去卵巢大鼠骨组织的变化

目的：观察去卵巢对大鼠骨组织的改变，以建立妇女绝经后骨质疏松的动物模型。方法：选用３月龄ＳＤ雌性大鼠１６只，随机分为对照组和去卵巢组。去卵巢组的大鼠的双侧卵巢被切除，对照组做假手术，持续９０天。用骨矿测定仪测量大鼠股骨的骨密度及在半自动图像分析仪观测胫骨近端骨小梁的静、动态指标，并在扫描电镜下观察大鼠股骨松质骨结构的改变。结果：与对照组比较，去卵巢组大鼠股骨远端的骨密度明显降低。胫骨骨小梁的面积减     

去卵巢大鼠骨组织的变化

目的:观察去卵巢对大鼠骨组织的改变,以建立妇女绝经后骨质疏松的动物模型。方法:选用3月龄SD雌性大鼠16只,随机分为对照组和去卵巢组。去卵巢组的大鼠的双侧卵巢被切除,对照组做假手术,持续90天。用骨矿测定仪测量大鼠股骨的骨密度及在半自动图像分析仪观测胫骨近端骨小梁的静、动态指标,并在扫描电镜下观察大鼠股骨松质骨结构的改变。结果:与对照组比较,去卵巢组大鼠股骨远端的骨密度明显降低。胫骨骨小梁的面积减少,骨小梁间隙增加。股骨的骨小梁减少,变细,断裂,连接不紧密,表面常见骨吸收形成的陷窝。结论:用切除卵巢的方法造成雌激素缺乏,导致骨质疏松,是研究因绝经引起原发性骨质疏松的可靠动物模型。     

去卵巢大鼠骨组织的变化

目的:观察去卵巢对大鼠骨组织的改变,以建立妇女绝经后骨质疏松的动物模型。方法:选用3月龄SD雌性大鼠16只,随机分为对照组和去卵巢组。去卵巢组大鼠的双侧卵巢被切除,对照组做假手术,持续90天。用骨矿测定仪测量大鼠股骨的骨密度及在半自动图像分析仪观测胫骨近端骨小梁的静、动态指标,并在扫描电镜下观察大鼠股骨松质骨结构的改变。结果:与对照正常组比较,去卵巢组大鼠股骨的远端的骨密度降低(P<0.05)。胫骨骨小梁的面积减少,骨小梁间隙增大。股骨的骨小梁变少,变细,断裂,连接不紧密,表面常见骨吸收形成的陷窝。结论:用切除卵巢的方法造成雌激素缺乏,导致骨质疏松,作为研究因绝经引起的原发性骨质疏松的可靠动物模型。     

Micro CT定量研究去卵巢山羊胫骨平台松质骨微结构特点

背景：骨质疏松时胫骨平台松质骨微结构发生显著变化,Micro CT是一种能够全面、立体、无创测量骨微结构、评估骨质量及预测骨强度的新兴技术,近年来在骨质疏松研究领域得到日益广泛的应用。 目的：应用Micro CT技术定量研究去卵巢山羊胫骨平台松质骨的微结构特点。 方法：将12只2.5岁健康雌性山羊随机分为去卵巢组和假手术组,去卵巢组行卵巢切除,假手术组切除等量腹腔脂肪组织,每组各6只。两组实验动物分别在术后2,4年处死,分离并截取左侧胫骨平台,行Micro CT扫描,分别测量胫骨平台骨骺松质骨和干骺端松质骨微结构参数。 结果与结论：术后2和4年,与假手术组相比,去卵巢组胫骨平台骨骺和干骺松质骨微观结构参数-骨体积分数、骨小梁数量和骨小梁厚度均降低(P < 0.05),骨小梁分离度均升高(P < 0.05),基本呈时间依赖性变化。仅在术后4年,去卵巢组骨骺松质骨微观结构参数骨小梁厚度与假手术组相比差异无显著性意义(P > 0.05),其骨小梁分离度、骨小梁厚度与去卵巢组术后2年相比差异无显著性意义(P > 0.05)。无论术后2或4年,与假手术组相比,去卵巢组干骺端松质骨微结构参数的改变均比骨骺松质骨明显。结果证实,山羊胫骨平台骨骺松质骨微结构参数与干骺端松质骨具有一定的差异;骨质疏松时山羊胫骨平台松质骨微结构改变呈现出区域性特点,干骺端松质骨较骨骺松质骨微结构退变更为显著。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程全文链接：     

