柚皮苷对骨质疏松大鼠拔牙创骨愈合的影响

背景：柚皮苷作为一种中药单体化合物,具有抗炎、促成骨的作用,但其对拔牙创愈合速度的影响并不明确。目的：建立骨质疏松大鼠拔牙模型,通过体内实验探究柚皮苷对拔牙创愈合速度的影响。方法：48只雌性SD大鼠随机分为假手术组14只与去势组34只。去势组去除双侧卵巢建立骨质疏松模型,6周后两组各随机取4只大鼠行MicroCT检测确认建模结果。建模成功后将剩余大鼠随机分为对照组、柚皮苷及雌二醇组,均拔除左上颌第二磨牙,柚皮苷组予以300 mg/(kg·d)柚皮苷灌胃,雌二醇组予以20μg/(kg·d)17β雌二醇皮下注射,对照组予以等体积生理盐水处理。干预4周后,分离各组大鼠上颌骨进行苏木精-伊红染色、Masson染色、MicroCT检测,检测拔牙创周围骨组织骨保护素、核因子κB受体活化因子配体(receptor activator of nuclear factor-κB ligand,RANKL) mRNA及蛋白表达量。结果与结论：(1)去势6周后,去势组骨体积分数降低,证明骨质疏松建模成功;(2)拔牙4周后,与对照组相比,柚皮苷组、雌二醇组骨小梁间距小、骨小梁数量多,牙槽骨高度丢失更少,说明柚...     

川芎嗪对类风湿性关节炎外周血RANK／RANKL／骨保护素途径干预作用的研究

目的观察川芎嗪对类风湿性关节炎（RA）模型大鼠RANK／RANKL／0PG在外周血中CD3^＋T淋巴细胞、中性粒细胞、CD14单核细胞的表达率及平均荧光强度,探讨川芎嗪在RA骨破坏和炎症过程巾的意义。方法大鼠随机分成5组,正常对照组、模型对照组、川芎嗪大剂量组、川芎嗪小剂量组、阳性药物对照组,每组10只。给药7d后,应用间接免疫荧光标记和流式细胞技术对各组大鼠外周血相关指标进行检测分析。结果与正常对照组相比,RA大鼠骨保护素（OPG）表达明显降低,从正常的24．7降至18．7（q=4．2,P〈0．05）,RANK、RANKL变化不明显,经过川芎嗪治疗后,大剂量组OPG有明显的回升,至23．8％（q=3．97,P〈0．05）,小剂量组变化不明显。RANK在CD3^＋细胞、中性粒细胞、CD14单核细胞上的平均荧光强度明显降低,分别为20．6、135．4、84．2,经川芎嗪大剂量治疗后明显升高,分别达到31．0、192．1、95．6（q=10．4、q=8．6、q=6．3,P〈0．05）。结论大剂量川芎嗪可以通过调节OPG／RANK／RANKL途径对RA起一定的作用。     

OPG/RANKL/RANK信号通路在骨巨细胞瘤发病机制中的作用

文题释义：OPG/RANKL/RANK 信号通路：是骨代谢中至关重要的一条信号通路,它是成骨细胞与破骨细胞之间相互作用的信号通道,同时也是骨巨细胞瘤影响骨代谢的主要途径。 骨巨细胞瘤(Giant cell tumor of bone,GCTB)：是常见的原发性骨肿瘤之一,其发病率占所有原发性骨肿瘤的4%-10%,多发生于20-40岁的青壮年患者,好发于股骨远端、胫骨近端或桡骨远端。骨巨细胞瘤组织学来源尚不清楚,一般认为起始于骨髓内间叶组织。该肿瘤具有较强的侵袭性,对骨质有较大的破坏和侵蚀作用,但很少有患者出现反应性新骨生成或是自愈倾向。 背景：研究表明,骨保护素/核因子κB受体活化因子配体/核因子κB受体活化因子(OPG/RANKL/RANK)信号通路与骨巨细胞瘤发病机制之间有一定的相关性,通过控制OPG/RANKL/RANK信号通路影响成骨细胞与破骨细胞之间相互作用,对该病起到一定的治疗作用。 目的：介绍 OPG/RANKL/RANK信号通路与骨巨细胞瘤发病机制的关系,总结并讨论OPG/RANKL/RANK信号通路在骨巨细胞瘤发病机制中的最新研究进展。 方法：检索 PubMed 数据库、Web of science数据库及万方数据库中2001至2019年相关文献,检索词分别为“OPG/RANKL/RANK,giant cell tumor of bone,pathogenesis,signal pathway, bone metabolism,OPG/RANK/RANKL,骨巨细胞瘤,发病机制,信号通路,骨代谢”。排除较陈旧及重复的文献,通过整理,共纳入53篇文献进行分析探讨。 结果与结论：①骨保护素抑制破骨细胞增殖及分化,降低成熟破骨细胞活性,阻断核因子κB受体活化因子配体与核因子κB受体活化因子结合,减缓破骨;②核因子κB受体活化因子配体与破骨细胞前体细胞表面的核因子κB受体活化因子结合,促进破骨细胞前体细胞分化,增殖,进而加速破骨;③核因子κB受体活化因子配体与其受体结合后,激活核因子κB等信号因子促进破骨细胞的增殖、分化并激活破骨细胞,同时调节相关基因的转录及表达;④OPG/RANK/RANKL与骨巨细胞瘤发病机制相关。 ORCID: 0000-0002-2756-4848(梁晨亮) 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     

