雌激素缺乏对大鼠牙槽骨吸收影响的实验研究

目的观察雌激素缺乏对大鼠牙槽骨吸收的影响。方法34只雌性SD大鼠随机分为4组。第1组假手术(n=8),第2组卵巢切除(n=9),第3组卵巢切除加牙周结扎(n=9),第4组卵巢切除、牙周结扎加雌激素治疗(n=8)。适应性喂养7天后行假手术或双侧卵巢切除术。第4组于术后第二天起皮下注射苯甲酸雌二醇．20μg／kg体重／次,三天一次。第3、4两组于卵巢切除术后28天,结扎丝结扎上颌第一磨牙诱导牙周炎。第63天处死全部大鼠。常规取材。观察牙用组织组织学改变。测量牙用骨丧失值(PBL)。比较牙用骨支持率(PBS)。检测血清碱性磷酸酶(ALP)。结果采用成组f检验,第1、2两组的PBL分别为0．398±O．147mm,0．663±0．132哪。PBS分别为O．588±O．058。0．440±0．197,组间差异均有统计学意义(P<0．05);第2、3两组的PBL、PBS组间差异均有统计学意义(P<0．05)。第3组的PBL为0．875±0．197mm,PBS为0．336±O．087;第3、4两组的PBL、PBS组间差别没有统计学意义(P>0．05),第4组的PBL为O．823±0．119mm,PBS为0．360±0．950。结论雌激素缺乏促进牙槽骨吸收,茵斑刺激加剧骨质疏松大鼠牙槽骨的吸收,雌激素替代治疗不能预防骨质疏松大鼠因茵斑刺激引发的牙槽骨吸收。     

雌激素对骨质疏松熏烟大鼠种植体周围骨的影响

目的:评价雌激素对骨质疏松熏烟大鼠种植体周围骨的影响.方法:40只3月龄雌性SD大鼠随机均分为4组:假手术组(sham)、卵巢去势组(OVX)、卵巢去势+吸烟组(OVX+S)、卵巢去势+吸烟+雌激素组(OVX+S+E),分别进行假手术和卵巢去势术,术后OVX+S和OVX+S+E组持续熏烟24周.去势术后12周,在大鼠右...     

大鼠实验性牙周炎对胰岛的影响

目的:通过观测实验性牙周炎大鼠胰岛组织形态、检测外周血胰岛素水平和胰岛环氧化酶(cyclooxygenase,COX-2)表达情况,探讨慢性牙周炎对胰岛的影响。方法:将25只SD大鼠随机分为对照组10只和慢性牙周炎组15只,慢性牙周炎组行双侧上颌磨牙结扎法建立牙周炎模型。基线和12周采集外周血,12周处死大鼠,取颌骨和胰腺组织标本做切片,观察牙周和胰腺的组织学改变,测量牙槽骨吸收高度,并采用免疫组织化学法检测胰岛COX-2表达情况。结果:12周时牙周炎组外周血中肿瘤坏死因子(tumor necrosis factor-α,TNF-α)达(10.02±2.16)pg/mL,较对照组(7.64±1.59)pg/mL有明显升高(P<0.05)。但牙周炎组的血清胰岛素水平、胰岛形态和COX-2的表达水平均未见明显差异。结论:中等程度慢性牙周炎尚不足以造成大鼠胰岛组织形态和功能的改变。     

绝经后骨质疏松大鼠实验性牙周炎动物模型研究

目的:通过卵巢切除术及钢丝结扎法建立绝经后骨质疏松大鼠实验性牙周炎动物模型。方法:选用3~4月龄雌性SD大鼠16只,随机分为假手术组(SHAM)、卵巢切除组(OVX),每组8只,卵巢切除术1周后进行钢丝结扎,于实验第8周处死大鼠,通过体重、骨密度测量、血清生化检测及组织学观察对动物模型进行评价。结果:与SHAM组相比,OVX组大鼠术后体重明显增加,血清碱性磷酸酶水平显著增高,而雌二醇水平及全身骨密度值明显降低(P<0.01)。股骨骨小梁数量减少,较为稀疏不连续。钢丝结扎侧磨牙牙龈乳头炎症明显,上皮钉突增生,牙槽嵴顶高度降低,OVX组牙槽骨呈疏松性改变,骨吸收明显高于SHAM组。结论:采用卵巢切除术及钢丝结扎法可建立绝经后骨质疏松大鼠实验性牙周炎动物模型,为探讨绝经后骨质疏松与牙周炎的相互作用及其机制提供了有效的手段。     

