仙茅苷调节lncRNA MEG3/miR-181a-5p通路对骨质疏松大鼠成骨细胞自噬的影响

目的 探讨仙茅苷（Curculigoside，CUR）对骨质疏松症（osteoporosis，OP）大鼠成骨细胞自噬的影响以及对lncRNA MEG3/miR-181a-5p信号轴的调节作用。方法 体外培养骨髓间充质干细胞（BM-MSCs）诱导成骨细胞分化，CCK-8法筛选CUR浓度；数据库预测lncRNA MEG3与miR-181a-5p结合位点；利用转染技术将BM-MSCs细胞分为NC组、CUR组、CUR+3-MA组、CUR+pc-NC组和CUR+pc-LncRNA MEG3组，qRT-PCR检测lncRNA MEG3、miR-181a-5p的表达水平，碱性磷酸酶（ALP）染色法检测细胞ALP活性，MDC法检测细胞自噬体数量，免疫荧光检测细胞微管相关蛋白1-轻链3（LC3）、自噬效应蛋白（Beclin1）的表达。肌肉注射地塞米松磷酸钠建立OP大鼠，大鼠分为对照组（CT组）、模型组（OP组）、OP+CUR组（灌胃15 mg/kg CUR），CT检测大鼠胫骨骨形态学，Western blot和qRT-PCR分别检测LC3Ⅱ/Ⅰ、Beclin1与lncRNA MEG3、miR-181a-5的表达。结果 25 μg/mL以上浓度的CUR显著提高BM-MSCs细胞增殖活力（P＜0.05）；lncRNA MEG3与miR-181a-5p具有靶向结合位点；与NC组相比，CUR组细胞ALP活性、自噬体数量以及LC3、Beclin1表达增加（P＜0.05）；与CUR组相比，CUR+3-MA组细胞ALP活性、自噬体数量以及LC3、Beclin1表达减少（P＜0.05）；与CUR+pc-NC组相比，CUR+pc-LncRNA MEG3组细胞ALP活性、自噬体数量以及LC3、Beclin1表达减少（P＜0.05）。OP组大鼠骨形态学评价以及LC3Ⅱ/Ⅰ、Beclin1、miR-181a-5p表达较CT组下降，lncRNA MEG3表达增加（P < 0.05）；OP+ CUR组大鼠骨形态学评价以及LC3Ⅱ/Ⅰ、Beclin1、miR-181a-5p表达较OP组增加，lncRNA MEG3表达降低（P＜0.05）。结论 CUR可能通过调节LncRNA MEG3/miR-181a-5p信号轴促进OP大鼠成骨细胞自噬活性。     

狼疮肾炎患者自噬水平及其对足细胞相关蛋白表达水平的影响

目的探讨狼疮肾炎(lupus nephritis,LN)患者自噬水平及其对足细胞相关蛋白表达水平的影响。方法选择2017年5月至2019年5月于榆林市第一医院收治的69例LN患者为LN组,50例系统性红斑狼疮(systemic lupus erythematosus,SLE)患者为SLE组,50例肾切除手术患者为对照组,观察3组肾脏足细胞内自噬体数量,比较3组肾脏组织中自噬相关蛋白、微管相关蛋白轻链3(LC3)、B淋巴细胞瘤蛋白质-2-相互作用蛋白(Beclin1)的表达,以及足细胞相关蛋白,肾病蛋白(Nephrin)、足突蛋白(Podocin)的表达。分离狼疮肾炎患者肾脏足细胞,将足细胞分为自噬抑制组和自噬诱导组,自噬抑制组加入100 nmol/L 3-甲基腺嘌呤(3-MA),自噬诱导组加入100 nmol/L雷帕霉素(RAPA),比较3组足细胞内自噬体数量及LC3、Beclin-1、Podocin、Nephrin等蛋白的表达。结果LN组、SLE组肾脏足细胞内自噬体数量及LC3、Beclin-1、Podocin、Nephrin蛋白表达量显著高于对照组(P<0.05);SLE组肾脏足细胞内自噬体数量及LC3、Beclin-1、Podocin、Nephrin蛋白表达量显著高于LN组(P<0.05);自噬诱导组足细胞内自噬体数量及LC3、Beclin-1、Podocin、Nephrin蛋白表达量显著高于正常对照组、自噬抑制组(P<0.05);正常对照组足细胞内自噬体数量及LC3、Beclin-1、Podocin、Nephrin蛋白表达量显著高于自噬抑制组(P<0.05)。结论LN患者自噬水平呈升高状态,自噬水平升高可能通过上调足细胞相关蛋白Podocin、Nephrin水平而减轻足细胞损伤,抑制LN病情进展。     

