激素对股骨头微血管及组织细胞的影响

目的通过建立激素性股骨头缺血性坏死动物模型,研究股骨头微血管密度(microvas-culardensity,MVD)和股骨头组织细胞超微结构的变化,探讨长期大剂量使用糖皮质激素引起股骨头缺血性坏死的机制。方法健康日本白兔40只,1.86～2.21kg,平均2.06kg。随机分为两组,实验组31只,对照组9只。实验组每周皮下注射醋酸氢化泼尼松8mg/kg,对照组每周皮下注射生理盐水0.32ml/kg。在实验的第4、8和12周分别对实验组和对照组的股骨头行微血管墨汁灌注,研究股骨头MVD的变化;制作半薄切片,在透射电镜下分别观察实验组和对照组的股骨头组织细胞的超微结构。拍摄兔耳背微血管网观察用药前后的变化。结果实验组双侧股骨头松质骨和密质骨的单位面积内MVD与对照组相比在用药3个月后明显下降(P<0.01)。兔耳背微血管网随用药时间的延长逐渐变稀疏。股骨头各系组织细胞内均发现有脂质堆积;骨细胞核膜失去连续性、碎裂,染色质溶解;血管内皮细胞内出现脂滴,胞膜结构不完整,可见明显的裂隙,线粒体肿胀、变圆,结构不清;脂肪细胞异常肥大,核内出现脂滴,并压迫小静脉,管腔变窄;小静脉内可见红细胞相互重叠呈“缗线状”。结论骨内压升高是激素性骨坏死病理过程中的一个表现,与肥大的脂肪细胞压迫小静脉有关。长期大剂量使用糖皮质激素可抑制     

“人”位、动力蛙式位及传统蛙式位固定对幼兔股骨头及骺板软骨凋亡实验研究

[目的]幼兔双髋行人位、动力蛙式位及传统蛙式位固定,探讨对股骨头及骺板软骨细胞凋亡影响。[方法]44只3周龄幼兔随机分4组(n=11):人位组(A组),动力蛙式位组(B组),传统蛙式位组(C组)及正常对照组(D组),固定3周后处死取股骨头。采用HE染色观察股骨头及骺板软骨细胞组织形态,免疫组化检测软骨bcl-2、bax蛋白表达情况。[结果](1)HE示A、B、C实验组股骨头表面软骨不光滑,细胞柱状紊乱,层次不清,细胞数量减少,基质染色不均匀,纤维组织增多;对照组软骨表面光滑,细胞柱状排列整齐规则,数量多,基质染色均匀;(2)免疫组化示股骨头关节软骨A、B、C实验组bax表达强度均显著高于对照组(P<0.05),对照组bcl-2/bax比值最高,动力蛙式位组bcl-2/bax比值显著高于传统蛙式位组和人位组(P<0.05);股骨头骺板软骨对照组和动力蛙式位组肥大、增殖区细胞bcl-2/bax比值显著高于传统蛙式位和人位组(P<0.05),静止区各组之间无显著差异(P>0.05)。[结论]3种髋固定体位均能影响股骨头及骺板软骨细胞凋亡,其中,传统蛙式位及人位固定加速软骨细胞的凋亡,不利于细胞存活,而动力蛙式位固定...     

激素诱发兔股骨头坏死发生过程中组织学和影像学动态对比研究

目的 研究兔激素性股骨头缺血坏死发生、发展过程中组织学改变和影像学表现之间的关系,探讨股骨头缺血坏死早期最佳诊断方法及治疗.方法 健康成年日本大白兔46只,随机分为实验组30只,肌肉注射甲强龙(20 mg/kg,单次),对照组16只肌肉注射相同剂量生理盐水.分别于注射后2、4、8、12周行X线、CT、MRI、股骨头血管动脉造影,以及处死动物前股骨头血管墨汁灌注后进行组织学检查、常规HE染色以及微血栓染色.结果 组织学:实验组2周时出现骨髓细胞碎片集聚,骨小梁出现空骨陷窝骨髓造血组织消失,大量脂肪细胞堆积,墨汁灌注,血管数量减少;4～12周时骨髓内脂肪细胞增大,骨小梁开始萎缩、变细,骨细胞核边聚、固缩;空骨陷窝数增多,骨髓造血组织几乎完全消失,被脂肪组织、脂肪细胞替代填充,墨汁灌注血管消失.影像学:2～12周X线、CT均未见异常,MRI在应用激素2周双侧股骨头T1WI显示信号强度明显降低,低信号区呈线样,T2WI和准,T2WI呈不均匀高信号,高信号区呈线样,并延续至12周.动脉介入造影2周后即出现股骨头血管管腔变细,4及8周时血管数量减少、尚存在的血管变得纤细.对照组均未见明显异常.结论 股骨头缺血坏死发生发展过程中组织学变化和MRI表现密切相关,MRI是早期检查发现、诊断股骨头缺血坏死最具灵敏度、特异性的非侵入性检查方法.     

