胫骨干骨折后的骨质丢失

临床上注意到：胫骨干骨折后会发生松质骨的骨质丢失。表现为Ｘ线片上骨小梁变细、稀疏、整体透Ｘ线增强。但这通常是肉眼观察所得，缺乏定量测定。为此，我们以计算机辅助的Ｘ线片密度分析研究了这一问题。１材料与方法３２例胫骨干骨折。收集原始和伤后２周和６月的随访...     

中药复方干预3周模拟失重大鼠骨丢失的初步研究

目的：研究中药复方对3周模拟失重大鼠骨骼改变的干预作用,初步观察模拟失重情况下,复方对钙剂（牡蛎醋酸水解物）的协同作用。方法：Wistar大鼠,雄性,30只,随机分为3组,空白组、模型组、中药组,每组10只。尾吊模拟失重3周,中药复方（含熟地黄、怀牛膝、黄芪、当归、牡蛎醋酸水解物等）水煎剂灌胃。观察中药对模拟失重大鼠血清钙与磷水平、后身骨密度、骨矿盐含量、力学强度的影响。结果：模拟失重3周后,与空白组比较,模型组血清钙磷均显著升高（P〈0.01）,后身骨密度、骨力学强度均显著降低（P〈0.01）;中药组血钙磷升高程度有减小趋势,骨密度显著提高（P〈0.01或0.05）,骨力学强度有较大改善趋势。结论：3周尾吊模拟失重可造成大鼠后身骨量显著丢失和强度下降,中药可较好地改善上述情况。单纯补充钙剂不足以对抗模拟失重所致骨丢失,复方中熟地黄、怀牛膝、黄芪、当归等可能对钙剂牡蛎起到了协同作用。     

蛇床子素对模拟微重力引起的骨质流失的防治作用

目的研究蛇床子素对模拟微重力导致大鼠骨质流失的防治作用。方法将Wistar大鼠随机分为3组:对照组(Ctrl)、尾吊组(HLS)、尾吊给药组(OST)。4周后取后肢骨用双能骨密度仪及万能试验机分别测量各组股骨骨密度及生物力学,并通过micro CT分析骨小梁参数;用Van Gieson(VG)染色观察胫骨形态变化。通过qRT-PCR检测胫骨骨保护素(OPG)和核因子-κB受体激活剂配体(RANKL)mRNA表达水平。用ELISA试剂盒检测血清中骨特异性碱性磷酸酶(BALP)、骨钙素(OCN)和抗酒石酸酸性磷酸酶-5b(TRACP-5b)的含量变化。结果与对照组相比,尾吊组大鼠股骨骨密度及生物力学参数显著降低(P0.05),与尾吊组相比,尾吊给药组骨密度及生物力学显著上升(P0.05);尾吊组骨小梁体积分数(BV/TV)、厚度(Tb.Th)显著降低(P0.01),间距(Tb.Sp)显著升高(P0.01),尾吊给药后BV/TV、Tb.Th及Tb.Sp显著降低(P0.01);VG染色观察尾吊组胫骨骨小梁间隙变大,数量减少,而尾吊给药组骨小梁骨髓腔减少,数量增多;尾吊组血清BALP和OCN浓度显著降低(P0.05),TRACP-5b浓度显著升高(P0.05),当给予蛇床子素后,BALP浓度显著升高(P0.05),而TRACP-5b浓度显著降低(P0.05);尾吊组胫骨OPG/RANKL比值显著降低(P0.05),尾吊给药后,OPG/RANKL比值显著升高(P0.05)。结论蛇床子素可通过促进骨形成和抑制骨吸收两方面有效防治模拟微重力导致的骨质流失。     