应力刺激与骨保护蛋白、核因子κB受体活化因子及其配体骨代谢信号通路**

背景：骨保护蛋白、核因子κB受体活化因子及其配体(osteoprote-gerin/ ligand of receptor activator of NF-κB/receptor activator of NF-κB,OPG/RANKL/RANK)骨代谢信号通路是对应力敏感的通路之一。不同性质的运动会产生不同的机械应力刺激,影响骨代谢信号通路。 目的：观察不同性质的运动对OPG/RANKL/RANK信号通路的影响。 方法：由第一作者于2000/2011通过计算机检索 CNKI,HighWire和Elsevier数据库中关于“应力刺激与OPG/RANKL/RANK”的相关的论文报告。以“应力刺激,OPG/RANKL/RANK”或“应力刺激,骨代谢”为检索词进行检索。选择的文章内容与应力刺激对信号通路的影响有关,选择相关近期发表的文献或者是发表在权威期刊的文献。共检索到215篇文章,按纳入和排除标准对文献进行筛选,共纳入31篇文章。 结果与结论：运动对骨骼不断产生机械应力刺激,这种机械应力刺激可以通过影响成骨细胞和破骨细胞的OPG/RNAKL/RANK信号调节系统而调节骨组织代谢。但是相关文献中的研究结果不一致,有待进一步的研究。      

补肾健脾活血方干预骨质疏松模型大鼠骨代谢、氧化应激及自噬的变化

背景:氧化应激被认为是骨质疏松发生的最重要的始动因素之一,氧化应激除直接激活经典的线粒体和内质网凋亡途径外,还激活细胞自噬信号通路,而骨质疏松发病中成骨细胞抗氧化功能的调控机制并未被清晰阐述。目的:探讨补肾健脾活血方改善氧化应激与自噬对骨质疏松大鼠磷脂酰肌醇3-激酶、蛋白激酶B、哺乳动物雷帕霉素靶蛋白的影响。方法:72只6月龄雌性SD大鼠随机分为假手术组24只及手术组48只,去除卵巢造模;术后3个月两组各取12只检测骨密度及血清中骨钙素、骨特异性碱性磷酸酶、Ⅰ型前胶原N端前肽、骨保护素水平。剩余手术组的36只大鼠分为模型组、补肾健脾活血方组及阿仑膦酸钠组,每组12只,药物组给予相应药物灌胃,假手术组和模型组灌胃等体积生理盐水。12周后处死各组大鼠,双能X射线法检测大鼠腰椎和股骨骨密度,ELISA法测定血清骨代谢指标及氧化应激指标,实时荧光定量PCR检测股骨组织中LC3、Beclin1、ATG5、哺乳动物雷帕霉素靶蛋白的mRNA表达情况,Western blot法检测磷脂酰肌醇3-激酶、磷酸化蛋白激酶B、哺乳动物雷帕霉素靶蛋白的蛋白表达情况。结果与结论:(1)造模3个月及药物干预3个月后...     