雌激素对去卵巢大鼠牙槽骨组织结构和MT1-MMP表达的影响

目的:研究雌激素对去卵巢大鼠牙槽骨组织结构、MT1-MMP表达的影响.方法:对大鼠牙槽骨组织石蜡切片进行HE染色和MT1-MMP免疫组化染色,观察不同时期的正常大鼠、去卵巢大鼠和去卵巢后补充雌激素大鼠的牙槽骨组织结构情况和牙槽骨中MT1-MMP的表达及其分布特征.结果:雌激素缺乏会导致大鼠牙槽骨的骨代谢失衡,牙槽嵴与固有牙槽骨吸收、破坏;成骨细胞和骨细胞MT1-MMP表达降低,而破骨细胞MT1-MMP表达升高.结论:雌激素缺乏引起牙槽骨吸收,MT1-MMP表达水平和分布部位变化可能对其有调节作用.     

2种给药方式下辛伐他汀对牙周炎骨质疏松大鼠上颌骨骨丢失的影响

目的比较辛伐他汀(Simvastatin,SIM)在不同给药方式下抑制牙周炎骨质疏松大鼠上颌骨骨丢失的作用效果。方法 24只4月龄雌性SD(Sprague Dawley)大鼠,随机分成4组:假手术组(SHAM),去势+绑线组(OVX+LIG),去势+绑线+辛伐他汀灌胃给药组(OVX+LIG+Oral SIM),去势+绑线+辛伐他汀局部用药组(OVX+LIG+Local SIM)。适应性喂养1周后,进行骨质疏松造模手术——双侧卵巢切除术(OVX),4周后,进行牙周炎造模手术——分别于双侧上颌骨第一、第二磨牙进行8字结扎绑线术(LIG),4周后拆除绑线,用药组开始辛伐他汀给药。8周后处死所有大鼠,收集双侧上颌骨和血清,分别进行进一步检测。检测包括micro-CT扫描,硬组织切片观察、染色,酶联免疫吸附实验(ELISA)。结果相比于对照OVX+LIG组,OVX+LIG+Local SIM组可见明显釉牙骨质界-牙槽嵴顶(CEJ-ABC)距离的减少(P<0.05),OVX+LIG+Oral SIM组与OVX+LIG+Local SIM组可见明显牙槽骨的骨密度(BMD)和骨体积分数(BVF)升高,OVX+LIG+Oral SIM组可见明显骨钙素(OC)上升,抗酒石酸酸性磷酸酶5b(TRAP5b)下降。结论局部或全身系统应用辛伐他汀能减缓牙周炎伴骨质疏松大鼠上颌骨的骨丢失,其中局部注射辛伐他汀对牙槽嵴顶骨形成具有促进作用。     

雌激素缺乏对大鼠核因子C（Nfic）与成骨相关基因表达的影响

目的：通过检测分析骨质疏松大鼠股骨组织核因子C(Nuclear Factor I-c,Nfic)与成骨相关基因表达情况,探讨雌激素缺乏状况下两类基因表达的相关性,探寻雌激素相关的骨质疏松发生原理。方法：3月龄未交配雌性SD大鼠20只,随机分为两组： A、假去势手术组(SHAM); B、去势手术组(OVX)。对A组大鼠行假去势手术,B组大鼠行去势手术。去势手术前、去势手术后1、2、3、4、5、6周及处死前称重,观察大鼠体重变化。卵巢切除术后1.5个月,采用双能骨密度测量仪测量大鼠腰椎及股骨远中骨密度,处死后,取双侧后肢股骨进行Q-PCR,检测核因子C(Nfic)、核心结合因子2(Runx2)、碱性磷酸酶(Alp)的mRNA表达情况。结果：去势手术前,两组大鼠体重差异无统计学意义(P>0.05);术后2、4、6周, OVX组大鼠体重较SHAM组显著增加(P<0.05, P<0.01, P<0.01)。术前,两组大鼠腰椎及左股骨骨密度差异无统计学意义(P>0.05);术后1.5个月, OVX组大鼠腰椎及左股骨骨密度较SHAM组显著降低(P<0.01, P<0.05)。去势组大鼠的Nfic、 Runx2、 Alp基因表达量明显低于假去势手术组(P<0.05)。结论：雌激素缺乏大鼠较正常组肥胖,骨密度减低,骨质改变,成骨能力减弱,成脂功能提高; Nfic基因与Runx2、 Alp成骨相关基因表达量呈正相关。     