营养素合剂对模拟失重大鼠股骨的影响

目的观察营养素合剂对抗模拟失重条件下大鼠骨丢失的效果，并初步探讨其机理。方法SPF级SD大鼠30只，随机平均分为3组：A组为自由活动对照组，人鼠自由活动；B组和C组为尾吊模拟失重组；A组和B组大鼠饲喂基础饲料；C组大鼠饲喂基础饲料添加2％(w／w)的营养素合剂，喂养21d。结果A组大鼠股骨的最大载荷、弹性载荷、最大应力、股骨密度、血清中骨钙素浓度、股骨钙量以及饲料钙的表观吸收率显著高于B组大鼠相应的指标；C组大鼠股骨的最大载荷、弹性载荷、最大应力、血清中骨钙素的浓度、左侧股骨钙量、对饲料钙的表观吸收率均显著性高于B组大鼠。结论营养素合剂能明显提高模拟失重大鼠股骨质量。     

五加补骨方及阿仑膦酸钠对模拟失重大鼠骨丢失干预比较

目的:比较五加补骨方及阿仑膦酸钠对3周尾吊模拟失重大鼠前后肢骨胳及肌肉丢失的干预作用.方法:自2009年3月至5月,6周龄雄性Wistar大鼠40只,按体重用随机区组法分为:五加补骨方组(HUC)、阿仑膦酸钠组(HUA)、空白组(CON)、模型组(HU),每组10只.动物实验周期为4周,HUC组全程给予五加补骨方(含刺五加、熟地黄、怀牛膝、牡蛎等)水煎剂,按体重10 ml/kg剂量每日灌胃1次,药液浓度0.704 g/ml;HUA组全程给定量阿仑膦酸钠片溶解混悬剂灌胃,按体重10 ml/kg剂量每周灌胃1次,药液浓度0.9 mg/ml;CON组和HU组均以上述方法全程给予蒸馏水.自第2周始,HU、HUC、HUA组均以尾部悬吊模拟失重3周.第4周末处死大鼠,分别测量血清钙、磷含量及碱性磷酸酶活性(ALP),肱骨和股骨骨密度(BMD)、肱骨和胫骨生物力学性能(biomechanical property)以及肱二头肌和腓肠肌重量指数.结果:与CON组比较,HU组血清Ca显著升高(P＜0.05),后肢BMD、力学性能及肌肉指数均显著降低(P＜0.01);与CON组比较,HUA组血清Ca显著升高(P＜0.05).HUC组血清ALP显著高于其他3组(P＜0.01).与HU组比较,HUC组及HUA组股骨BMD均显著升高,胫骨最大载荷、最大桡度及弹性载荷均有升高趋势;与HU组相比,HUC组及HUA组腓肠肌萎缩分别缓解12.5%和50%(P＞0.05),肱骨BMD均无显著变化,而HUA组肱骨最大桡度(P＜0.01)及弹性桡度(P＜0.05)均较HU组有显著降低.结论:中药复方和阿仑膦酸钠均可有效抑制模拟失重造成的后肢骨及肌肉丢失,改善其力学结构.中药复方在缓解上肢力学性能改变方面表现出一定优势.在治疗航天失重骨丢失类疾病上,五加补骨方与阿仑膦酸钠效果相当.     

G-B-R复配物对模拟微重力效应诱导骨丢失的防护作用

目的 从天然产物中寻找到对微重力效应诱导骨丢失具有防护作用的复配物。方法 通过24种天然产物对骨髓干细胞和成骨细胞的增殖活性,筛选出具有较强效果的天然产物并对其进行复配;随后通过复配物对模拟微重力效应下昆明小鼠骨质丢失的影响来评价其骨丢失防护作用。结果银杏叶和荞麦花粉的复配物显示出最强的骨髓干细胞增殖活性;熟地黄显示出最强的成骨细胞增殖活性;在模拟微重力环境下不同剂量的银杏叶、荞麦花粉与熟地黄的复配物均显示出不同程度的骨丢失防护作用;高剂量组可以显著提高模型组小鼠血清中碱性磷酸酶的活性及股骨中的有机物含量。结论 通过对天然产物促骨髓干细胞和成骨细胞增殖活性进行筛选和复配,发现所获得的G-B-R复配物对微重力效应诱导的骨丢失具有良好的防护作用。     