七氟醚激活海马线粒体自噬诱导老年小鼠认知功能损伤

目的探讨七氟醚对老年小鼠海马线粒体自噬和认知功能的影响。方法雄性C57BL/6J小鼠48只,18~20月龄,体重35~40 g。采用随机数字表法将小鼠为三组:对照组(C组)、吸入3%七氟醚组(S组)和吸入3%七氟醚+自噬抑制剂三甲基腺嘌呤组(3-MA组),每组16只。C组小鼠吸入空氧混合气体6 h。S组和3-MA组吸入3%七氟醚6 h。3-MA组吸入七氟醚前1 h腹腔注射三甲基腺嘌呤30 mg/kg。七氟醚吸毕24 h后采用Morris水迷宫实验观察小鼠行为学变化,第1~4天训练,第5天进行空间探索实验。行为学测试结束后立即处死小鼠。采用HE染色法观察海马组织病理学改变,免疫荧光法观察海马组织中自噬情况,Western blot法检测海马组织中PINK1、Parkin、LC3和Beclin1蛋白含量。结果与C组比较,S组、3-MA组水迷宫实验第2~4天逃避潜伏期明显延长(P<0.05),第5天目标象限停留时间明显缩短(P<0.05),穿越次数明显减少(P<0.05),海马组织出现病理形态学损伤,海马组织中LC3阳性细胞数明显增多(P<0.05),海马组织PINK1、Parkin、Beclin1蛋白含量和LC3Ⅱ/LC3Ⅰ比值明显升高(P<0.05)。与S组比较,3-MA组水迷宫实验第2~4天逃避潜伏期明显缩短(P<0.05),第5天目标象限停留的时间明显延长(P<0.05),穿越次数明显增多(P<0.05),海马组织病理形态学损伤程度减轻,海马组织中LC3阳性细胞数明显减少(P<0.05),海马组织PINK1、Parkin、Beclin1蛋白含量和LC3Ⅱ/LC3Ⅰ比值明显降低(P<0.05)。结论吸入3%七氟醚6 h的老年小鼠,海马病理形态学发生改变,伴随学习和记忆能力下降,其机制可能与七氟醚激活线粒体自噬有关。     