左归丸对实验性骨质疏松牙周炎大鼠牙周组织OPG、RANKL表达的影响

选取6月龄纯种雌性SD大鼠46只,随机分为4组,正常组(N组)10只,去势牙周炎组(OVX-PD组)12只,去势牙周炎戊酸雌二醇治疗组(ERT组)12只,去势牙周炎左归丸治疗组(ZGT组)12只。建立骨质疏松牙周炎动物模型并按分组用药,3个月后处死动物,检测牙周组织中的骨保护因子(OPG)、破骨细胞核因子КB受体活化因子配体(RANKL)。ZGT组、ERT组可见牙周袋变浅,牙槽骨可见新骨生成;ZGT组及ERT组牙周组织中OPG含量明显高于OVX-PD组(P<0.01),RANKL含量明显低于OVX-PD组(P<0.01)。     

淫羊藿苷口服给药对骨质疏松牙周炎小鼠牙槽骨吸收的影响

目的:研究口服淫羊藿苷（ICA）对骨质疏松小鼠牙周炎引起的牙槽骨吸收的抑制作用。方法:3月龄、雌性、C57BL/6J小鼠随机分为3组,即正常组（SHAM组）、卵巢切除+口腔涂布牙龈卟啉单胞菌（Pg）+淫羊藿苷组（OVX+Pg+ICA）、卵巢切除+Pg口腔涂布组（OVX+Pg）。小鼠适应性喂养1周,第2周进行双侧卵巢切除术,诱导小鼠骨质疏松形成。从第4周开始,对小鼠牙周涂布Pg,1次/d,连续1周。第12周收集左侧下颌骨进行固定切片及染色,分析各组之间牙槽骨吸收高度的差异。收集右侧下颌骨进行亚甲蓝染色,分析各组间牙槽骨吸收面积的差异;收集双侧上颌骨牙周组织蛋白,分析成骨相关蛋白的表达差异。采用SPSS16.0软件包对数据进行统计学分析。结果:小鼠股骨及牙周组织切片染色显示,成功建立了小鼠骨质疏松牙周炎模型。对牙槽骨吸收距离和面积的测量分析显示,相比于OVX+Pg组,口服淫羊藿苷可显著减少釉-牙骨质界-牙槽嵴顶（CEJ-ABC）的距离及颊舌侧牙槽骨吸收面积（P<0.05）;Western免疫印迹显示,相比于OVX+Pg组,OVX+Pg+ICA组中Runx2、OSX、OCN及OPN蛋白表达水平显著升高（P<0.05）。结论:口服淫羊藿苷在预防小鼠骨质疏松发生的同时,可有效减少牙周炎引起的牙槽骨吸收。     

Effect of an estrogen-deficient state and its therapy on bone loss resulting from an experimental periodontitis in rats

OBJECTIVE: The aim of this study was to evaluate the impact of an estrogen-deficient state and its therapies (estrogen and calcitonin administration) upon bone loss resulting from an experimental periodontitis. METHODS: Fifty-eight Wistar rats were divided into four groups: group 1 (n = 15): sham operated; group 2 (n = 15): ovariectomized; group 3 (n = 14): ovariectomized plus calcitonin administration; group 4 (n = 14): ovariectomized plus estrogen administration. Twenty-one days after ovariectomy or sham surgeries, the ligature was randomly placed. Sixty days later, the animals were killed and the specimens routinely processed. In addition, serum levels of alkaline phosphatase and calcium were assessed. RESULTS: Intergroup analysis revealed that an estrogen-deficient state significantly increased bone loss resulting from periodontitis and that such an effect could not be prevented either by estrogen or calcitonin administration (0.34 +/- 0.13, 0.65 +/- 0.06, 0.63 +/- 0.19, 0.67 +/- 0.28 for groups 1, 2, 3 and 4, respectively). Furthermore, an estrogen-deficient state presented a direct effect on the alveolar bone regardless of plaque accumulation and this effect may be significantly reduced by estrogen administration (p < 0.05). Serum analysis demonstrated a higher bone turnover for the animals with estrogen deficiency, and estrogen therapy restored bone metabolism. CONCLUSION: Estrogen administration may prevent the direct effect of an estrogen-deficient state on alveolar bone; however, neither estrogen nor calcitonin administration could prevent this effect when associated with a response to a plaque-related inflammatory process.     