低钙透析液对血液透析患者钙磷代谢及骨质重塑的影响

目的比较低钙透析液对长期血液透析患者钙磷代谢及骨重塑的影响。方法45例血清矫正钙≥9.5mgdl且iPTH≤150pgml患者随机分为透析液钙浓度1.25、1.5及1.75mmolL3组透析治疗3个月,观察3组患者血清Ca、P、Ca×P、iPTH、BGP、IGF1及IGFBP3水平差异。结果观察结束时,DCa1.5与DCa1.75组,血清Ca×P水平DCa1.5组无变化、DCa1.75组升高(P<0.05),IGF1水平2组均保持稳定;iPTH及BGP水平DCa1.5组升高(P<0.05)及DCa1.75组降低(P<0.05)。DCa1.25组血清Ca×P及IGF1水平明显降低(P<0.01),iPTH及BGP水平有显著升高(P<0.01)。透析前血清iPTH及BGP水平呈正相关(r=0.155,P<0.05)。结论低钙透析液可在有限时间内有效降低钙负荷及改善骨代谢。长期应用低钙透析液很可能通过增加iPTH、BGP水平及降低IGF1水平引发骨质疏松。     

腹部手术后TPN治疗中的低血磷症及其防治

本文选择了16例腹部手术后TPN治疗的患者为观察对象,并随机分为补磷组(9例)及对照组(7例),连续测定血浆中磷水平和24小时尿中磷排出量。结果发现,对照组在TPN治疗后第4、7天血磷明显降低(P<0.01),既使无磷摄入,仍有相当的磷从尿排出;而补磷组则无低血磷现象发生。     

模拟失重对大鼠肝脏Hsp70及其基因表达的影响

目的 探讨模拟失重环境中大鼠肝脏组织Hsp70及Hsp70mRNA表达变化.方法 成年Wistar大鼠48只,体重(300±20)g).随机分为6组,按模拟失重时相分别为6、12、24、48、96、0 h组(地面对照组).采用尾悬吊法建立模拟失重动物模型.应用RT-PCR和Western blot技术分别检测各组大鼠肝组织Hsp70蛋白和mRNA的表达.结果 不同时相模拟失重环境下大鼠肝脏Hsp70mRNA水平均显著高于对照组(P<0.05),模拟失重6 h组肝脏Hsp70mRNA表达显著升高,12 h组达高峰,24 h和48 h略有下降,但仍然显著高于对照组(P<0.05).Hsp70蛋白表达水平在6 h组形成高峰,随模拟失重时间的延长,则呈明显下降趋势.96 h组降低到对照组水平.结论 模拟失重使大鼠肝脏组织中Hsp70蛋白和基因表达发生明显变化,提示肝脏Hsp70表达变化与失重应激反应和失重耐受有密切关系.     

膳食中添加骨糊对大鼠钙磷吸收和骨质的影响

畜禽骨骼中含丰富的蛋白质和矿物质元素，尤其钙的含量高，钙磷比值适宜。本实验用新鲜猪长骨和肋骨，经破碎、研磨制成鲜骨糊，再经烘干、碾细、制成骨糊粉，添加到膳食中。实验动物选用Ｗｉｓｔａｒ刚断乳的雄性大白鼠２８只，按体重配对随机分成４组。实验期４周。实验表明，低钙膳食中添加骨糊，可显著增加肠钙吸收量（Ｐ＜０．０５），提高股骨灰分绝对含量（Ｐ＜０．０１）、骨矿盐含量（灰分重／干重）（Ｐ＜０．０１）和骨矿盐密度（灰分重／体积）（Ｐ＜０．０５）。结果表明，低钙摄入时补充骨糊能改善人体钙的营养，对身体没有不良影响     