泼尼松对大鼠松质骨结构的影响

目的：探讨泼尼松对松质骨结构的影响。方法：用泼尼松４．５ｍｇ／ｋｇ,给３月龄ＳＤ雄性大鼠灌胃,每周２次,持续９０ｄ。扫描电镜观察大鼠腰椎松质骨结构的改变。结果：与正常组比较,泼尼松组的大鼠骨小梁变少、变细、断裂、连接不紧密,表现常见骨吸收形成的陷窝。结论：糖皮质激素可造成松质骨三维结构的损害,使力学强度降低,增加骨折的危险性。     

芪霍肾宝抗泼尼松所致大鼠松质骨结构破坏的作用

目的：观察芪霍肾宝对糖皮质激素引起松质骨结构破坏的防治作用。方法：选用3月龄SD雄性大鼠24只，随机分为对照组、激素组和治疗组。激素组用泼尼松4.5mg/kg灌胃．每周二次；治疗组给予芪霍肾宝O.38g/kg，每周6次．持续90天。扫描电镜观察大鼠腰椎松质骨结构的改变。结果：与正常组比较，激素组的大鼠骨小梁变少．变细，断裂，连接不紧密．表面常见骨吸收形成的陷窝；治疗组大鼠骨小梁粗大．排列整齐，连接紧密。结论：芪霍肾宝能有效防止糖皮质激素所引起的松质骨三维结构的损害，保持骨的正常力学强度，避免骨折。     

去势大鼠5种骨转换生化指标的动态变化

目的： 对去势大鼠骨质疏松动物模型形成过程中5种骨转换指标的变化及其相关性进行研究。方法: 将3月龄SD雌性大鼠分为3组：切除卵巢组(OVX)，假手术组(sham)和对照组(control)，术前和术后分别于1、1.5、2、2.5、3和4月检测血清骨钙素(OC)、碱性磷酸酶(ALP)、 骨碱性磷酸酶(BALP)、抗酒石酸酸性磷酸酶(TRAP)和羟脯氨酸(HYP)水平，并作大鼠胫骨病理切片检查。结果: OVX组血清OC、ALP、BALP、TRAP和HYP水平均明显高于sham组，其变化顺序依次为：TRAP/HYP→OC→ALP/BALP；5种指标之间呈显著正相关；术后3月OVX组大鼠胫骨小梁结构有病理改变。结论: 去势大鼠属于高转换型骨质疏松；在模型形成过程中，骨吸收指标的变化早于骨形成指标的改变；骨转换指标是反映绝经后早期骨量丢失的灵敏指标。     

去睾丸大鼠骨形态计量学的研究

目的：探讨4月龄雄性大鼠去睾丸后骨量的变化，重点比较松质骨和皮质骨骨代谢的变化。方法：20只4月龄SD雄性大鼠，随机分为假手术组（A组）和去睾丸组（B组），同等条件下饲养90d后，取腰椎和胫骨中段行不脱钙制片进行骨形态计量学观察。结果：去睾丸组与假手术组比较，前者腰椎松质骨吸收增加、骨形成下降（P〈0．05），出现明显骨质疏松；皮质骨外膜的骨形成动态参数如矿化沉积率、骨形成率下降（P〈0．05），内膜骨形成和吸收均有增加趋势。结论：去睾丸90d能使大鼠松质骨出现骨质疏松，皮质骨丢失不如松质骨显著。松质骨对去睾丸敏感性比皮质骨高。     

卵巢切除对大鼠骨组织结构改变的影响

目的：探讨卵巢切除对大鼠骨组织形态学改变的影响。方法：将１８只３月龄雌性大鼠随机分为卵巢切除组及假手术组（对照组）。术后３周处死两组大鼠，获取股骨远端１／３处骨，分别进行石蜡包埋，塑料包埋切片及扫描电镜观察。结果：卵巢切除可引起大鼠骨小梁变细、中断，骨小梁表面钙盐沉积减少。结论：卵巢切除可使大鼠骨吸收增加，影响骨的稳定性，增加骨折发生的危险性。     