骨质疏松大鼠股骨骨折骨痂及腰椎的生物力学研究

目的 :探讨骨质疏松大鼠股骨骨折骨痂及腰椎的生物力学。方法 :8月龄雌性Wistar大鼠摘除卵巢 ,3个月后制作左股骨中段骨折克氏针内固定的模型。术后鲑鱼降钙素 (密盖息 )组每天皮下注射密盖息 2IU / 。雌激素组每隔 2d皮下注射苯甲酸雌二醇 0 .1mg/ 。另设假手术组和骨质疏松组对照。8周后处死大鼠 ,左股骨行扭转实验 ;第 4腰椎行凹入实验。结果 :降钙素组 ,雌激素组股骨的最大扭矩 ,扭转刚度和腰椎的最大载荷 ,松质骨刚度都明显高于骨质疏松组 (P <0 .0 5 ) ,与假手术组相似 (P >0 .0 5 )。结论 :鲑鱼降钙素和雌激素能改善骨质疏松大鼠股骨骨痂及腰椎的生物力学性能 ,提高骨质量 ,增强抗骨折能力。     

仙灵骨葆胶囊干预糖尿病模型大鼠的骨代谢

背景:研究发现仙灵骨葆胶囊可改善骨代谢、防治骨质疏松,但是否对糖尿病并发的骨质疏松症具有预防作用或可能的机制却鲜有报道.目的:观察仙灵骨葆胶囊对糖尿病并发骨质疏松症大鼠的骨代谢以及相关成骨标志物因子Wnt3a、β-连环蛋白、骨形态发生蛋白2的影响并探讨其作用机制.方法:将36只雄性健康8周龄SD大鼠腹腔单剂量注射60 ...     

补肾壮骨方干预去卵巢骨质疏松模型大鼠骨代谢及骨密度的变化

背景：中医药以其良好的治疗效果及安全性越来越多的应用于骨质疏松症的治疗中,补肾壮骨方目前作为山东中医药大学附属医院协定方被广泛应用于临床中,获得了极好的治疗效果。目的：评价补肾壮骨方对去卵巢骨质疏松大鼠骨代谢及骨密度的影响。方法：60只SD大鼠随机分为6组,分别为假手术组、模型组、阿仑膦酸钠组、补肾壮骨方高、中、低剂量组,每组10只,后5组制备去卵巢骨质疏松症模型,假手术组只切除卵巢周围脂肪组织。造模8周后,补肾壮骨方高、中、低剂量组分别予以2.34,1.17,0.58 g/(kg·d)补肾壮骨方,阿仑膦酸钠组予阿仑膦酸钠1 mg/(kg·d),假手术组及模型组给予等体积的生理盐水,1次/d灌胃。连续灌胃12周后检测各组大鼠血清碱性磷酸酶、Runt相关转录因子2及核因子κB受体活化因子配体水平;取右侧股骨观察骨密度及骨微结构;苏木精-伊红染色观察组织病理改变;免疫组化法检测骨组织Wnt1、骨形态发生蛋白2蛋白表达。结果与结论：(1)造模8周后,与假手术组对比,模型组大鼠骨密度、骨小梁数明显降低(P <0.05),提示造模成功;(2)与模型组大鼠对比,补肾壮骨方低、中、高剂量组及阿...     

红茴香提取物干预骨质疏松性大鼠骨折后的血管生成

背景：红茴香提取物是一种具有消炎镇痛和活血化瘀等功效的中药制剂,其乙醇提取物对大鼠软组织损伤具有显著疗效,而红茴香是否对骨质疏松性骨折具有治疗效果尚未报道。目的：探讨红茴香提取物对骨质疏松性骨折大鼠血管生成的保护作用及可能机制。方法：(1)体内实验：应用去势法和闭合性骨折法建立骨质疏松性骨折大鼠模型。36只健康雌性SD大鼠随机选取30只分为假手术组、模型组和红茴香提取物组(建模后给予0.05 mL/kg红茴香提取物),每组10只,其余6只纳入空白对照组。采用双能X射线和三点弯曲力学试验法检测大鼠股骨骨密度值和股骨弹性段终点载荷;苏木精-伊红染色法测定骨痂组织血管数量和血管面积;ELISA法检测血清中血管内皮生长因子、碱性成纤细胞生长因子、血小板衍生生长因子和一氧化氮水平。(2)体外实验：对人微血管内皮细胞进行药物干预,分为对照组、红茴香提取物(50,100或200 mg/L)组、Vector+二甲基亚砜组、NRF1过表达组、LY294002(10μmol/L)组和NRF1过表达+LY294002组。MTT法检测人微血管内皮细胞增殖;Transwell法检测人微血管内皮细胞迁移率;血管生...     