1，25(OH)2D3对模拟失重大鼠股骨远端松质骨的扫描电镜观察

目的 观察1,25-二羟维生素D3对模拟失重状态下大鼠股骨远端松质骨超微结构的影响.方法 SPF级雄性SD大鼠66只,随机分为自由活动组、悬吊对照组和悬吊实验组,同时悬吊实验组给予1,25-二羟维生素D3皮下注射（0.05 μg/kg·d）,实验期为14 d、28 d.取股骨远端沿冠状面切开,蒸馏水冲洗净骨髓腔,乙醇梯度脱水,表面喷金后利用扫描电镜对大鼠股骨远端松质骨的形态结构进行观察.结果 悬吊对照组与自由活动组比较大鼠骨小梁变细,断裂,数目减少,胶原纤维排列杂乱,微损伤增多;悬吊实验组较悬吊对照组大鼠骨小梁数目增多,胶原纤维排列规整,未见明显微骨折发生,且悬吊14 d实验组较悬吊28 d实验组保持了更好的微结构.结论 1,25-二羟维生素D3能够对模拟失重状态下大鼠股骨远端松质骨的超微结构产生有利影响.     

益生元对饮用银化水模拟失重大鼠骨代谢与骨生物力学的影响

目的　研究饮用银化水对模拟失重大鼠骨代谢与骨生物力学的影响及益生元的调整作用。方法　 40只SPF级SD雄性大鼠随机分为地面对照组 (GC)、模拟失重对照组 (SC)、模拟失重饮用银化水组 (SS)、银化水与益生元模拟失重组 (SPS) ,实验期 2 1d。EDTA滴定法测定饲料钙表观吸收率和骨钙含量 ,双能X射线测右侧股骨密度 ,质构仪测右侧股骨生物力学指标。结果　骨代谢指标SC组显著低于GC组 (P <0 0 0 1 ) ,SS组也低于SC组 (P <0 0 5) ,SPS组高于SS组 (P <0 0 5) ;SC组骨结构力学和材料力学指标均显著低于GC组 (P <0 0 0 1 ) ,SS组材料力学指标低于SC组 (P <0 0 5) ,SPS组材料力学指标高于SS组 (P <0 0 5)。结论　饮用 0 2 0mg/L银化水加重了模拟失重大鼠骨代谢的紊乱和骨材料力学的下降 ,而益生元可以缓解饮用银化水模拟失重大鼠骨代谢的紊乱和骨材料力学的下降。     

The relative effect of endogenous estradiol and androgens on menopausal bone loss: a longitudinal study

OBJECTIVE: The aim of this study was to assess the relative strength of the association of endogenous estradiol and androgens with bone loss at the lumbar spine and femoral neck during the menopausal transition. DESIGN: A longitudinal study of a population-based cohort of 159 Australian-born women who at baseline had a mean age of 50.0 years (SD=2.4) and had menstruated in the prior 3 months. BMD was measured by dual-energy X-ray absorptiometry at the lumbar spine and femoral neck on up to three occasions. RESULTS: Of the 159 participants, 50 had two BMD measurements and 109 had a third measure. The mean time between the first and final measures for the whole group was 39 months and at the time of the final measures 49% of the participants had become postmenopausal. The mean percentage change/year in lumbar spine BMD was -0.9% (95% CI, -1.1 to -0.6) and at the femoral neck, -0.5% (95% CI, -0.7 to -0.2). A highly significant association with estradiol at the final time point was found, whereas the contribution of estradiol at baseline was negligible. The variance explained by estradiol levels was 19% and 11% for change in BMD at the LS and FN, respectively. Excluding baseline estradiol values and using the average of change in BMD at the LS and FN, the final regression equation estimated that an estradiol level of 330 pmol/l (95% CI, 274 to 386) and 245 pmol/l (95% CI, 194 to 296) is required for preservation of LS and FN BMD, respectively. A stepwise linear regression model was used to assess the effect of age, BMI, estradiol, testosterone, DHEAS, SHBG, and free testosterone index on changes in BMD and found that only the final estradiol level had a significant association with change in BMD. CONCLUSION: Endogenous estradiol was the only hormone among those investigated to have a significant effect on bone mineral density during the menopausal transition.     

