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雌激素对骨质疏松大鼠牙槽骨改建及IL-1表达的影响 总被引:12,自引:5,他引:7
目的:探讨雌激素对骨质松牙槽骨改建中IL-1的表达与分布的影响及意义。方法:在建立SD大鼠骨质疏松模型的基础上,用免疫组化染色方法,观察IL-1在骨质疏松以及雌激素治疗后的牙槽骨中的表达变化。结果:IL-1在骨质疏松牙槽骨中有较强的表达,阳性反应主要分布于破骨细胞,部分成骨细胞及骨细胞中,而在用雌激素治疗骨质疏松组中,IL-1的阳性表达程度明显下降。 相似文献
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目的:探讨大豆异黄酮对绝经后牙槽骨骨质疏松的防治作用。方法:将32只3月龄雌性SD大鼠随机分为4组,适应性喂养1周后,A组为假手术组,B、C、D组均摘除双侧卵巢。C组大鼠于术后1周开始肌肉注射苯甲酸雌二醇(0.1mg/kg),每周1次。而A、B和D组肌肉注射等量橄榄油。D组大鼠于术后1周开始每天给予大豆异黄酮混悬液灌胃(100mg/kg)。其余3组用等量生理盐水灌胃。各组动物在同等条件下饲养,自由进食、饮水。实验结束后处死动物,收集大鼠下颌骨标本。对组织HE染色切片进行骨形态及计量学分析。结果:去卵巢后,大鼠牙槽骨呈疏松样改变。大豆异黄酮治疗后的D组.骨小梁面积、骨小梁周长、骨小梁面积比、骨小梁数量及分离度与去卵巢的B组有显著性差异,而与雌激素治疗的C组无显著性差异。结论:雌激素缺乏可引起牙槽骨骨质疏松。大豆异黄酮与雌激素一样。可以抑制破骨细胞性骨吸收.并对骨形成有刺激作用。 相似文献
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目的:探讨RANKL-RANK-OPG轴在丹参素防治牙槽骨骨质疏松中的作用。方法:SD大鼠随机分为3组:对照组、去卵巢组和丹参素治疗组。实验90 d后取大鼠牙槽骨,HE染色观察牙槽骨组织形态学改变,组织化学染色方法检测牙槽骨组织中TRAP的活性,免疫组化的方法检测牙槽骨组织中RANKL和OPG的表达情况。结果:与去卵巢组相比:丹参素治疗组牙槽骨骨量明显增多,TRAP阳性的破骨细胞数减少,RANKL/OPG减小。结论:丹参素防治牙槽骨骨质疏松可能与其调控RANKL-RANK-OPG轴有关。 相似文献
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雌激素对骨质疏松大鼠牙槽骨改建过程中IL-1表达的影响 总被引:3,自引:0,他引:3
目的:研究雌激素对骨质疏松牙槽骨改建过程中白细胞介素-1(IL-1)的分布及表达的影响,探讨雌激素对骨质疏松牙槽骨改建影响的机制。方法:利用大鼠卵巢切除术制成骨质疏松模型,并运用免疫组化染色方法及半定量分析,观察IL-1在骨质疏松及雌激素治疗后的牙槽骨中的表达变化。结果:IL-1在骨质疏松牙槽骨中的表达明显增强,阳性反应主要分布于破骨细胞、部分成骨细胞中,而经雌激素治疗后,IL-1的阳性表达明显下降。结论:雌激素对骨质疏松大鼠牙槽骨中IL-1的表达有明显的抑制作用。 相似文献
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雄激素对大鼠牙槽骨骨量的影响 总被引:2,自引:1,他引:1
目的:探讨去睾丸对大鼠牙槽骨骨量的影响。方法:24只雄性SD大鼠随机分为3组:假手术组(Con)、去睾丸组(ORX)和雄激素治疗组(TP)。除Con组外,其余行双侧睾丸摘除术。Con组和ORX组给予溶媒5ml/kg/d灌胃,TP组给予丙酸睾丸酮5mg/kg/d灌胃。实验12周后取大鼠的牙槽骨,脱钙,切片,染色,用骨形态计量学方法测量牙槽骨松质骨的骨量,计算牙槽骨的骨静态学参数。结果:与Con组相比较,ORX组牙槽骨骨小梁厚度降低(P〈0.05),其他变化均不明显。结论:雄激素缺乏使大鼠牙槽骨有丢失趋势,但不明显。 相似文献
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Alendronate阻止牙槽骨骨吸收的实验研究 总被引:3,自引:1,他引:2
目的:评价双膦酸盐Alendronate抑制牙槽骨骨吸收的作用。方法:建立骨质疏松及牙槽骨吸收动物模型,建模术后六周,给实验组皮下注射Alendronate每周3次,共6周;用血生化指标骨生物力学、骨密度测量、组织形态学等方法进行药效评价。结果:股骨骨密度对照组与用药组相比明显降低(P<0.01);血清碱性磷酸酶对照组与用药组相比明显升高(P<0.01);骨生物力学各项指标实验组与对照组也有明显差异。组织形态学:实验组牙龈轻度炎症,牙槽骨水平吸收与对照组相比明显减少;对照组牙龈乳突炎症明显,上皮钉突增生。炎细胞浸润,牙槽骨明显水平吸收。结论:Alendronate治疗骨质疏松有明显的疗效,能够增加骨量,阻止骨丢失;对病理性牙槽骨骨吸收有显著的治疗作用。 相似文献