去卵巢山羊长骨生物力学性能的变化

采用生物力学方法研究雌性山羊双侧卵巢切除后１８０天其长骨生物力学性能的变化。１５±岁雌性成都山羊１０只，体重２２±ｋｇ，随机分为对照组（Ｃｏｎｔｒｏｌ５只）和双侧卵巢切除组（ＯＶＸ５只）。术后１８０天处死动物，取出双侧股，胫，跖，肱，桡和掌骨。用三点弯曲法测整体骨弯曲结构力学性能的变化。分别取断端密质骨，用三点弯曲，压缩和拉伸方法测骨试件的材料力学特性的变化。结果显示：与对照组比较，双侧卵巢切除组各长骨相应的骨密度，断端骨组织厚度和整体三点弯曲的破坏荷载均明显下降（Ｐ＜００５）；除股骨外，各长骨的整体三点弯曲极限强度，弹性模量和骨试件的弯曲与压缩极限强度，弹性模量以及部分长骨拉伸极限强度明显低于对照组（Ｐ＜００５）。本研究结果提示：雌性山羊双侧卵巢切除后１８０天，其长骨的整体抗弯强度和骨试件的抗弯，抗压，以及抗拉强度均有不同程度的下降，易于骨折。这与临床绝经后妇女雌激素降低，导致骨质疏松，使骨折的倾向性增大是一致的；也与大鼠双侧卵巢切除骨质疏松模型所表现出的骨结构变化和骨量减少相符合。作者认为，骨生物力学参数是评价骨质疏松的重要指标。切除双侧卵巢的雌性山羊有可能成为骨质疏松的大动物模型。     

多尺度分析骨质疏松大鼠骨微结构变化

目的 多尺度分析骨质疏松大鼠的骨微结构变化。 方法 20只5月龄雌性SD大鼠随机选取12只实施双侧去卵巢(ovariectomy, OVX)手术,术后 8 周形成骨质疏松大鼠模型,另外 8 只作为假手术( SHAM) 对照组。 利用Micro-CT 和 SR-Nano-CT 定量分析骨质疏松大鼠在组织尺度下皮质骨和松质骨以及细胞尺度下骨细胞、骨陷窝小管和细胞外基质的微结构变化。 结果 组织尺度下,OVX 组皮质骨的截面积较 SHAM 组显著增大(P<0. 05),皮质骨骨密度和厚度较 SHAM 组虽有变化,但不显著;OVX 组骨小梁的骨密度、体积分数、厚度和骨小梁数量较 SHAM组显著降低(P<0. 01),骨小梁分离度显著增加(P<0. 01)。 细胞尺度下,OVX 组骨陷窝半轴长较 SHAM 组没有显 著差异,但 OVX 组骨陷窝厚度和骨小管直径较 SHAM 组显著增大(P<0. 05);同时,细胞尺度下 OVX 组皮质骨孔隙率较 SHAM 组显著增大(P<0. 05)。 结论 OVX 大鼠骨在组织和细胞尺度出现不同程度的微结构变化。 其中,组织尺度主要是松质骨丢失,皮质骨变化不大;细胞尺度骨陷窝小管网络孔隙显著增大,将直接影响皮质骨骨密度和强度。 多尺度分析骨质疏松大鼠骨微结构变化对于骨质疏松症的临床诊断及病理分析有潜在的应用价值。     

雌激素干预吸烟骨质疏松大鼠种植体周围的骨沉积

背景：骨质疏松、吸烟可致口腔种植失败率显著增高。 目的：观察雌激素对吸烟骨质疏松大鼠种植体周围骨沉积的影响。 方法：50只雌性大鼠均分为5组：除假手术组外,卵巢去势组、卵巢去势+雌激素组、卵巢去势+吸烟组、卵巢去势+吸烟+雌激素组均制备卵巢去势模型,去势术后后两组持续熏烟24周。去势术后12周,在大鼠右侧胫骨近骺端植入钛种植体,种植后对卵巢去势+雌激素组和卵巢去势+吸烟+雌激素组肌注雌激素。实验24周时行动物活体骨密度测量及X射线观察,处死动物采集标本行种植体骨硬组织切片观察。 结果与结论：骨密度及X射线观察结果显示,雌激素可提高种植体周围骨沉积。硬组织切片观察结果显示,卵巢去势+雌激素组种植体骨包绕范围基本形成骨结合,松质骨区结合骨板与周围骨小梁相连。卵巢去势+吸烟+雌激素组种植体周围结合骨板较卵巢去势+吸烟组明显增厚,骨板周围小梁骨增多。提示雌激素可在一定程度上提高吸烟骨质疏松大鼠种植体周围骨沉积,促进种植体骨结合。     