积雪草酸对高血脂小鼠骨量丢失的保护作用

目的探讨积雪草酸对高血脂小鼠骨量丢失的保护作用。方法 60只8周龄SPF级雄性C57BL/6 J小鼠按体重随机分为6组,每组10只:空白对照组[CON,生理盐水:5 m L/(kg·d)]、高脂饲料组[HFD,生理盐水:5 m L/(kg·d)]、高脂饲料+低剂量积雪草酸组[HFD+AA-L:5 mg/(kg·d)]、高脂饲料+中剂量积雪草酸组[HFD+AA-M:10 mg/(kg·d)]、高脂饲料+高剂量积雪草酸组[HFD+AA-H:20 mg/(kg·d)]、高脂饲料+辛伐他汀组[HFD+SIM:20 mg/(kg·d)]。除空白组之外,其他组别采用高脂饲料连续喂养16周并同时给药进行干预。实验结束后,经眼眶采血收集血清、两侧股骨和胫骨。结果高脂饲料引起小鼠血清胆固醇(TC)、丙二醛(MDA)和I型胶原C末端肽(CTX-I)水平升高,超氧化物歧化酶(SOD)和I型前胶原氨基端前肽(PINP)水平下降(均P0.05),且胫骨近端骨密度下降,骨微结构受损,骨形成率下降,其股骨生物力学指标降低。HFD+AA-M、HFD+AA-H和HFD+SIM组均可明显降低小鼠血清TC、MDA、CTX-I水平,升高SOD和PINP水平(均P0.05),增加骨密度和改善骨微结构,提高骨生物力学指标,HFD+AA-H组效果稍优于HFD+AA-M,但稍逊于HFD+SIM组。HFD+AA-L组小鼠血指标、骨密度、骨微结构和骨生物力学均无明显改善(P0.05)。结论积雪草酸[10、20 mg/(kg·d)]灌胃给药可预防高血脂小鼠的骨量丢失,其机制可能通过促进骨形成,抑制骨吸收,增加机体的抗氧化能力。     

Reduced bone density in women with fractures: Contribution of low peak bone density and rapid bone loss

Osteoporosis is regarded as a disease of the elderly because fractures occur late in life. Although excessive bone loss during aging is likely to contribute to the deficit in bone density, patients with fractures do not consistently have more rapid bone loss, greater bone resorption or lower bone formation (measured using biochemical or histomorphometric markers of bone turnover). The pathogenesis of the low bone density and bone fragility that characterize osteoporosis may begin during the first two decades of life. There are differences in the hormonal regulation of regional growth and mineral accrual, differences in the age of onset, rate and duration of linear growth and mineral accrual of the axial and appendicular skeleton, of cortical and trabecular bone, and of proximal and distal limb segments. Illnesses, risk or protective factors, and disorders of hormonal deficiency or excess may affect longitudinal growth, mineral accrual, or both, depending on the timing of exposure. Quantitatively larger and qualitatively different effects on bone density may result when exposure occurs during growth rather than during adulthood. The magnitude of these deficits and their location are likely to establish the relevance of regional age-related and sex hormone dependent bone loss. Thus, any unifying hypothesis concerning the epidemiology and pathogenesis of osteoporosis must consider the relative contributions of low peak bone density and bone loss to the deficit in bone density in adulthood. A great deal of research is needed to examine the physiology of longitudinal growth and mineral accrual as the pathogenesis of osteoporosis is at least partly explained by events occurring during the first 20 years of life.     