调控自噬流对巨噬细胞粘附与迁移功能的影响

目的巨噬细胞浸润是包括糖尿病肾病(diabetic nephropathy, DN)在内的多种慢性肾脏疾病的重要组织病理特征。本研究通过调控巨噬细胞(RAW264.7)自噬流各阶段,探究其对巨噬细胞黏附迁移功能的影响。 方法体内实验,建立糖尿病肾病大鼠模型,于12周末分别处死正常大鼠、DN组大鼠,病理染色观察肾脏病理改变,检测肾组织巨噬细胞标志物及自噬相关标志物表达。体外实验,检测正常与高糖(30 mM)条件下,巨噬细胞自噬体数量变化,LC3、Beclin－1(自噬相关标志物)、P62(自噬体清除指标)的表达,以及巨噬细胞粘附迁移数量。分别加用自噬溶酶体降解抑制剂氯喹(CQ)、自噬体生成激活剂雷帕霉素(RAPA),观察其对巨噬细胞自噬标记物表达及其粘附迁移功能的影响,电镜观察巨噬细胞自噬体数量与自噬溶酶体形态的变化。 结果体内实验,DN大鼠肾脏损伤明显,肾小球体积增大,基底膜增厚,系膜基质增多,肾组织CD68(巨噬细胞标志物)、P62表达增加(t＝3.35、t＝16.27, P<0.05),LC3表达减少(t＝51.12, P<0.05);体外实验,在高糖组,电镜观察发现自噬体数量较正常组减少,Western印迹与免疫荧光显示自噬相关蛋白LC3、Beclin－1表达降低,P62表达升高(t＝27.02,t＝45.56、t＝32.71,P<0.05),巨噬细胞粘附和迁移数量增多(t＝6.87、t＝8.76,P<0.05)。用CQ处理后,电镜观察发现巨噬细胞自噬体溶酶体降解受到抑制,Western印迹与免疫荧光显示自噬相关蛋白LC3、Beclin－1表达降低,P62表达升高(t＝14.64、t＝12.45、t＝8.57,P<0.05);CQ进一步促进高糖诱导的巨噬细胞黏附迁移数量增多(t＝4.37、t＝7.27,P<0.05);RAPA增加巨噬细胞自噬体数量,Western与免疫荧光显示RAPA提高了被高糖抑制的巨噬细胞自噬水平,[LC3、Beclin－1表达升高,P62表达降低(t＝9.37、t＝11.53,t＝8.73;P<0.05)],减少高糖诱导的巨噬细胞黏附、迁移数量增多(t＝4.16、t＝5.74, P<0.05)。 结论高糖抑制自噬水平,促进巨噬细胞黏附迁移;抑制自噬溶酶体降解可降低自噬水平、促进巨噬细胞粘附迁移;激活自噬体生成能提高自噬水平,减轻巨噬细胞粘附迁移。     

AMPK在二甲双胍诱导结肠癌细胞SW480自噬中的作用

目的研究二甲双胍是否影响人结肠癌SW480细胞中AMPK活性,并探讨AMPK在二甲双胍诱导自噬中的作用。方法用不同剂量(0、1、5、10 mmol/L)二甲双胍处理SW480细胞24 h,Western blot检测AMPK、p-AMPK以及自噬相关蛋白LC3、p62蛋白表达;荧光定量PCR检测LC3 mRNA表达。二甲双胍与自噬抑制剂3-甲基腺嘌呤(3-Methyladenine,3-MA)单独或联合处理后,Western blot检测LC3、p62表达。沉默AMPK后,10 mmol/L二甲双胍处理SW480细胞24 h,Western blot检测LC3、p62蛋白表达,荧光定量PCR检测LC3mRNA表达情况。结果不同浓度二甲双胍(1、5、10 mmol/L)处理SW480细胞后,AMPK磷酸化水平递增上升,LC3蛋白及mRNA递增表达增加,p62递减表达降低。二甲双胍与3-MA联合处理SW480细胞后,LC3表达降低,p62表达升高。3-MA有抑制二甲双胍的作用。沉默AMPK后,LC3蛋白及mRNA表达下降,p62蛋白表达增加。结论二甲双胍可诱导SW480细胞中AMPK活化,AMPK的活化参与了二甲双胍诱导的自噬。     

自噬对于风湿性心脏病瓣膜间质细胞分化以及增殖能力的影响

目的探讨自噬对于风湿性心脏病的瓣膜间质细胞(VICs)生物学特征改变以及增殖能力的影响。方法使用肝素诱导人主动脉瓣膜间质细胞(购自上海赛百慷生物技术股份有限公司)向肌成纤维细胞分化, 而后使用自噬抑制剂LY294002(15 μmol/L)进行干预, 将细胞分为对照组、抑制剂组、诱导组、实验组。使用蛋白质印迹法(Western blot)检测各组细胞α-平滑肌肌动蛋白(α-SMA)、碱性磷酸酶(ALP)、Beclin1、微管相关蛋白轻链3-Ⅱ(LC3-Ⅱ)蛋白表达水平;采用细胞增殖及毒性检测试剂盒(CCK-8)分析自噬对4组细胞增殖的影响。结果蛋白印记结果显示对照组的ALP和α-SMA蛋白(0.827±0.123、0.716±0.141)显著低于诱导组(1.384±0.165、1.315±0.223), 差异有统计学意义(t=4.669, P<0.01、t=3.929, P<0.05);对照组Beclin1和LC3-Ⅱ(0.807±0.182、0.392±0.150)显著低于诱导组(1.271±0.067、1.404±0.018), 差异有统计学意义(t=4.131, P&...     

