分别检查大鼠的龈沟出血指数(SBI)、肺功能状况,ELISA法检测血清中TNF-α和IL-1含量,然后处死大鼠,取材观察牙槽骨吸收程度(ABL)、牙周组织和肺部组织病理学改变,对数据进行统计分析。结果:COPD伴CP组大鼠的肺功能明显降低,龈沟出血指数和牙周组织改变与CP组相似,实验组血清IL-1和TNF-α水平明显高于对照组(P<0.05)。结论:CP在COPD大鼠肺损伤的发生发展过程中具有促进作用。  相似文献   

10.
目的 应用SD大鼠建立慢性牙周炎(chronic periodontitis,CP)和慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)动物模型,探讨CP和COPD的相关机制.方法 将40只SD大鼠按随机数字法分为4组:A组:正常对照组;B组:CP组;C组:COPD组;D组:CP+COPD组,每组10只.各组按实验设计施加相应建模因素,于实验10周末处死动物.分别检查各组大鼠的牙周指标及肺功能状况,并观察牙周和肺部的组织病理学改变,酶联免疫吸附法检测血清中肿瘤坏死因子(TNF)-α水平,并行统计学分析.结果 A、C组出血指数分别为(0.25±0.04)、(1.30±0.25),附着丧失分别为(0.43±0.02)、(0.51±0.02)mm,与A、C组相比,B、D组大鼠的出血指数[分别为(3.85±0.34)、(4.01±0.44)]、附着丧失[分别为(0.90±0.27)、(0.98±0.18)mm]均明显升高(P<0.05);与A组0.2 s末用力呼气量与用力肺活最比值(forced expiratory volume in 0.2 second toforced vital capital ratio,FEV0. 2/FVC值)(65.34±2.63)相比,B、C、D组大鼠FEV0 2/FVC值[分别为(57.49±6.77)、(58.10±2.40)、(49.53±2.86)]明显降低,表明动物模型建造成功.其中D组肺功能与病理学改变均较C组更大,各实验组与正常对照组TNF-α比较差异均有统计学意义(P<0.05),D组TNF-α含量[(23.422±2.815)μg/L]升高最为明显.结论 在CP和COPD相关关系大鼠动物模型中,CP可能对COPD具有促进和诱发作用.  相似文献   

11.
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.  相似文献   

12.
ObjectiveTo determine serum adiponectin, C-reactive protein (CRP), TNF-α and IL-6 levels in impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) patients with periodontitis before and after periodontal intervention, and to investigate the relationship between T2DM and periodontitis.MethodsA total of 50 IGT and 106 T2DM patients with periodontitis were enrolled. The T2DM patients were divided into two groups: T2DM without macrovascular disease (DM1) group and T2DM with macrovascular disease (DM2) group. Each group was randomly divided into two subgroups according to whether they performed periodontal intervention. The normal control group (NC group) consisted of 30 healthy adults. The serum adiponectin, CRP, TNF-α and IL-6 levels were measured at baseline and 3 months after periodontal intervention.ResultsThe serum adiponectin levels at baseline had decreased tendency with significant difference between each two groups, while CRP, TNF-α, and IL-6 levels had increased tendency with significant difference between each two groups among NC, IGT, DM1 and DM2 groups (all P < 0.01). At 3 months after periodontal intervention, the serum adiponectin levels were increased than those without periodontal intervention (all P < 0.01), while CRP, IL-6 and TNF-α significantly decreased (all P < 0.05) in both IGT and DM1 groups. In DM2 group, only CRP levels at 3 months after periodontal intervention were significantly decreased (P < 0.05). Moreover, the HbAlc levels in T2DM patients were improved at 3 months after periodontal invention (P < 0.01).ConclusionPeriodontal intervention is helpful for glucose control, which may be associated with increased serum adiponectin levels and decreased inflammatory cytokine levels.  相似文献   