咀嚼力增强对骨质疏松大鼠颌骨骨丢失的保护作用及机制

为研究咀嚼力增强对骨质疏松大鼠颌骨骨丢失的保护作用及机制,选取30只雌性SD大鼠进行实验,行摘除卵巢术建立骨质疏松动物模型,喂食高硬度饲料建立咀嚼力增强动物模型,检测血清雌二醇(E2)、骨钙素(BGP)、碱性磷酸酶(ALP)、牙槽骨骨形态计量学指标、TGF-β与OPG、RANKL基因等指标.结果显示,与模型组相比,实验...     

丹皮酚对去卵巢骨质疏松大鼠叉头框蛋白O3a/Wnt信号通路及椎骨密度的影响

背景:丹皮酚可抑制炎症,减轻慢性骨关节炎临床症状,作为一种不良反应小、更为安全的天然药物成分,探讨其对骨质疏松症的治疗作用具有重要的临床意义。目的:探究丹皮酚对去卵巢骨质疏松大鼠叉头框蛋白O3a(forkhead box O3a,FoxO3a)/Wnt信号通路及椎骨密度的影响。方法:雌性SD大鼠随机分为6组,每组10只。假手术组仅切除卵巢旁部分脂肪组织;其余50只大鼠均采用双侧卵巢摘除法制备去卵巢骨质疏松大鼠模型,模型制备成功后分为模型组、雌激素组[炔雌醇10μg/(kg·d)]、丹皮酚低、中、高剂量组[丹皮酚125,250,500 mg/(kg·d)],每组10只,灌胃给药;假手术组、模型组灌胃等量生理盐水,持续干预12周。ELISA法测定血清雌激素、骨保护素、骨钙素水平;采用双能X射线动物骨密度测定仪检测大鼠股骨及椎骨骨密度;采用骨科生物力学测试仪检测大鼠股骨及椎骨生物力学指标:弹性模量、最大载荷、屈服载荷;实时荧光定量PCR检测椎骨组织FoxO3a、Wnt2 mRNA表达水平;免疫印迹法检测椎骨组织FoxO3a、Wnt2及核内β-catenin蛋白表达。结果与结论:①治疗后,与假手术组比较,模型组L4,5骨密度、弹性模量、最大载荷、屈服载荷、血清雌二醇、骨保护素水平、椎骨组织Wnt2 mRNA及蛋白水平、核内β-catenin蛋白水平均显著降低(P<0.05),骨钙素水平、椎骨组织FoxO3a mRNA及蛋白水平显著增加(P<0.05);②与模型组比较,丹皮酚低、中、高剂量组大鼠L4,5骨密度、弹性模量、最大载荷、屈服载荷、血清雌二醇、骨保护素水平、椎骨组织Wnt2 mRNA及蛋白水平、核内β-catenin蛋白水平依次增加(P<0.05),血清骨钙素水平、椎骨组织FoxO3a mRNA及蛋白水平依次降低(P<0.05),且丹皮酚高剂量组均优于雌激素组(P<0.05);③提示丹皮酚可增加去卵巢骨质疏松大鼠椎骨骨密度,改善其骨生物力学状况,减轻骨质疏松,该作用可能与抑制FoxO3a、促进Wnt2/β-catenin通路激活有关。     

运动联合福善美对去卵巢大鼠骨密度和神经传导的影响

目的: 观察运动是否可增强福善美对卵巢切除大鼠骨质疏松的治疗作用。方法: 将90只6月龄雌性SD大鼠随机分为假手术组(sham,18只)和卵巢切除模型组(OVX,72只)。大鼠卵巢切除8周后,测定大鼠第4腰椎骨密度(BMD)和血清雌二醇含量。随后,存活的OVX大鼠分为模型组(OVX)、福善美治疗组(OVX+FOX)、运动治疗组(OVX+EX)和福善美与运动联合治疗组(OVX+FOX+EX),分别给予1 mg·kg^-1·d^-1福善美灌胃和(或)跑台运动干预治疗12周后,双能X线骨密度仪测定各组大鼠第4腰椎BMD;肌电图机检测大鼠左侧股神经传导速度(MCV)、运动末端潜伏期(ML)和复合肌肉动作电位(CMAP);ELISA法测定大鼠血清Ⅰ型前胶原羧基端前肽(PICP)及Ⅰ型胶原羧基端交联端肽(ICTP)含量。结果: 卵巢切除大鼠福善美和(或)运动干预治疗12周后,OVX组与sham组相比,BMD显著降低(P<0.05),血清PICP和ICTP明显增高(P<0.05),左侧股神经ML未见明显改变。福善美和运动均可显著提高骨质疏松大鼠BMD,降低ICTP;福善美可显著降低骨质疏松大鼠ICTP,而运动对ICTP无明显影响。运动可明显缩短模型组左侧ML(P<0.05),福善美对ML无显著改善作用。运动与福善美联合对BMD、PICP、ICTP及ML的改善作用较两者单用效果显著(P<0.05);福善美与运动两治疗组间未见明显差异。各组大鼠左侧股神经MCV和CMAP未见明显差异。2×2析因设计的方差分析显示,福善美与运动2种处理方式之间不存在交互作用(P>0.05)。结论: 福善美和运动可能通过抑制破骨细胞的骨吸收而抑制大鼠卵巢切除对骨密度的影响。     