自噬和p53凋亡刺激蛋白在横纹肌溶解致大鼠急性肾损伤模型中的表达趋势

目的:观察自噬相关蛋白和p53凋亡刺激蛋白(apoptosis-stimulating protein of p53,ASPPs)在急性肾损伤(acute kidney injury,AKI)早期的表达变化,初步探讨自噬相关蛋白和ASPPs是否可能成为AKI早期损伤生物标志物。方法:建立横纹肌溶解致AKI大鼠模型,将74只雄性SD青年大鼠随机分为假手术组(Sham),甘油模型组;模型组大鼠一次性双下肢肌肉注射50%甘油8 ml/kg,Sham组相同途径注射生理盐水8 ml/kg,造模前大鼠禁水24 h;在给药6 h、12 h、1、2、3、5、7 d时检测大鼠Scr、BUN、Cys C和肌酸激酶(creatine kinase,CK)水平;光镜观察大鼠肾脏病理变化;透视电镜观察大鼠肾小管上皮细胞超微结构变化及自噬体的情况;免疫印迹法检测肾脏组织Atg5-Atg12、Beclin 1、LAMP-2、p62、p53及i ASPP和ASPP1表达情况。结果:青年大鼠暴露于甘油6 h时,与Sham组比较,顺铂模型组大鼠Scr、BUN、Cys C、CK水平显著升高(P0.05),Scr、BUN在2 d时达峰;光镜检查发现肾小管损害明显加重;电镜结果显示,与Sham组比较,顺铂组大鼠平均自噬体数量明显增多;甘油诱导后6 h开始,肾脏组织i ASPP蛋白表达明显减少(P0.05),LC3、Atg5-Atg12、Beclin 1、LAMP-2、p62、p53及ASPP1等蛋白表达即出现明显升高(P0.05)。与Sham组比较,LC3蛋白表达6h达峰后逐渐下降,至5 d时达最低值,后逐渐升高;p53蛋白表达12 h达峰后逐渐下降;p62蛋白表达1 d达峰后逐渐下降;Atg5-Atg12、Beclin 1、LAMP-2及ASPP1等蛋白表达3 d达峰后逐渐下降;i ASPP蛋白表达6 h开始减少,1 d时达最低值后逐渐升高。结论:自噬和ASPPs在AKI发生早期即可出现并参与了AKI的发生发展。自噬相关蛋白和ASPPs有望成为AKI更早期的损伤标志物,可能是AKI早期干预的新靶点,但仍需更深入的研究。     

精索静脉曲张大鼠睾丸自噬对生精细胞的影响

目的:研究精索静脉曲张(VC)大鼠模型中睾丸不同水平自噬对生精细胞凋亡的影响。方法:雄性SD大鼠54只随机分为6组:空白对照组、雷帕霉素对照组、氯喹对照组各6只,VC组、VC+雷帕霉素组、VC+氯喹组各12只。采用HE染色观察睾丸、附睾组织形态学变化,并对睾丸及附睾中精子形成情况进行评分,TUNEL染色检测生精细胞凋亡指数(AI),Western印迹检测LC3、p62、Bax、Bcl-2的表达。结果:空白对照组、雷帕霉素对照组、氯喹对照组大鼠睾丸及附睾组织均未发生明显形态学变化,精子形成情况评分及AI亦无显著差异(P>0.05);VC组大鼠睾丸及附睾组织发生明显病理损伤,精子形成情况评分显著降低(P<0.01),AI显著升高(P<0.01),但VC+雷帕霉素组较VC组明显改善,而VC+氯喹组较VC组轻度加重。此外,与空白对照组比较,VC组自噬相关蛋白LC3(包括LC3-Ⅱ/LC3-Ⅰ的比值)和促凋亡蛋白Bax表达显著增加(P<0.01),抑凋亡蛋白Bcl-2表达则显著降低(P<0.01);且VC+雷帕霉素组LC3与Bcl-2表达显著高于VC组(P<0.01),p62和Bax表达则显著低于VC组(P<0.01);而VC+氯喹组LC3与Bcl-2表达显著低于VC组(P<0.01),p62和Bax的表达则显著高于VC组(P<0.01)。结论:VC可诱导大鼠睾丸自噬和生精细胞凋亡,上调自噬可抑制生精细胞凋亡,阻滞自噬则可促进生精细胞凋亡。     