13.
Background: The aim of the present study is to evaluate the serum receptor activator of nuclear factor‐κβ ligand (RANKL)/osteoprotegerin (OPG) system in patients with chronic periodontitis (CP) and type 2 diabetes mellitus (T2DM) and its changes after periodontal intervention. Methods: Thirty‐five patients with CP + T2DM, 35 systemically healthy patients with CP, and 35 healthy controls were enrolled, and serum levels of RANKL and OPG were measured at baseline. Then the CP + T2DM group was divided into a well‐controlled subgroup and a poorly controlled subgroup according to their hemoglobin A1c (HbA1c), and initial periodontal therapy was performed. After 3 months, patients in both subgroups were recalled, and serum RANKL and OPG levels were tested again and compared with the baseline. Results: At baseline, serum levels of OPG in the T2DM + CP group were much lower than in the CP group and healthy controls (197.41 ± 57.05 pg/mL versus 232.60 ± 70.85 pg/mL [CP group] or 244.96 ± 85.13 pg/mL [healthy controls], P <0.05), whereas their RANKL levels were much higher than in the other two groups (324.35 ± 87.62 pg/mL versus 284.52 ± 90.35 pg/mL [CP group] or 163.01 ± 45.24 pg/mL [healthy control], P <0.05), as was the RANKL/OPG (R/O) ratio (1.68 ± 0.33 versus 1.26 ± 0.35 [CP group] or 0.72 ± 0.25 [healthy control], P <0.001). Serum levels of OPG in both disease groups had significant negative correlations with HbA1C, and serum levels of RANKL in all participants had significant positive correlations with periodontal parameters. After periodontal intervention, both the well‐controlled and poorly controlled subgroups exhibited significant increases in OPG and decreases in RANKL in serum, and the R/O ratio was also notably reduced. Additionally, the poorly controlled subgroup exhibited a greater reduction in HbA1c and a greater increase in OPG than the well‐controlled subgroup. Conclusions: The changing trend in the serum RANKL/OPG system in patients with T2DM + CP was similar to that seen in CP patients and may be even more pronounced. Periodontal intervention effectively improved glucose metabolism and changed the serum RANKL/OPG system regardless of whether patients’ HbA1c was well‐controlled or poorly controlled over the 3‐month observation period.  相似文献   

14.
Background : This study aims to assess visfatin concentrations in serum and gingival crevicular fluid (GCF) and investigate this relationship in patients with type 2 diabetes mellitus (T2DM) and chronic periodontitis (CP) before and after non‐surgical periodontal treatment. Methods: Fifty‐four patients with T2DM and CP were recruited. The patients were randomly divided into two groups: treatment and control. Serum and GCF visfatin concentrations and glycated hemoglobin (HbA1c) levels were measured by enzyme‐linked immunosorbent assay at different time points (at baseline and 3 and 6 months after non‐surgical periodontal treatment). Results: Serum and GCF visfatin concentrations showed no significant differences between the groups at baseline (t test, P >0.05). A significant decline of visfatin in the treatment group was found in serum and GCF 3 months after non‐surgical periodontal treatment (t test, P <0.01). Baseline and 3‐month HbA1c levels were not significantly different, but at 6 months, a statistically significant difference was detected (t test, P >0.05). Conclusions: The data suggest that non‐surgical periodontal treatment is helpful for glucose control, an effect that may be associated with reduced visfatin in patients with T2DM and periodontitis. Furthermore, the data suggest that visfatin may be considered an inflammatory marker for periodontal diseases.  相似文献   