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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。 相似文献
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长期超生理剂量的醋酸泼尼松对大鼠牙槽骨骨量的影响 总被引:1,自引:1,他引:0
目的:探讨长期超生理剂量的糖皮质激素对大鼠牙槽骨骨量的影响.方法:用醋酸泼尼松2.7 mg/kg/d给大鼠灌胃90 d,模拟建立类固醇性骨质疏松动物模型,实验90 d后取大鼠的牙槽骨,脱钙,切片,染色,用骨形态计量学方法测量牙槽骨松质骨的骨量,计算牙槽骨的骨静态参数.结果:与对照组相比,模型组牙槽骨骨小梁面积百分数、骨小梁厚度,骨小梁数量、骨小梁分离度差异均没有统计学意义.结论:本实验剂量醋酸泼尼松不能引起大鼠牙槽骨骨量丢失. 相似文献
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目的 比较不同去势时间对大鼠牙槽骨微结构的影响,探讨牙槽骨骨质疏松大鼠模型建立成功的参数。方法 24只6月龄雌性SD大鼠,随机分为4组:(1)对照组1(Sham1);(2)去势组1(OVX1);(3)对照组2(Sham2);(4)去势组2(OVX2)。分别在全麻下行假手术和双侧卵巢去势术。于术后3个月和4个月处死各组大鼠,取双侧上颌骨标本,通过Micro-CT扫描、HE染色、抗酒石酸酸性磷酸酶(TRAP)染色、Van Gieson染色、荧光双标观察并分析牙槽骨微结构的变化。结果 去势3个月后OVX1组与Sham1组大鼠相比,体重增加25.09%(P<0.01);牙槽骨骨体积分数(BV/TV)、骨小梁数目(Tb.N)、骨小梁分离度(Tb.Sp),牙骨质界-牙槽嵴顶(CEJ-ABC)距离无改变(P>0.05),骨小梁宽度(Tb.Th)降低了12.44%(P<0.05),破骨细胞数量增加了40.12%(P<0.01);骨形成沉积率(MAR)无明显改变(P>0.05);去势4个月后OVX1组与Sham1组大鼠相比,体重进一步增加了26.25%(P<0.01),BV/TV、Tb.Th、MAR分别降低了11.15%、17.22%和38.45%(P<0.01),Tb.Sp和破骨细胞数量分别增加了81.89%和35.67%(P<0.01),Tb.N和CEJ-ABC距离无变化(P>0.05),HE和Van Gieson染色均表明OVX2组大鼠牙槽骨骨量降低,骨髓腔面积增加,骨小梁微结构破坏、变细,部分区域发生断裂。结论 6月龄雌性SD大鼠去势4个月后,牙槽骨发生明显骨质疏松,可作为合适的牙槽骨骨质疏松大鼠模型参数的理论依据。 相似文献
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目的 :观察二膦酸盐对去卵巢骨质疏松大鼠下颌牙槽骨内破骨细胞以及牙本质基质蛋白1(dentin matrix protein1,DMP1)表达的影响。方法 :取6月龄SD大鼠30只,随机分为假手术组(Sham)、去卵巢模型组(OVX)和二膦酸盐药物治疗组(RIS),每组10只。Sham组大鼠仅术中暴露卵巢不切除,OVX组大鼠行"双侧卵巢切除术+生理盐水皮下注射",RIS组行"双侧卵巢切除术+利塞磷酸钠(2.4μg/kg)皮下注射"。术后3个月取各组大鼠下颌骨常规脱钙,甲苯胺兰染色观察下颌第一磨牙(M1)区域牙槽骨组织学结构,抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase,TRAP)染色观察M1区域牙槽纵隔破骨细胞的骨吸收情况,免疫组化染色观察各组M1牙槽骨DMP1分布表达情况,并进行相关半定量图像分析。结果:与Sham组相比,OVX组TRAP阳性细胞数增加;而较OVX组而言,RIS组TRAP阳性细胞数显著减少(P<0.05)。免疫组化染色显示,各组DMP1不仅表达在牙槽骨骨细胞内,牙槽间隔的松质骨骨基质、牙周韧带中均可见其表达,OVX组M1牙槽骨DMP1表达较Sham组减少(P<0.05),而RIS组表达较OVX组有升高。结论:二膦酸盐能减少骨质疏松大鼠下颌牙槽骨破骨细胞数量,并上调DMP1表达,从而影响下颌牙槽骨矿化。 相似文献
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丹参素防治去卵巢大鼠牙槽骨骨量的丢失 总被引:7,自引:0,他引:7
目的:探讨丹参素对大鼠牙槽骨骨量的影响、丹参素与雌激素防止牙槽骨骨丢失的疗效比较以及丹参素与雌激素是否具有防止牙槽骨骨丢失的协同效应.方法:40只SD大鼠随机分为5组:假手术组(Sham)、去卵巢组(OVX)、雌激素组(E2)、丹参素(Tan)及丹参素与雌激素联合用药组(E2 Tan).雌激素组、丹参素组和丹参素与雌激素联合用药组分别用雌激素100 μg·kg-1·d-1、丹参素12.5 mg·kg-1·d-1和丹参素12.5 mg·kg-1·d-1加雌激素50 μg·kg-1·d-1给大鼠灌胃,17欠/d,共90 d.实验90 d后取大鼠的牙槽骨,脱钙,切片,染色,用骨形态计量学方法测量牙槽骨松质骨的骨量,计算牙槽骨的骨静态参数.结果:与假手术组相比,去卵巢组牙槽骨骨小梁面积百分数减小(P<0.01)和骨小梁分离度增大(P<0.05).与去卵巢组相比,雌激素组牙槽骨骨小梁面积百分数、骨小梁厚度均增大(P<0.01),丹参素组及联合用药组牙槽骨骨小梁面积百分数增大(P<0.05).与丹参素组相比,雌激素治疗组及联合用药组各项测量指标差别均没有统计学意义.结论:丹参素都能防治牙槽骨骨质疏松且疗效与雌激素相当,但丹参素与雌激素在防治牙槽骨骨质疏松时没有协同作用. 相似文献