七氟醚预处理对大鼠脊髓缺血再灌注损伤的影响及自噬在其中的作用

目的 评价七氟醚预处理对大鼠脊髓缺血再灌注损伤的影响及自噬在其中的作用.方法 成年雄性SD大鼠45只,体重420～450 g,采用随机数字表法分为5组(n=9):对照组(Con组)、脊髓缺血再灌注组(I/R组)、七氟醚预处理组(Sevo组)、特异性自噬抑制剂3-甲基腺嘌呤组(3-MA组)和3-MA+七氟醚预处理组(3-MA+ Sevo组).I/R组胸主动脉球囊阻断+体循环低血压制备大鼠脊髓缺血再灌注模型,Sevo组于缺血前24h时吸入3.4％七氟醚2h,3-MA组和3-MA+ Sevo组分别于再灌注即刻和吸入七氟醚前15 min时鞘内注射20出3-MA(10 mmol/L).于再灌注24h时采用神经功能缺陷评分(NDS评分)法评价大鼠神经功能,随后处死取脊髓,Western blot法检测LC3B、Beclin 1、Bcl-2蛋白的表达水平.结果 与Con组比较,I/R组脊髓LC3B、Beclin 1蛋白表达上调,Bcl-2蛋白表达下调,NDS评分升高(P＜0.05);与I/R组比较,Sevo组、3-MA组和3-MA+ Sevo组脊髓LC3B、Beclin 1蛋白表达下调,Bcl-2蛋白表达上调,NDS评分降低(P＜0.05);Sevo组、3-MA组和3-MA+ Sevo组各指标比较差异无统计学意义(P＞0.05).结论 七氟醚预处理可减轻大鼠脊髓缺血再灌注损伤,其机制可能与上调Bcl-2,抑制自噬溶酶体途径,减轻自噬有关.     

缺氧条件下大鼠髓核细胞中缺氧诱导因子1α与自噬相关分子的表达及相关性分析

目的探讨缺氧条件下大鼠髓核细胞中缺氧诱导因子1α(hypoxia inducible factor 1α,HIF-1α)与自噬相关分子Beclin1、LC3B的表达及其相关性。方法取健康成年SD大鼠髓核组织,分离培养髓核细胞并传代。取第3代髓核细胞行HE染色和Ⅱ型胶原酶免疫荧光染色鉴定后,随机分为4组。A组细胞于常氧条件下(37℃、5%CO2、20%O2)培养,B组细胞于缺氧条件下(37℃、5%CO2、1%O2)培养,C组细胞转染HIF-1α-小干扰RNA后于缺氧条件下培养,D组细胞加入自噬抑制剂3-MA后于缺氧条件下培养。各组细胞培养8 h后,采用Western blot和实时荧光定量PCR(real-time fluorescence quantitative PCR,qRT-PCR)检测HIF-1α与自噬相关分子Beclin1、LC3B的表达情况。结果经分离纯化的第3代大鼠髓核细胞HE染色后细胞质呈淡粉色,细胞核呈蓝黑色;Ⅱ型胶原酶免疫荧光染色为阳性。Western blot和qRT-PCR检测示,B组HIF-1α、Beclin1和LC3B蛋白及mRNA相对表达量均显著高于A组(P<0.05),C组均显著低于B组,差异均有统计学意义(P<0.05)。D组HIF-1α蛋白和mRNA相对表达量与B组比较差异无统计学意义(P>0.05),Beclin1和LC3B蛋白和mRNA相对表达量均较B组显著降低(P<0.05)。结论缺氧条件能诱导大鼠髓核细胞中HIF-1α和自噬相关分子Beclin1、LC3B的表达,且HIF-1α与自噬相关分子的表达具有相关性,即HIF-1α下调能降低自噬相关分子的表达,而缺氧条件下自噬水平下调对HIF-1α的表达无明显影响。     