Effects of dietary-fiber levels on RANK/RANKL/OPG expression in the appendix of weanling rabbits

Background/purposeThe dietary fiber can regulate the intestinal mucosal immunity, and the M cell is the portal for initiating mucosal immunity. We investigated the effects of dietary fiber on the transport of Escherichia coli to assess the function of microfold (M) cells in the appendix.MethodA total of 150 New Zealand rabbits were fed three diets (high fiber (HF): 31.72%; control: 37.36%; low dietary fiber (LF): 41.84%; neutral detergent fiber (NDF). An infection model was established in vivo using E. coli containing green fluorescent protein as the indicator in appendix loops. Samples were collected before and after inoculation with indicator for 10, 30, or 60 min. The M cells number, differentiation-related genes and proteins were monitored by respectively using immunofluorescence, Q-PCR and Western-blot.ResultsThe number of M cells in HF group was significantly higher than that of LF group before and at 10 min, 30 min post injection with E.coli (P < 0.01), which has an opposite at 60 min. The number of fluorescent E. coli transported across the appendix was significantly increased in the HF group (P < 0.01) compared with the LF group at 30 min (P < 0.001); expression of RANKL gene and protein levels were no difference between HF and LF group. The variation tendency of RANK, OPG genes and proteins were consistent with the change of M cell transport indicator number in different time points.ConclusionOur study showed that a high-fiber diet can increase number of M cells and speed up antigen transfer under regulation of ANKL/OPG/RANK system.     

康力龙对类固醇性大鼠骨质疏松骨密度和生物力学的影响

目的　从生物力学和骨矿含量测定角度研究康力龙对类固醇性大鼠骨代谢的影响。方法　采用 3月龄雄性SD大鼠 2 8只 ,随机分为基础对照组、年龄对照组、激素模型组和康力龙预防组。后两组给醋酸泼尼松 4 5mg·kg-1,ig ,2次 /周 ;预防组还给康力龙 0 5mg·kg-1·d-1,ig。 3个月后取股骨和第 5腰椎行骨密度测定 ,再行扭转、3点弯曲和压缩试验。结果　与年龄对照组比较 ,激素模型组股骨和第 5腰椎的总骨密度减少了 14 6 4 % (P <0 0 1) ;股骨干在 3点弯曲试验时所承受的载荷减少了17 1% (P <0 0 5 ) ;其余的力学参数都出现减少的趋势。与激素模型组比较 ,康力龙预防组股骨和第 5腰椎的总骨密度有所增加 ;股骨扭转角度明显增加 72 5 % (P <0 0 5 ) ,其余的力学参数都出现增加的趋势。结论　长期使用糖皮生激素 (GC) ,会使大鼠皮质骨和松质骨的骨密度和力学性能下降 ,从而易致骨折 ;应用康力龙则能阻止GC所致骨量丢失 ,还能增加其力学性能。     

Hypoxia mimetic deferoxamine influences the expression of histone acetylation- and DNA methylation-associated genes in osteoblasts

Purpose of the study: Sufficient oxygen supply to bone tissue is essential for normal bone development and efficient bone repair. Hypoxia and hypoxia-inducible factor 1α (HIF1α) signaling pathway have been shown to exhibit profound effects on proliferation, differentiation as well as gene and protein expression in osteoblasts, osteoclasts and mesenchymal stem cells; however, as epigenetic mechanisms also perform an important regulatory role in these cells, our aim was to elucidate whether hypoxia mimetic deferoxamine could influence epigenetic mechanisms in bone cells by modulating the gene expression levels of chromatin-modifying enzymes.