非那雄胺对大鼠前列腺eNOS表达和微血管的影响

目的　评价非那雄胺对大鼠前列腺微血管的影响并探讨其机制。方法　①将雄性SD大鼠随机分为三组 ,每组 10只 ,按4 0mg/(kg·d)喂饲非那雄胺 7d(B组 )、14d(C组 ) ,以喂饲生理盐水为对照组 (A组 )。②HE染色观察采用墨汁灌注染色的大鼠前列腺微血管的改变。③免疫组织化学SP法检测大鼠前列腺组织中内皮型一氧化氮合酶 (eNOS)的蛋白表达。结果　①B、C组的微血管密度较A组分别下降了 35 .2 %、5 6 %。②eNOS的蛋白表达较A组分别减少 15 .7%、5 2 .5 %。结论　非那雄胺可抑制大鼠前列腺组织中eNOS的蛋白表达进而抑制前列腺的微血管生成。     

激素诱发兔股骨头坏死发生过程中组织学和影像学动态对比研究

目的 研究兔激素性股骨头坏死发生、发展过程中组织学改变和影像学表现之间的相关关系.方法 健康成年日本大白兔46只,随机分为实验组30只,肌内注射甲基泼尼松龙(20mg/kg,1次/d,连续3 d);对照组16只,肌内注射相同剂量生理盐水.分别于注射后2、4、8、12周行X线、CT、MRI与股骨头血管动脉造影检查,并于处死动物前股骨头血管墨汁灌注后进行组织学检查,常规HE染色以及微血栓染色.结果 组织学:实验组2周时出现骨髓细胞碎片集聚,骨小梁出现空骨陷窝,骨髓造血组织消失,大量脂肪细胞堆积,墨汁灌注,血管数量减少;4-12周时骨髓内脂肪细胞增大,骨小梁开始萎缩、变细,骨细胞核边聚、固缩,空骨陷窝数增多,骨髓造血组织几乎完全消失,被脂肪组织、脂肪细胞替代填充,墨汁灌注血管消失.影像学:2-12周X线、CT均未见异常,在应用激素2周双侧股骨头MR T_1加权像显示信号强度明显降低,低信号区呈线样,T_2和准T_2加权像呈不均匀高信号,高信号区呈线样,并延续至12周.动脉介入造影,2周后即出现股骨头血管管腔变细,4、8周时血管数量减少,尚存在的血管变细.各时间点股骨头坏死组织学改变与MRI异常表现密切相关.对照组均未见明显异常.结论 糖皮质激素诱发兔股骨头坏死发生、发展过程中,骨坏死组织学变化和股骨头MRI异常表现密切相关;MRI异常表现在一定程度上可以反映股骨头坏死后的组织学改变;MRI是早期诊断股骨头坏死最具灵敏度、特异性,并能反映骨坏死真实情况的非侵入性检查方法.     

小鼠激素性股骨头坏死的组织学演变

目的通过激素性股骨头坏死小鼠模型，了解其组织学变化过程及其规律。方法选用2个月龄FVB小鼠，分为6组，每组5只，A、B、C、D组行甲基强的松龙每日21mg／kg体重皮下注射，分别持续1、2、3、4周，在处死前10和3d以30mg／kg体重腹腔注射盐酸四环素，E组为对照组；F组母鼠行双侧卵巢切除。股骨头行苏木素-伊红（HE）染色、甲苯胺蓝染色、四环素标记、TUNEL和Micro-CT。结果4周时股骨头软骨下骨板和骨小梁出现坏死和空的骨陷窝；有跨越骨骺的骨桥形成；部分骨小梁见双荧光标记带，其中大量骨细胞和成骨细胞TUNEL阳性。Micro-CT发现1～3周骨量逐步下降，股骨头三维重建可见桔皮样改变。结论FVB小鼠作为激素性股骨头坏死的早期病理过程的动物模型有其一定应用价值。     