人骨保护素质粒转染抑制大鼠实验性牙周炎骨吸收的研究

目的:将自行构建的质粒载体pcDNA3.1-h OPG,通过体内转染,评价OPG直接基因转染疗法对大鼠实验性牙周炎牙槽骨吸收的影响,为牙周炎以及种植体周炎的生物治疗提供实验依据.方法:将30只SD大鼠随机分为3组,即I组生理盐水组(n=10,100μg/只)、Ⅱ组pcDNA3.1(-)组(n=10,100μg/只)、Ⅲ组pcDNA3.1-hOPG组(n=10,100μg/只).通过丝线结扎、接种牙周炎可疑致病菌、喂高糖软食诱发实验性牙周炎.结扎28d后处死,通过大体标本、组织学等观察牙槽骨吸收、OPG及破骨细胞变化.结果:Ⅲ组结扎侧OPG表达强度增加,牙槽骨吸收量减少(P＜0.05),活化破骨细胞数降低(P＜0.05).结论:OPG重组质粒转染,减少破骨细胞数量,有效减缓实验性牙周炎引起的牙槽骨吸收破坏.     

Effect of sodium alendronate on alveolar bone resorption in experimental periodontitis in rats

BACKGROUND: Bisphosphonates are potent inhibitors of bone resorption and were shown to inhibit bone resorption in experimental periodontitis by unknown mechanisms. We studied the effect of the aminobisphosphonate sodium alendronate (SA) in experimental periodontitis. Wistar rats were subjected to ligature placement around the second upper left molars. METHODS: Animals were treated with SA 0.01 to 0.25 mg/kg subcutaneously (sc), either 1 hour before (prophylactic) or starting 5 days after (therapeutic) periodontitis induction and daily until the rats were sacrificed (11 days). Controls received saline. Animals were weighed daily. Alveolar bone loss was measured as the difference (in millimeters) between the cusp tip and the alveolar bone. The periodontium and the surrounding gingivae were examined at histopathology, and the neutrophil influx into the gingivae was assayed using myeloperoxidase activity. The local bacterial flora was assessed through culture of the gingival tissue in standard aerobic and anaerobic media. RESULTS: Alveolar bone loss was significantly and dose dependently inhibited by SA either as a prophylactic or therapeutic treatment compared to the control. SA reduced tissue lesion at histopathology, with partial preservation of the periodontium, coupled to decreased myeloperoxidase activity compared to the control. The reduced neutrophil influx was also shown in carrageenan-induced peritonitis, used as a control experiment for this parameter. SA also significantly inhibited the growth of pigmented bacilli and Fusobacterium nucleatum, which are important in the pathogenesis of periodontal disease. SA also inhibited the in vitro growth of isolated Peptostreptococcus sp. CONCLUSION: Sodium alendronate preserves alveolar bone resorption and has anti-inflammatory and antibacterial activities in experimental periodontitis.     

环肌酸抑制大鼠牙周炎周围牙槽骨吸收的实验研究

目的:通过体外和体内实验探讨环肌酸对牙周炎造成的牙槽骨吸收的抑制作用.方法:体外实验通过细胞活力测定、碱性磷酸酶染色和茜素红染色、抗酒石酸酸性磷酸酶染色和实时反转录聚合酶链反应(RT-PCR)等检测,评价环肌酸对成骨细胞和破骨细胞增殖和分化的影响.动物实验将20只大鼠分为4组,A组为对照组,B组采用牙周结扎+生理盐水注...     