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We have investigated the effect of ovariectomy combined with a low Ca diet on bone healing following the implantation of bioactive glass into extraction sockets, in rats. Ovariectomized rats received a low Ca diet from the day of surgery until sacrifice while sham-operated animals were fed a standard laboratory chow. Two weeks after surgery the upper incisors were extracted and the alveolar sockets in both groups were partially filled with a particulate bioglass (PerioGlas®). The animals were killed 1, 2, 3 and 9 weeks after tooth extraction and the relative volume fraction of the healing components (bone trabeculae, connective tissue and coagulum remnants) was estimated in histological paraffin sections by a histometric differential point-counting method. The bioglass particles persisted inside the socket for all the experimental periods and, as bone repair proceeded, they were progressively enclosed in newly formed bone trabeculae which in some cases established a close contact with their surface. The volume fraction of neoformed bone trabeculae relative to the volume fraction of connective tissue and coagulum remnants was greater in the sockets of ovariectomized animals implanted with bioglass than in those of the overiectomized non-implanted groups. 相似文献
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目的: 研究骨碎补总黄酮对合并牙列缺损或缺失的骨质疏松症患者牙槽骨高度、厚度、骨密度及牙槽嵴顶宽度的影响。方法: 将符合纳入标准的46例患者随机分为实验组和对照组,每组23例,实验组服用强骨胶囊,对照组服用阿仑膦酸钠片;于药物治疗前及治疗后1、3、6个月时分别行锥形束CT(CBCT)检查,应用Anatomage invivo 5软件测量并观察牙槽骨高度、厚度、骨密度及牙槽嵴顶宽度的变化,采用SPSS17.0软件包进行统计学分析。结果: 对照组牙槽骨颊(唇)侧皮质骨的骨密度在药物治疗后1个月时较实验组显著升高(P<0.05),实验组牙槽骨的颊(唇)侧皮质骨骨密度在药物治疗后3个月和6个月时均较对照组显著升高(P<0.05)。对照组牙槽嵴顶宽度和牙槽骨的颊(唇)侧皮质骨厚度在药物治疗后3个月较实验组显著升高(P<0.05),在药物治疗后6个月时,2组间差异无统计学意义(P>0.05)。不同时点实验组和对照组在基骨的颊(唇)侧皮质骨、松质骨、腭(舌)侧皮质骨的厚度变化均无显著差异(P>0.05)。结论: 骨碎补总黄酮能显著增加骨质疏松症患者牙槽骨骨密度,在增加牙槽骨的颊(唇)侧皮质骨的骨密度上较阿仑膦酸钠存在优势;骨碎补总黄酮能增加骨质疏松症患者牙槽骨的颊(唇)侧皮质骨厚度,对牙槽嵴顶宽度、牙槽骨高度影响不大。 相似文献