Osteogenesis after Bone and Bone Marrow Transplantation: II. The Initial Cellular Events Following Transplantation of Decalcified Allografis of Cancellous Bone

An experimental study was done in rabbits to investigate the fate of allogeneic iliac cancellous bone, both non-decalcified and decalcified with hydrochloric acid, transplanted to a muscular site for up to 14 days. Some of the treated allografts were impregnated with autologous bone marrow cells, obtained from the femoral medulla by aspiration, and each was compared with allografts alone. Combined myelo-osseous grafts produced bone after 7 to 8 days implantation, as did marrow autografts alone. In addition non-decalcified implants stimulated the production of multinucleated giant cells. Three different types of wash solution were used but these did not influence the cell population seen, nor the new bone formation. It is concluded that the critical events in bone formation after transplantation occur less than 8 days after the transplantation and that marrow cells have osteogenic capacity. This has relevance to the clinical aspects of bone grafting.     

Bone cement with reduced proportion of monomer in total hip arthroplasty: Preclinical evaluation and randomized study of 47 cases with 5 years' follow-up

Bone cement with reduced amount of monomer and low curing temperature may improve implant fixation due to reduced toxicity. We analyzed the mechanical, chemical and thermal properties of such a cement (Cemex Rx) using Palacos R as control. The in vivo performance of the 2 cements was also evaluated in a prospective randomized study of 47 hips, where either of the cement types was used to fixate Lubinus SP2 prostheses with the stem made of titanium alloy. Cemex Rx had a reduced tensile strength, probably because this cement was manually mixed, as recommended by the manufacturer. A standardized laboratory test showed lower curing temperature for Cemex, but measurements at 37° and with prechilled Palacos R and Cemex Rx, as in clinical work, showed no difference. In the clinical study radiostereometric measurements of cup and stem migration showed similar values in the 2 groups up to 5 years after the operation. The cement mantle was stable in both groups, but the stems migrated similarly inside the cement mantle regardless of the type of cement used. Proximal wear was low (0.04-0.05 mm/year) and tended to be lower in the Cemex group (p = 0.02). Aluminum and vanadium levels in serum increased 5 years after the operation, but no difference was noted between the 2 groups. Collagen markers (PICP, ICTP) showed similar increases in bone turnover 6 weeks and 6 months after operation in both groups.     

重组合异种骨植骨修复骨囊肿所致骨缺损

2001年10月～2003年9月，笔者共收治28例骨囊肿患者，均采用病灶刮除，瘤腔灭活和重组合异种骨植骨治疗，获得满意疗效，体会如下。     

感染性骨缺损的治疗及研究进展

感染性骨缺损由于存在感染及骨缺损双重病变,治疗棘手,疗程长,且易出现肌肉萎缩、局部瘢痕而致肢体功能受到严重影响.近年来随着外固定技术、显微外科技术、生物材料技术及骨组织工程技术等的发展,感染性骨缺损的治疗取得明显进步,短缩了治疗时间,且效果显著,笔者对其研究进展综述如下.     