15.
Background: The objectives of the present study are to: 1) determine whether gingival crevicular fluid (GCF) chemerin is a novel predictive marker for patients with chronic periodontitis (CP) with and without type 2 diabetes mellitus (t2DM); 2) analyze the relationship between chemerin and interleukin (IL)‐6 in periodontally healthy individuals and in patients with CP and with and without t2DM; and 3) evaluate the effect of non‐surgical periodontal therapy on GCF chemerin levels. Methods: Eighty individuals were split into four groups: 20 who were systemically and periodontally healthy (CTRL), 20 with t2DM and periodontally healthy (DM‐CTRL), 20 systemically healthy with CP (CP), and 20 with CP and t2DM (DM‐CP). Individuals with periodontitis were treated with non‐surgical periodontal therapy. GCF sampling procedures and clinical periodontal measures were performed before and 6 weeks after treatment. Enzyme‐linked immunosorbent assay was used to measure chemerin and IL‐6 levels. Results: Greater values for GCF chemerin and IL‐6 levels were found in CP groups than in periodontally healthy groups, in DM‐CP than in CP, and in DM‐CTRL than in CTRL (P <0.008). GCF chemerin and IL‐6 levels decreased following therapy in CP groups (P <0.02). A comprehensive overview of all groups showed a statistically significant positive correlation of chemerin with IL‐6, glycated hemoglobin, sampled‐site clinical attachment level, and gingival index (P <0.05). Conclusions: In this study, periodontitis and t2DM induced aberrant secretion of chemerin, and non‐surgical periodontal therapy influenced the decrease of GCF chemerin levels in patients with CP with and without t2DM. Furthermore, it suggests GCF chemerin levels may be considered a potential proinflammatory marker for diabetes, periodontal disease, and treatment outcomes.  相似文献   

16.
目的 探讨牙周非手术治疗对伴二型糖尿病(T2DM)慢性牙周炎(CP)大鼠模型中血清白细胞介素6(IL-6)的表达及颈动脉血管壁的影响。方法 将28只6周龄清洁级SD大鼠随机分为A组(正常对照组,7只)、B组(T2DM+CP组,21只),将B组按照不同干预措施随机分成B1(自然进程组)、B2(机械治疗组)、B3(机械治疗+盐酸米诺环素+抗生素组),用酶联免疫吸附测定法进行血清IL-6的测定,苏木精-伊红(HE)染色后光镜下观察颈动脉组织的病理变化。结果 A组血管壁形态正常;B1组内皮细胞脱落消失,中膜弹性纤维排列紊乱,平滑肌组织局部坏死呈无定型颗粒,少量钙盐沉积,管壁增厚明显;B2、B3组内皮细胞脱落消失,中膜部分平滑肌细胞空泡变性,血管壁无明显增厚。B1组血清IL-6含量随时间持续升高,高于A组(P<0.001)。各干预组血清IL-6的含量在第一次干预后1周达到峰值,随后逐渐下降,在第二次干预后5周,B2、B3组均显著低于B1组(P<0.001)。结论 对于伴有糖尿病的牙周炎大鼠,单纯牙周机械治疗在短期内可能会引起血清IL-6水平升高,远期疗效则可能会降低机体的炎症状态,且伴有颈动脉血管病变的改善;联合使用局部及全身抗生素可能优化其疗效。  相似文献   

17.
目的 探讨牙周非手术治疗对伴二型糖尿病(T2DM)慢性牙周炎(CP)大鼠模型中血清白细胞介素6(IL-6)的表达及颈动脉血管壁的影响。方法 将28只6周龄清洁级SD大鼠随机分为A组(正常对照组,7只)、B组(T2DM+CP组,21只),将B组按照不同干预措施随机分成B1(自然进程组)、B2(机械治疗组)、B3(机械治疗+盐酸米诺环素+抗生素组),用酶联免疫吸附测定法进行血清IL-6的测定,苏木精-伊红(HE)染色后光镜下观察颈动脉组织的病理变化。结果 A组血管壁形态正常;B1组内皮细胞脱落消失,中膜弹性纤维排列紊乱,平滑肌组织局部坏死呈无定型颗粒,少量钙盐沉积,管壁增厚明显;B2、B3组内皮细胞脱落消失,中膜部分平滑肌细胞空泡变性,血管壁无明显增厚。B1组血清IL-6含量随时间持续升高,高于A组(P<0.001)。各干预组血清IL-6的含量在第一次干预后1周达到峰值,随后逐渐下降,在第二次干预后5周,B2、B3组均显著低于B1组(P<0.001)。结论 对于伴有糖尿病的牙周炎大鼠,单纯牙周机械治疗在短期内可能会引起血清IL-6水平升高,远期疗效则可能会降低机体的炎症状态,且伴有颈动脉血管病变的改善;联合使用局部及全身抗生素可能优化其疗效。  相似文献   