A cat model for the evaluation of mechanisms of bone resorption: Induction of bone loss by simulated immune complexes and inhibition by indomethacin

Summary When simulated immune complexes (SIC) (heat-aggregated IgG) possessing many of the properties of true antigen-antibody complexes were injected via the root canal into the periapical tissues of cat maxillary cuspids, radiographically and histologically evident bone resorption occurred at these sites within 7 days. Bone loss was accompanied in all cases by inflammation of the surrounding collagenous connective tissues and was characterized by the presence of osteoclasts. Bone resorption, but not the accumulation of inflammatory cells, was blocked by the systemic administration of indomethacin, an inhibitor of prostaglandin synthetase. The most likely explanation is that SIC-activated mechanisms such as the complement cascade, prostaglandin synthesis, and neutrophil degranulation were responsible for the bone loss. The minor inflammation and bone loss that followed the repeated injections of BSA and of monomeric IgG can best be explained as a response to trauma. The data presented establish that the cat maxillary cuspid is a useful model in which to explore the mechanism underlying pathological bone resorption.     

Cyclical behavior of bone remodeling and bone loss in healthy women after menopause: results of a prospective study

Annual changes in lumbar bone mineral density (LBMD) and bone remodeling markers were measured in 238 healthy pre- and postmenopausal women, aged 45–74 years. The subjects were divided into groups according to their menstrual status and years since menopause. The results obtained indicate that bone loss is not a constant process over time but rather exhibits cyclical damping oscillations. When the log-linear trend of LBMD decrement was transformed into a constant by considering annual percentage changes, the presence of a cyclical component of 7 years was evident. By employing a harmonic regression model, the cyclical component was also statistically significant on baseline data. The cyclical behavior of LBMD decrement corresponded to an analogous behavior of the bone remodeling markers. These results suggest that a lack of estrogen acts as a synchronizer on bone remodeling by triggering a latent cyclical rhythm of bone loss that persists throughout life after menopause. The existence of a chronobiological rhythm of bone loss starting after menopause, if confirmed, could have important clinical implications.     

Natural history and risk factors for bone loss in postmenopausal Caucasian women: a 15-year follow-up population-based study

SUMMARY: In this 15-year follow-up study, we found that the estimated rate of bone loss at the femoral neck (FN) for women aged 45-68 was linear at a rate of 1.67% per year, but quadratic for lumbar spine (LS) at a rate of 3.12% initially, and slowing down with age. We also confirmed the protective role of HRT, increasing weight, and lean mass in long-term bone loss. INTRODUCTION: The objective was to describe the natural history of bone loss and explore the role of environmental factors in postmenopausal women over a 15-year period. METHODS: Bone mineral density (BMD) at the FN and the LS were measured in postmenopausal women from the Chingford Study. Height, weight, HRT status, and calcium/vitamin D supplement were assessed at each visit. Osteoarthritis of hip and spine was assessed by X-ray at baseline and at year 8. RESULTS: A total of 955 postmenopausal women with an average age of 54.7 at baseline were included. Both FN and LS BMD decreased significantly with age (p<0.0001). The decline was larger in the LS (-3.12% per year), which showed a quadratic relationship, than in the FN (-1.67% per year) with a linear relationship. The rate of bone loss was reduced by one third annually for the FN and LS respectively in current HRT users. Change in weight was positively associated with both DeltaFN and DeltaLS BMD (beta=0.16% and 0.09% change in DeltaFN and DeltaLS BMD per kilogramme change in weight respectively, p<0.0001 for both sites). Spine OA and progression were positively associated with DeltaLS BMD (beta=1.22% change in DeltaLS BMD per grade in spine OA and 0.45% change in DeltaLS BMD for patients who progressed, p<0.0001 for spine OA and p=0.002 for spine OA progression). Spine OA (beta=0.54% change in DeltaFN BMD per grade, p<0.0001), but not progression, and hip OA were positively associated with DeltaFN BMD. Furthermore, both age and body weight at baseline were positively associated with both DeltaFN and DeltaLS BMD (beta=0.02-0.04% change in DeltaFN and DeltaLS BMD per year increase in age at baseline and 0.004-0.007% change in DeltaFN and DeltaLS BMD per kilogramme increase in weight at baseline, all p<0.0001). CONCLUSION: This large population-based longitudinal study demonstrated that the decline of BMD over 15 years is linear with age for the FN, but quadratic for the LS. The study confirmed the protective role of HRT, increased weight and lean mass in long-term bone loss.