Effects of glucocorticoid on BMD, micro-architecture and biomechanics of cancellous and cortical bone mass in OVX rabbits

The incidence of osteoporosis continues to increase with progressively aging populations. The purpose of this study was to detect the effects of glucocorticoid (GC) treatment on bone mineral density (BMD), biomechanical strength and micro-architecture in cancellous and cortical bone in ovariectomized (OVX) rabbits. Twenty adult female New Zealand white rabbits were randomly divided into three groups. The OVX-GC group (n=8) received a bilateral ovariectomy first and then daily GC treatment (methylprednisolone sodium succinate, 1mg/kg/day) for 4 weeks beginning 2 weeks after ovariectomy treatment. The OVX group (n=4) received a bilateral ovariectomy without GC treatment. The sham group (n=8) only received the sham operation. BMD was determined prior to and 6 weeks after the operation in the spine. Six weeks after the operation, the animals were sacrificed, and cancellous bone specimens were harvested from the femoral condyle and lumbar vertebrae. Cortical bone specimens were obtained from the femoral midshaft. The femoral specimens were scanned for apparent BMD. All specimens were tested mechanically and analyzed by microcompute tomography (micro-CT). In cancellous bone, GC treatment resulted in significant decreases in BMD, bone biomechanical strength and micro-architecture parameters in lumbar vertebrae. Similar trends in BMD and micro-architectural changes were also observed in the femoral condyle in the OVX-GC group compared with the sham group. However, there was no significant decline in any parameter in either lumbar vertebrae or femoral condyle in the OVX group. Similarly, no significant difference was found in any parameter in cortical bone among the three groups. Thus, the 4-week GC treatment in OVX rabbits could result in a significant bone loss in cancellous bone but not in cortical bone. This model is comparable to the osteoporosis-related changes in humans. OVX alone was not sufficient to induce osteoporosis.     

Effects of vitamin K2 on the development of osteopenia in rats as the models of osteoporosis

Vitamin K2 is widely used for the treatment of osteoporosis in Japan. To understand the effects of vitamin K2 on bone mass and bone metabolism, we reviewed its effects on the development of osteopenia in rats, which characterizes models of osteoporosis. Vitamin K2 was found to attenuate the increase in bone resorption and/or maintain bone formation, reduce bone loss, protect against the loss of trabecular bone mass and its connectivity, and prevent the decrease in strength of the long bone in ovariectomized rats. However, combined treatment of bisphosphonates and vitamin K2 had an additive effect in preventing the deterioration of the trabecular bone architecture in ovariectomized rats, while the combined treatment of raloxifene and vitamin K2 improved the bone strength of the femoral neck. The use of vitamin K2 alone suppressed the increase in trabecular bone turnover and endocortical bone resorption, which attenuated the development of cancellous and cortical osteopenia in orchidectomized rats. In addition, vitamin K2 inhibited the decrease in bone formation in prednisolone-treated rats, thereby preventing cancellous and cortical osteopenia. In sciatic neurectomized rats, vitamin K2 suppressed endocortical bone resorption and stimulated bone formation, delaying the reduction of the trabecular thickness and retarding the development of cortical osteopenia. Vitamin K2 also prevented the acceleration of bone resorption and the reduction in bone formation in tail-suspended rats, which counteracted cancellous bone loss. Concomitant use of vitamin K2 with a bisphosphonate ameliorated the suppression of bone formation and more effectively prevented cancellous bone loss in tail-suspended rats. Vitamin K2 stimulated renal calcium reabsorption, retarded the increase in serum parathyroid hormone levels, and attenuated cortical bone loss primarily by suppressing bone resorption in calcium-deficient rats while maintaining the strength of the long bone in rats with magnesium deficiency. These findings suggest that vitamin K2 may not only stimulate bone formation, but may also suppress bone resorption. Thus, vitamin K2 could regulate bone metabolism in rats, which represented the various models of osteoporosis. However, the effects of vitamin K2 on bone mass and bone metabolism seem to be modest.     