Materials and methods: Osteoblast cell line HOS was exposed to deferoxamine, a widely used hypoxia mimetic, and expression profile of 40 genes associated with histone acetylation, deacetylation and DNA methylation was determined using quantitative real time polymerase chain reaction (qPCR) array followed by individual qPCR analyses. In addition, genes associated with hypoxia response, RANK/RANKL/OPG system, WNT/β-catenin signaling pathway and oxidative stress were also analyzed.

Results: We observed induced expression of histone deacetylase 9 (HDAC9) and suppressed expression of K(lysine) acetyltransferase 5 (KAT5) and DNA methyltransferase 3A (DNMT3A) demonstrating for the first time that expression of genes encoding chromatin-modifying enzymes could be influenced by hypoxia mimetic in HOS cells.

Conclusions: Based on our results we can conclude that hypoxia mimetic deferoxamine influences expression of histone acetylation- and DNA methylation-associated genes in osteoblasts and that further studies of hypoxia-induced epigenetic changes in bone cells should be undertaken.     

Effect of resveratrol on abnormal bone remodeling and angiogenesis of subchondral bone in osteoarthritis

Purpose: The effect of resveratrol on subchondral bone in osteoarthritis was explored by constructing a mouse model of osteoarthritis and giving resveratrol as intervention. Methods: The degree of proteoglycan loss in articular cartilage was assessed by safranine fast green staining. The expressions of Lubricin and Aggrecan, COLX, and MMP-13, the co-expression of CD31 and Endomucin, and the expression of angiogenesis-related factors were determined by immunohistochemistry. TRAP stain and immunostaining were used to assess abnormal subchondral bone resorption and bone formation. Angiography was employed to analyze the effect of resveratrol on the proliferation of subchondral bone vessels. Results: Resveratrol inhibited cartilage thickening and the increase of COLX and MMP-13 expression, delayed the loss of proteoglycan, Lubricin, and Aggrecan, and inhibited osteoclast differentiation by up-regulating osteoprotegerin (OPG) and down-regulating the expression of RANKL. Angiography showed that resveratrol can reduce the abnormally elevated number and volume of blood vessels in the subchondral bone. Immunostaining showed that resveratrol inhibited CD31^hiEmcn^hi angiogenesis and high expression of VEGFA and Angiopoietin-1. Conclusion: Resveratrol inhibits osteoclast differentiation and reduces active bone resorption by regulating the OPG/RANKL/RANK pathway, and inhibits the abnormal proliferation of CD31^hiEmcn^hi blood vessels by downregulating the expression of VEGFA and Angiopoiein-1, thereby eliminating the pathologic coupling mechanism of osteogenesis and vascularization, and delaying the progression of osteoarthritis.     

Ovariectomy-associated changes in bone mineral density and bone marrow haematopoiesis in rats

The relationship between the bone mass loss and bone marrow haematopoiesis in osteoporosis remains obscure. We selected 3-month-old female Sprague–Dawley rats and randomly divided them into six groups. Three groups were ovariectomized (OVX), while the other three groups were sham operated (Sham). Four, 8 and 12 weeks after the surgical procedure, the rats were euthanized and sampled. The left femur was used for measurement of bone mineral density (BMD). The right femur distal metaphysic cancellous bone was processed for morphological evaluation. Our results showed that the femur BMD in the 4-week OVX group was not significantly decreased compared with that of the 4-week Sham group, but that the volume of adipose tissue in the bone marrow was markedly increased. The femur BMD in the 8-week OVX group was decreased significantly compared with that of the 8-week Sham group ( P   <   0.05). Meanwhile, the volume of haematopoietic tissue decreased and the volume of adipose tissue increased. The number of megakaryocytes was decreased ( P   <   0.05). Interestingly, the osteoclasts and mast cells were increased in number in the 8-week OVX group ( P   <   0.05). These changes became obvious in the 12-week OVX rats, in contrast to the Sham groups. The volume of trabecular bone and the number of osteoblasts in the 12-week OVX group decreased significantly. Increased reticulin fibres were observed only in the 12-week OVX group. Our studies demonstrated a reciprocal correlation between bone-forming osteoblasts and marrow adipose tissue and suggest that OVX rats may be valuable as an animal model to study hypohaemopoiesis.