18.
目的:建立慢性牙周炎(chronic periodontitis,CP)合并高脂血症(hyperlipidemia,HL)的SD大鼠模型并对其进行牙周基础治疗,观察血清白介素-6(interleukin 6,IL-6)炎症因子及牙槽骨的影响。方法:SD大鼠随机分为4组,对照组(A)、HL组(B)、CP组(C)、HL+CP组(D);进行相应的建模处理,从建模开始15周后随机处死B组大鼠1只,取颈动脉分叉血管组织进行油红O染色,观察到泡沫细胞形成,则建模成功。再将C/D组随机分为2小组,C1/D1为自然进程组,C2/D2为牙周基础治疗组,进行2次牙周干预,分别于干预前1周、第1次干预后1周、第2次干预后1、3、5周采血,酶联免疫吸附法测定血清IL-6含量。实验结束后处死所有大鼠,取单侧上颌骨,剥离牙龈,进行亚甲基蓝染色,使用电子数显卡尺在徕卡显微镜(16X)下测量离体上颌骨实验牙釉质牙骨质界至牙槽嵴顶(cementoenamel junction and alveolar bone crest,CEJ- ABC)的距离(第一、二磨牙共12个位点)作为牙槽骨吸收值以检测牙槽骨吸收情况。使用SPSS21.0软件对所得数据进行统计学分析。结果:血清IL-6含量C、D组明显高于A组(P<0.05),其中,C1/D1组随时间推移一直呈现上升趋势,C2/D2组则在第2次干预后1周血清IL-6含量达到高峰,随观察时间延长则逐渐下降并低于基线水平(P<0.05);牙槽骨丧失量:C、D组>A组(P<0.001),而C2/D2组较C1/D1组牙槽骨丧失略有改善,但差异无统计学意义;牙槽骨吸收与血清IL-6水平呈Pearson正相关关系(P<0.01)。结论:高脂血症可加重牙周炎病变,牙周干预后短期内表现为机体炎症反应加重,远期则可能因炎症因子水平的降低而减轻全身病变进程。血清IL-6水平升高后,牙周局部表现为牙槽骨的吸收量增加。牙周基础治疗一定程度上可改善伴或不伴有高脂血症的牙周炎大鼠牙槽骨丧失的进程。  相似文献   

19.
Background: Overproduction of interleukin (IL)‐6 may play a pathologic role in rheumatoid arthritis (RA) and chronic periodontitis (CP). The present study assesses IL‐6 receptor (IL‐6R) inhibition therapy on the periodontal condition of patients with RA and CP. Methods: The study participants were 28 patients with RA and CP during treatment with IL‐6R inhibitor, and 27 patients with RA and CP during treatment without IL‐6R inhibitor. Periodontal and rheumatologic parameters and serum levels of cytokine and inflammatory markers and immunoglobulin G against periodontopathic bacteria were examined after medication with IL‐6R inhibitor for 20.3 months on average (T1) and again 8 weeks later (T2). Results: No differences were observed between the groups in any parameter values at T1, except for serum IL‐6 levels. The anti–IL‐6R group showed a significantly greater decrease in gingival index, bleeding on probing (BOP), probing depth (PD), clinical attachment level (CAL), and serum levels of IL‐6 and matrix metalloproteinase (MMP)‐3 from T1 to T2 than the control group (P <0.05). A significant correlation was found between changes in serum anticyclic citrullinated peptide levels and those in PD and CAL in the anti–IL‐6R group (P <0.05), whereas both groups exhibited a significant association between changes in serum MMP‐3 levels and those in BOP (P <0.05). Conclusion: Changes in periodontal and serum parameter values were different between the patients with RA and CP during treatment with and without IL‐6R inhibitor.  相似文献   

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