骨形态形成蛋白复合纤维蛋白载体修复全厚关节软骨缺损的实验研究

目的：用骨形态形成蛋白（BMP）复合纤维蛋白载体修复创伤性全厚关节软骨缺损,方法：60只新西兰家兔,体重2．5－3kg,雌雄不限,随机分为5组,每侧股骨髌髁关节面低速电钻钻一直径为4mm全厚关节软骨缺损,一侧缺损填充BMP／FS,对照侧缺损填充单纯FS,单纯BMP和空白组,膝关节不做固定,允许笼中自由活动,术后2,4,8,12周空气栓塞分批处死动物,大体观,组织学切片HE染色,S－100蛋白免疫组化染色和透射电镜观察实验结果,结果：术后4周,BMP／HF填充的部分关节软骨缺损由类透明软骨修复,术后8周,实验组缺损大部分由类透明软骨修复,而对照组则由纤维软骨或纤维组织修复,术后12周,实验组修复组织主要是透明软骨或类透明软骨,修复面较平整光滑,与周围组织愈合良好,但部分修复软骨面变薄,纤维化。结论：BMP／FS复合物促进了关节软骨的早期修复,并且最终的修复组织更接受正常的关节软骨,但术后12周修复的关节软骨出现退行性改变。     

脂质代谢及破骨细胞活性在激素性股骨头坏死塌陷发生过程中的作用研究

目的:通过诱导激素性股骨头坏死的动物模型并观测模型的相关指标,研究脂质代谢及破骨细胞活性在激素性股骨头坏死塌陷发生过程中的作用.方法:将雄性SD大鼠40只(150 g左右),随机分为空白对照组和激素实验组,腹腔注射大肠杆菌内毒素后,实验纽每周1次臀肌注射醋酸强的松龙35.5 mg/kg,对照组每周1次臀肌注射生理盐水2 ml,于第12周用药结束后处死动物,进行血清抗酒石酸酸性磷酸酶5b(Trap-5b)、总胆固醇(TC)、甘油三酯(TG)、软骨下骨生物力学、股骨骨密度测定,制作HE染色病理切片,进行茜红素和抗酒石酸酸性磷酸酶(TRACP)染色,并进行统计分析.结果:实验组的血清总胆固醇、甘油三酯、抗酒石酸酸性磷酸酶5b含量显著升高(P<0.01),局部骨髓内出现大量破骨细胞,骨质丢失严重(P<0.01),软骨下骨生物力学性能显著下降(P<0.01).结论:脂质代谢紊乱是激素性股骨头坏死重要的发病机制;破骨细胞活性增强、数量增加,引起骨质严重丢失导致的软骨下骨生物力学性能下降是股骨头塌陷的直接原因.     

激素联合脂多糖诱导兔早期股骨头坏死实验研究

目的观察激素联合脂多糖诱导早期兔股骨头坏死的实验效果。方法键康雄性新西兰大白兔30只,随机分为实验组（25只）和对照组（5只）。实验组连续2d每日静脉注射脂多糖10μg／kg．再连续3d每日肌肉注射甲泼尼龙20mg/kg;对照组注射同等剂量的生理盐水。5周后行CT扫描所有兔髋关节．并随机处死实验组和对照组兔各4只．行显微CT扫描股骨近端和组织切片观察。结果CT扫描显示实验组兔股骨头有不同程度的骨密度不均匀。显做CT显示骨质疏松和软骨下骨囊性化．周围可见硬化骨。组织学切片见骨细胞陷窝空疏、脂肪细胞增多及部分血管俭塞。结论激素联合脂多糖能安全便捷地诱导兔早期股骨头坏死模型。     