雌二醇对铅中毒模型大鼠骨组织及骨代谢指标不能产生影响

背景：关于铅中毒能否引起骨质疏松症及雌激素对其治疗是否有效尚无共识。 目的：观察雌二醇对去卵巢大鼠和铅中毒大鼠所致骨质疏松症的治疗效果。 方法：雌性大白鼠100只等分成正常对照组、去卵巢模型组、染铅模型组、雌二醇+去卵巢组和雌二醇+染铅模型组。建模后1周雌二醇+去卵巢组和雌二醇+染铅模型组皮下注射雌二醇(100 μg/kg),2次/1周,连续12周。 结果与结论：在去卵巢模型组和铅中毒组中骨钙、骨磷、血钙及血磷均出现降低(P < 0.01),血碱性磷酸酶升高(P < 0.01),骨组织形态呈现骨质疏松的病理改变。雌二醇+去卵巢组的骨代谢生化指标血钙、磷、和碱性磷酸酶和骨组织形态均恢复正常,而雌二醇+铅中毒组的骨代谢生化指标和骨组织形态呈现骨质疏松未出现明显改善迹象。铅中毒组和雌二醇+铅中毒组的骨铅和血铅明显高于正常对照组(P < 0.01)。说明铅中毒可引起骨质疏松的病理改变,雌二醇对去卵巢大鼠的骨质疏松症有良好治疗效果,而对铅中毒所致的骨质疏松症无明显疗效。     

低剂量唑来膦酸对去势拔牙大鼠破骨及成骨细胞的影响

文题释义：去势大鼠：即通过去势法建立骨质疏松动物模型,该模型建造方法主要有3种：去势法、维甲酸灌胃法和糖皮质激素肌注法,而去势法是目前最常用、最成熟的造模方法,主要是通过去除大鼠双侧卵巢至少3个月,构建骨量少、骨显微结构退化而引起骨脆性增加及骨折发生率升高的一种全身性骨病,即骨质疏松疾病模型。 TUNEL细胞凋亡检测：用于检测细胞在凋亡过程中细胞核DNA的断裂情况,其原理是生物素标记的dUTP在脱氧核糖核苷酸末端转移酶的作用下,可以连接到凋亡细胞中断裂DNA的3’-OH末端,并可与连接辣根过氧化酶的链霉亲和素特异结合,在显色剂DAB的存在下,产生很强的颜色反应(呈深棕色),特异准确定位正在凋亡的细胞。 背景：目前唑来膦酸虽能有效地预防绝经后妇女的骨丢失,但其对下颌骨的影响及其机制尚不清楚。 目的：观察去势大鼠经低剂量唑来膦酸作用后下颌骨组织病理学改变,探讨RANKL/RANK/OPG信号系统在唑来膦酸抑制骨吸收过程中的调控效应与机制。 方法：取36只雌性SD大鼠随机分为对照组、模型组和治疗组,后2组大鼠行两侧卵巢切除术,建立骨质疏松模型;对照组行假手术去除同等质量卵巢周围的脂肪。去卵巢3个月后,治疗组皮下一次性注射唑来膦酸20 μg/kg,对照组和模型组皮下注射相应剂量的盐水;用药1周后拔除大鼠左侧下颌磨牙,拔牙后4周麻醉动物取出拔牙侧下颌骨组织。通过影像学X 射线大致观察大鼠拔牙窝剩余牙槽骨状况,苏木精-伊红染色检测下颌骨皮质和骨松质的病理结构改变,TUNEL凋亡实验检测凋亡的成骨细胞数量,利用免疫组织化学技术检测下颌牙槽骨内细胞核因子κB受体活化因子配基(RANKL)、骨保护素、细胞核转录因子(NF-κB)的表达情况,最后Western blot检测核因子κB受体活化因子配基、细胞核转录因子蛋白的表达。 结果与结论：①拔牙4周后,治疗组相较模型组牙槽骨骨吸收减少,拔牙窝底有新骨形成;②苏木精-伊红染色可见,模型组的骨皮质变薄,骨小梁结构变细,甚至出现断裂,大量骨吸收陷窝,成骨细胞较少;治疗组骨皮质增厚,骨小梁结构正常,只有少量骨吸收陷窝,成骨细胞增多;③治疗组的成骨细胞凋亡数目显著低于模型组(P < 0.001);④免疫组织化学染色可见,治疗组RANKL蛋白、NF-KB p65蛋白表达显著低于模型组(P < 0.001,P < 0.002),骨保护素蛋白表达显著高于模型组(P < 0.001);⑤Western Blot结果显示,与对照组相比较,模型组的RANKL、NF-κB蛋白高表达,治疗组其表达量显著降低(均P < 0.001);⑥结果说明,唑来膦酸可通过下调细胞核转录因子信号通路抑制破骨细胞的分化,同时调控成骨细胞的凋亡。 ORCID: 0000-0002-0300-0460(程余婷) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