Drinking green tea alleviates alveolar bone resorption in ligature-induced periodontitis in mice

ObjectivesIt has been reported that green tea exerts antibacterial, anti-inflammatory, and antioxidant effects. The purpose of the present study was to evaluate the effects of drinking green tea on bone resorption in ligature-induced periodontitis in mice.MethodsSixty C57BL/6 eight-week-old male mice were used. To induce periodontitis, a ligature was placed for 7 days around the upper left second maxillary molar. After ligature removal, the animals were administered different concentrations of green tea (1.5 g/60 mL, 3 g/60 mL, or 6 g/60 mL) or distilled water. At 1 and 2 weeks of administration, the animals were sacrificed and micro-CT images of the maxillae were taken. Next, the depth and area of alveolar bone loss in the buccal and palatal sides were measured. The number of inflammatory cells and osteoclasts in histological sections were counted.ResultsThe result showed ligature-induced alveolar bone loss. Green tea inhibited ligature-induced bone loss in the buccal side in a dose-dependent manner. Histologically, ligature increased the number of inflammatory cells and osteoclasts, but this effect was alleviated by green tea.ConclusionsEvidence from this animal experiment suggested that drinking green tea would be potentially beneficial to reduce alveolar bone loss in ligature-induced periodontitis.     

Effects of glucocorticoid-induced osteoporosis on bone tissue of rats with experimental periodontitis

ObjectiveTo evaluate the effects of osteoporosis induced by glucocorticoid (GIOP) on bone tissue of rats with experimental periodontitis (EP).Design48 male Wistar rats divided into groups: Naïve, EP, GIOP and GIOP + EP. Rats of GIOP and GIOP + EP groups received 7 mg/kg of dexamethasone intramuscularly once a week for 5 weeks. Following, EP and GIOP + EP groups were subjected to ligature-induced periodontitis. Naïve group experienced no manipulation. After 11 days, the animals were euthanized and left maxillae collected for macroscopic, radiographic, micro-tomographic and microscopic analysis of alveolar bone loss (ABL). Blood samples were collected for determination of bone-specific alkaline phosphatase (BALP) levels and the right femurs were removed for radiographic and biomechanical analysis.ResultsEP caused ABL and reduced BALP levels (p < 0,05), but it did not change the architecture or biomechanics of femur, compared to Naïve. GIOP did not cause ABL, but it significantly decreased alveolar bone mineral density (ABMD), bone percentage and trabecular thickness (Tb.Th) and increased alveolar bone porosity (p < 0.05) and significantly reduced BALP serum levels, as well as radiographic density and Young’s module of femur, compared to Naïve. There was a greater ABL in group GIOP + EP when compared to EP (p < 0.05). GIOP + EP caused a greater decrease on ABMD, Tb.Th, bone percentage and increased bone porosity (p < 0.05) and also presented a significant reduction in BALP levels (p < 0.05), in radiographic density and in Young’s module of femur compared to EP (p < 0.05).ConclusionsGIOP can potentiate the destructive effects of EP on alveolar bone and alter the systemic bone loss, by promoting bone resorption and reducing osteoblast activity.     

尼古丁对实验性牙周炎大鼠牙槽骨影响的显微CT观察

目的 建立牙周炎大鼠的牙槽骨三维模型,采用显微CT观察尼古丁对大鼠牙槽骨的影响.方法 36只SD大鼠,丝线结扎上颌右侧(实验侧)第二磨牙颈部,左侧不予结扎,作为自身对照(对照侧),使用完全随机分组方法分为对照组(A)及尼古丁注射低剂量(B)和高剂量(C)组,每组12只.分别给予生理盐水和尼古丁0.83、1.67 mg·kg-1·d-1腹腔注射.每组分别于给药后第14、28天各处死6只,取双侧上颌磨牙区牙体牙周复合组织,行显微CT扫描、重建、测最和分析.结果 随尼古丁给药剂量增加,双侧牙槽骨骨密度、骨体积分数、骨小梁厚度逐渐降低,牙槽骨高度丧失与骨小梁间隙逐渐升高.28 d时C组牙槽骨高度丧失[对照侧和实验侧分别为(0.61±0.14)、(1.39±0.09)mm]显著高于B组[对照侧和实验侧分别为(0.39±0.10)、(1.31±0.06)mm]和A组[对照侧和实验侧分别为(0.30±0.06)、(0.94±0.07)mm];C组牙槽骨骨密度[对照侧和实验侧分别为(617.86±34.27)、(572.46±31.62)mg/cm3]显著低于B组[对照侧和实验侧分别为(660.04±36.73)、(604.97±32.59)mg/cm3]和A组[对照侧和实验侧分别为(709.15±34.95)、(657.04±30.06)mg/cm3].结论 尼古丁可加重丝线结扎造成的大鼠牙槽骨骨量丧失和骨质微观结构的变化,导致牙槽骨骨质疏松.