降钙素对兔骨关节炎关节软骨的保护作用

[目的]研究降钙素（ealcitonin，CT）对骨关节炎关节软骨的保护作用。[方法]6个月龄新西兰大白兔20只，随机分为两组均行右膝关节前交叉韧带切断术。1周后实验组开始皮下注射降钙素5 IU／kg，每日1次：对照组注入等剂量生理盐水；术后6周处死动物。取股骨内髁制成切片行HE、番红“O”和Ⅱ型胶原免疫组化染色。HE切片按照Mankin评分表评分。番红“O”染色和Ⅱ型胶原免疫组化染色切片用图像分析仪，测量平均灰度值。[结果]（1）对照组术侧膝关节组织学Mankin评分结果、番红“O”染色和Ⅱ型胶原免疫组化染色平均灰度值测量结果高于健侧，（P〈0．01）。（2）对照组手术膝关节组织学评分、番红“O”染色和Ⅱ型胶原免疫组化染色平均灰度值测量结果高于实验组手术膝关节，（P〈0．05）。[结论]降钙素5IU／kg每日1次皮下注射够明显减轻兔膝关节不稳定诱发的骨关节炎关节软骨的退变。降钙素可能通过提高软骨基质糖胺多糖（glycosaminoglycaris,GAG）和Ⅱ型胶原含量保护关节软骨。     

一氧化氮对股骨头微循环的作用

目的 研究一氧化氮对股骨头微循环的作用及与股骨头血流量的量效关系,证实一氧化氮的前体一左旋精氨酸能否成为改善股骨头微循环的有效药物。方法 随机采用新西兰兰兔２１只,分为三组。右股动脉插管,分别将左旋精氨酸（０、３０、４０、６０、８０、１００ｍｇ／ｋｇ）、Ｎ＾Ｇ－硝工－左旋精氨酸甲酯（０、５、１０、１５、２０、２５ｍｇ／ｋｇ）、Ｎ＾Ｇ－硝基－左旋精酸甲酯（１０ｍｇ／ｋｇ）＋左旋精氨酸（０、３０、６０     

Effect of methylprednisolone on reperfusion after femoral head ischemia

An episode of ischemia and reperfusion of the femoral head is thought to be the common pathway in the pathogenesis of femoral head necrosis. The influence of short-term high-dose steroid treatment on femoral head reperfusion after ischemia was investigated in a porcine model. Twenty-two pigs were randomized to receive methylprednisolone 20 mg/day/kg bodyweight intramuscularly for 3 days followed by methylprednisolone 10 mg/day/kg bodyweight for 11 days (n = 11), whereas the control group (n = 11) received no treatment. Femoral head ischemia was achieved by 6 hours of unilateral intraarticular hip pressure increase to 250 mm Hg. Femoral head blood flow was estimated using radiolabeled microspheres (15 microm in diameter) before ischemia, during hip tamponade, and 4 hours after tamponade release. Femoral head blood flow was lower in the corticosteroid treated pigs. Subtotal femoral head ischemia was documented in both groups during joint tamponade. Apart from two femoral head epiphyses in either group, reperfusion after tamponade release on the average occurred to a blood flow level similar to that before ischemia. Short-term high-dose methylprednisolone treatment depressed bone perfusion in general, but had no effect on reperfusion after femoral head ischemia in the porcine model.     

The effect of surgical approach on blood flow to the femoral head during resurfacing

We determined the effect of the surgical approach on perfusion of the femoral head during hip resurfacing arthroplasty by measuring the concentration of cefuroxime in bone samples from the femoral head. A total of 20 operations were performed through either a transgluteal or an extended posterolateral approach. The concentration of cefuroxime in bone was significantly greater when using the transgluteal approach (mean 15.7 mg/kg; 95% confidence interval 12.3 to 19.1) compared with that using the posterolateral approach (mean 5.6 mg/kg; 95% confidence interval 3.5 to 7.8; p < 0.001). In one patient, who had the operation through a posterolateral approach, cefuroxime was undetectable. Using cefuroxime as an indirect measure of blood flow, the posterolateral approach was found to be associated with a significant reduction in the blood supply to the femoral head during resurfacing arthroplasty compared with the transgluteal approach.     

自体骨髓移植治疗股骨头无菌性坏死

目的 探讨自体骨髓移植治疗股骨头坏死的疗效及其作用机制.方法 选用成年新西兰雄兔60只,造模后随机分为A、B、C三组.左侧股骨头作为对照组,不予处理,右侧为实验组.A组用米托蒽蓖按0.1 mg/kg量在数字减影型x射线机(DSA)导视下注入右侧股骨头内;B组在DSA下直接注入自体骨髓1 ml;C组先予以化疗(方法同A组),72h后注入自体骨髓1 ml.4个月后处死所有动物,取股骨头进行组织病理学及电镜观察.结果 A、B组内左右股骨头对比破骨细胞坏死数差异无统计学意义(P>0.05),而c组左右股骨头坏死数分别为40.60±4.11、21.23± 2.16,差异有统计学意义(P<0.05).C实验组镜下见大部分骨细胞结构清晰、完整,偶见坏死.结论 局部化疗+自体骨髓移植在细胞水平上对股骨头无菌性坏死具有一定的治疗作用.     