Building better bone: The weaving of biologic and engineering strategies for managing bone loss

Segmental bone loss remains a challenging clinical problem for orthopaedic trauma surgeons. In addition to the missing bone itself, the local tissues (soft tissue, vascular) are often highly traumatized as well, resulting in a less than ideal environment for bone regeneration. As a result, attempts at limb salvage become a highly expensive endeavor, often requiring multiple operations and necessitating the use of every available strategy (autograft, allograft, bone graft substitution, Masquelet, bone transport, etc.) to achieve bony union. A cost‐sensitive, functionally appropriate, and volumetrically adequate engineered substitute would be practice‐changing for orthopaedic trauma surgeons and these patients with difficult clinical problems. In tissue engineering and bone regeneration fields, numerous research efforts continue to make progress toward new therapeutic interventions for segmental bone loss, including novel biomaterial development as well as cell‐based strategies. Despite an ever‐evolving literature base of these new therapeutic and engineered options, there remains a disconnect with the clinical practice, with very few translating into clinical use. A symposium entitled “Building better bone: The weaving of biologic and engineering strategies for managing bone loss,” was presented at the 2016 Orthopaedic Research Society Conference to further explore this engineering‐clinical disconnect, by surveying basic, translational, and clinical researchers along with orthopaedic surgeons and proposing ideas for pushing the bar forward in the field of segmental bone loss. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1855–1864, 2017.

     

The Penetration of Lincomycin into Normal Human Bone: Determinations of Penetration into Compact Bone, Spongy Bone and Bone Marrow

The penetration of lincomycin into normal bone was studied in 10 patients with fracture of the neck of the femur, a separate determination being made of the lincomycin concentration in serum, bone marrow, spongy bone and compact bone. The concentration of lincomycin in bone marrow was found to be at the same level as that in the serum. The concentration in spongy bone amounted in most cases to 50 to 75 per cent of the concentration in the serum, whereas the concentration in compact bone varied from 0 to 15 per cent of that in the serum.     

No adverse effects of early weight bearing after uncemented total hip arthroplastyA randomized study of 20 patients

Experimental fibular defects in 16 rats were filled with an acid decalcified homogenous bone matrix (bone inductive material). Autogenous bone grafts in corresponding defects in the other legs of the same rats served as controls. After 3 months, 11 of the 16 defects filled with bone inductive material healed with bony union, but only 4 of the 16 defects treated with autogenous bone grafts had healed. The results suggest that bone inductive material can repair bone defects which are too large to be healed by autogenous bone grafts.     

Repair of Bone Defects by Bone Inductive Material

Experimental fibular defects in 16 rats were filled with an acid decalcified homogenous bone matrix (bone inductive material). Autogenous bone grafts in corresponding defects in the other legs of the same rats served as controls. After 3 months, 11 of the 16 defects filled with bone inductive material healed with bony union, but only 4 of the 16 defects treated with autogenous bone grafts had healed. The results suggest that bone inductive material can repair bone defects which are too large to be healed by autogenous bone grafts.     

The benefit of bone marrow concentrate in addition to a glass‐reinforced hydroxyapatite for bone regeneration: An in vivo ovine study

This study evaluates the ability of a Glass Reinforced Hydroxyapatite Composite (GRHC), in a new microporous pellet formulation with autologous bone marrow concentrate (BMC), to enhance bone regeneration and new bone formation. Ninety non‐critical sized bone defects were created in the femurs of nine Merino breed sheep and randomly left unfilled (group A), filled with GRHC pellets alone (group B) or filled with GRHC pellets combined with BMC (group C). The sheep were sacrificed at 3 weeks (three sheep), 6 weeks (three sheep) and 12 weeks (three sheep) and histological analysis (Light Microscopy‐LM), scanning electron microscopy (SEM) and histomorphometric analysis (HM) were performed. At 3, 6, and 12 weeks, HM revealed an average percentage of new bone of 48, 72, 83%; 25, 73, 80%, and 16, 38, 78% for Groups C, B and A respectively (significantly different only at 3 weeks p < 0.05). LM and SEM evaluation revealed earlier formation of well‐organized mature lamellar bone in Group C. This study demonstrates that the addition of a bone marrow concentrate to a glass reinforced hydroxyapatite composite in a pellet formulation promotes early bone healing. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1176–1182, 2017.