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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. 相似文献
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Effect of Healing Time on New Bone Formation After Tooth Extraction and Ridge Preservation With Demineralized Freeze‐Dried Bone Allograft: A Randomized Controlled Clinical Trial
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Background: Clinicians and patients continually search for procedures to decrease time from tooth extraction to restoration. Evidence to date is limited concerning timing of ridge preservation healing and reentry for implant placement. The first objective of this study is to histologically evaluate new bone formation 8 to 10 weeks versus 18 to 20 weeks after extraction of non‐molar teeth and ridge preservation using demineralized freeze‐dried bone allograft (DFDBA). The second objective is to compare dimensional changes including ridge width and height at the two healing time points. Methods: Forty‐four patients had tooth extraction and ridge preservation with DFDBA that was obtained from a single donor. Clinical measurements were made to evaluate ridge height and width. Patients were randomly allocated to short‐term (8 to 10 weeks) and long‐term (18 to 20 weeks) healing groups. Sites were reentered at the appropriate healing time, core biopsy was obtained, and a dental implant was placed. The same ridge dimensions were measured at time of implant placement. Histomorphometric analysis was performed to determine percentage of new vital bone formation, residual graft, and connective tissue (CT)/other. Results: A significantly higher percentage (47.41%) of new vital bone formation was found in the long‐term healing group compared with the short‐term healing group (32.63%) (P = 0.01). There was no significant difference in percentage of residual graft, percentage of CT/other, or ridge dimensional changes. Conclusion: This study indicates significantly greater new vital bone formation occurs after tooth extraction and ridge preservation with DFDBA when sites healed for 18 to 20 weeks compared with 8 to 10 weeks prior to dental implant placement. 相似文献