Femoral head blood flow reduction and hypercoagulability under 24 h megadose steroid treatment in pigs.

The pathogenesis of corticosteroid-induced femoral head necrosis is assumed to be ischemia. The purpose of this study was to investigate the perfusion pattern of the femoral head and plasma coagulability during 24 h corticosteroid megadose treatment, as recommended by the National Acute Spinal Cord Injury Studies (NASCIS), in the awake big animal model. Blindedly, 9 animals underwent megadose methylprednisolone infusion (30 mg/kg intravenously as an initial bolus, followed by 5.4 mg/kg/h for further 23 h) while 9 animals served as placebo treated controls. Regional blood flow of the systematically subdivided femoral head, proximal femur, acetabulum, and soft tissue hip regions was investigated by the microsphere technique at steady state (phase 1), after the initial bolus infusion (phase 2), and after the completed treatment (phase 3). Plasma coagulability was examined in phases 1 and 3. Blood flow of the femoral head epiphysis and metaphyseal cancellous bone was unchanged after one hour of steroid infusion, but decreased after the completed treatment at 24 h in the experimental group. Femoral head blood flow reduction was global without a tendency to more pronounced blood flow decrease in any subregion. Plasma fibrinogen was significantly higher after 24 h of steroid infusion than in the placebo control group. 24 h high dose methylprednisolone treatment causes femoral head blood flow reduction and hypercoagulability of plasma in the normal awake immature pig. These findings may be pathogenetic factors in the early stage of steroid-induced osteonecrosis.     

Selective reduction of bone blood flow by short-term treatment with high-dose methylprednisolone. An experimental study in pigs

Treatment with corticosteroids is a risk factor for non-traumatic avascular necrosis of the femoral head, but the pathological mechanism is poorly understood. Short-term treatment with high doses of methylprednisolone is used in severe neurotrauma and after kidney and heart transplantation. We investigated the effect of such treatment on the pattern of perfusion of the femoral head and of bone in general in the pig. We allocated 15 immature pigs to treatment with high-dose methylprednisolone (20 mg/kg per day intramuscularly for three days, followed by 10 mg/kg intramuscularly for a further 11 days) and 15 to a control group. Perfusion of the systematically subdivided femoral head, proximal femur, acetabulum, humerus, and soft tissues was determined by the microsphere technique. Blood flow in bone was severely reduced in the steroid-treated group. The reduction of flow affected all the segments and the entire epiphysis of the femoral head. No changes in flow were found in non-osseous tissue. Short-term treatment with high-dose methylprednisolone causes reduction of osseous blood flow which may be the pathogenetic factor in the early stage of steroid-induced osteonecrosis.     

Zoledronic acid improves femoral head sphericity in a rat model of perthes disease.

We hypothesized that the bisphosphonate zoledronic acid (ZA) could improve femoral head sphericity in Perthes disease by changing the balance between bone resorption and new bone formation. This study tests the effect of ZA in an established model of Perthes disease, the spontaneously hypertensive rat (SHR). One hundred and twenty 4-week old SHR rats were divided into three groups of 40: saline monthly, 0.015 mg/kg ZA weekly, or 0.05 mg/kg ZA monthly. At 15 weeks DXA measurements documented that femoral head BMD was increased by 18% in ZA weekly and 21% in ZA monthly compared to controls (p<0.01). Femoral head sphericity in animals with osteonecrosis was improved in ZA-treatment groups (p<0.01) as measured by epiphyseal quotient (EQ). The proportion of "flat" heads (EQ0.40) was significantly reduced from 32% in saline-treated animals to 12% in weekly ZA and 3% in monthly ZA (p<0.01). Histologically there was a similar prevalence of osteonecrosis in all groups. The prevalence of ossification delay was significantly reduced by ZA treatment (p<0.01). Zoledronic acid favorably altered femoral head shape in this spontaneous model of osteonecrosis in growing rats. Translation of these results to Perthes disease could mean that deformity of the femoral head may be modified in children, perhaps reducing the need for surgical intervention in childhood and adult life.     