Influence of ferutinin on bone metabolism in ovariectomized rats. II: Role in recovering osteoporosis

The aim of the present investigation, which represents an extension of a previous study, was to investigate the effect of ferutinin in recovering severe osteoporosis due to estrogen deficiency after rat ovariectomy and to compare phytoestrogen effects with those of estrogens commonly used in hormone replacement therapy (HRT) by women with postmenopausal osteoporosis. The animal model used was the Sprague–Dawley ovariectomized rat. Ferutinin was orally administered (2 mg kg⁻¹ per day) for 30 or 60 days starting from 2 months after ovariectomy (i.e. when osteoporosis was clearly evident) and its effects were compared with those of estradiol benzoate (1.5 μg per rat twice a week, subcutaneously injected) vs. vehicle-treated ovariectomized (OVX) and sham-operated (SHAM) rats. Histomorphometric analyses were performed on trabecular bone of lumbar vertebrae (4th and 5th) and distal femoral epiphysis, as well as on cortical bone of femoral diaphysis. Bone histomorphometric analyses showed that ferutinin seems to display the same effects on bone mass recorded with estradiol benzoate, thus suggesting that it could enhance the recovery of bone loss due to severe estrogen deficiency in OVX rats. On this basis, the authors propose listing ferutinin among the substances representing a potential alternative for the treatment of postmenopausal osteoporosis, which occurs as a result of estrogen deficiency.     

Long-term osteopenic changes in cancellous bone structure in ovariectomized rats

Cancellous bone mass decreases following ovariectomy in rodents, providing a useful model for post-menopausal bone loss in humans. This study describes and quantifies the longer-term changes in cancellous bone structure in the ovariectomized (OVX) rat. Rats were OVX or sham-OVX at 100 days of age and bones were collected 540 days later. Lumbar vertebral bodies were prepared for microradiography and structural analyses (nodal analyses and star volume analyses) of cancellous bone. Proximal humerii were prepared for scanning electron microscopy (SEM). Microradiography confirmed the loss of cancellous bone from the central spongiosa regions of the vertebral bodies and the humerii in the OVX rats. Changes in trabecular structural elements included relative increases in the number of free to free, cortical to free, cortical to node struts and decreases in the node to node struts in the OVX animals compared with controls. There were increases in average lengths of the node to free, node to node, and free to free trabecular struts in the OVX animals. The marrow star volume was increased in the OVX animals indicating a greater trabecular separation in these animals compared with controls. Viewed by SEM, metaphyseal trabeculae in the controls consisted of rods and plates but in the OVX animals the remaining trabeculae were mostly longitudinal rods with smaller transverse connecting rods. The remaining bone in the OVX animals was found in the lateral metaphyseal areas and is consistent with maintenance of the structural capacity of the bone. These long-term changes in cancellous bone structure are likely due to the continuation of functional skeletal loading but a decrease in gonadal hormones resulting in a decreased necessity to maintain a skeletal mineral store for reproduction (e.g., pregnancy and lactation). © 1993 Wiley-Liss, Inc.