一氧化氮对激素性股骨头缺血坏死治疗的生化研究

目的　分析一氧化氮 (NO)在前凝血状况下诱导实验性激素性股骨头缺血坏死过程中的作用。方法　 36只成年新西兰兔随机分为三组 ,A组 (正常对照组 ) 12只 ;B组 (疾病模型组 ) 12只 ,间隔三周于兔耳缘静脉注射马血清 ,共 2次 ,每次10ml/kg。于第二次注射后 2周 ,腹腔连续 3d注射甲基强的松龙 ,共 3次 ,每天 1次 ,每次 4 0mg/kg,建立激素性股骨头缺血坏死模型 ;C组 (治疗组 ) 12只 ,模型诱导方式同B组 ,模型复制成功后 ,将硝酸甘油作为一氧化氮外源供体 ,采用介入疗法 ,通过微泵导管直接注入双侧股骨头供血动脉内 ,持续泵注药液治疗 2周。三组动物均于实验完成后行心内穿刺抽取全血标本 ,测定血小板α颗粒膜蛋白 (GMP - 14 0 ) ,氧化型低密度脂蛋白 (OX -LDL) ,NO的血浆含量 ,而后处死 ,切取双侧股骨头行HE染色 ,光镜下观察病理改变 ,统计空骨陷窝率和软骨下区血管数 ,进行组间t检验。结果　A、C组血浆OX -LDL和GMP - 14 0水平明显低于B组 ,而血浆NO水平明显高于B组。C组空骨陷窝率及软骨下区血管数虽未完全达到A组正常水平 ,但较B组有明显改变。结论　NO生成减少导致的OX -LDL合成增多是引发激素性股骨头缺血坏死过程中系统血管内凝血的重要环节 ,以一氧化氮供体作为药物 ,采用介入疗法治疗激素性股骨头缺     

Zoledronic acid treatment results in retention of femoral head structure after traumatic osteonecrosis in young Wistar rats.

Osteonecrosis (ON) of the femoral head in childhood can lead to loss of femoral head architecture and subsequent deformity. When femoral head ON was surgically induced in 24 rats, zoledronic acid treatment and prophylaxis improved sphericity and maintenance of architecture at 6 weeks. This preliminary experiment supports the use of bisphosphonates in childhood ON. INTRODUCTION: We hypothesized that the bisphosphonate zoledronic acid could preserve femoral head structure while allowing bone repair. MATERIALS AND METHODS: Osteonecrosis (ON) was surgically induced in the right femoral head of 24 female Wistar rats. The rats were randomized into three treatment groups and dosed subcutaneously with saline, zoledronic acid (0.1 mg/kg) at 1 and 4 weeks postoperation (ZA post), or zoledronic acid (0.1 mg/kg) given 2 weeks preoperation and at 1 and 4 weeks postoperation (ZA pre-post). After death at 6 weeks postoperation, undecalcified specimens were analyzed by DXA and standardized histomorphometric analysis. RESULTS: Seventy-one percent of saline-operated femoral heads were aspherical (Mose score > 1), whereas only 13% and 0% of operated heads in the ZA-treated groups were aspherical (p < 0.05). DXA-measured bone mineral density in saline-treated femoral heads was reduced by 34% and 43% compared with the ZA-treated groups (p < 0.01). Histomorphometry showed decreases of 12% and 17% in bone volume (BV/TV) in saline groups compared with ZA post and ZA pre-post (p < 0.05), and a decrease in trabecular number (Tb.N) of 18% and 14% (p < 0.05), respectively. Bone formation rate (BFR) was increased by 56% in saline-treated operated heads over ZA post and was 4.8 times increased over the ZA pre-post group (p < 0.05). The differences in BV/TV and Tb.N in treated groups must therefore be caused by a reduction in bone turnover. Observational histology confirmed the retention of necrotic architecture in treated groups. CONCLUSIONS: Zoledronic acid treatment and prophylaxis preserved femoral head architecture after traumatic ON in this rat model at 6 weeks. These data indicate that, by conserving femoral head architecture, bone repair may occur in conjunction with improved femoral head shape.