构建预制个性化骨瓣修复下颌骨缺损的灵长类动物模型

背景：预制个性化骨瓣具有创伤小、血运好、可带软组织、形状可定制等优点,可用来修复血管床欠佳的骨缺损。 目的：建立预制骨瓣修复灵长类下颌骨缺损的动物模型。 方法：对9只恒河猴进行头颅扫描并制作个性化钛网。将复合或者未复合人重组骨形态发生蛋白2的脱钙冻干骨、珊瑚装入个性化钛网,植入背阔肌中进行个性化、血管化组织工程骨瓣的预制或者原位植入下颌骨节段性缺损。13周时,个性化、血管化组织工程骨瓣预制成功,将其转移修复下颌骨节段型缺损。采用临床和组织学方法观察异位预制个性化骨瓣及原位植入人重组骨形态发生蛋白2修复下颌骨缺损的效果。 结果与结论：预制骨瓣和原位植入的复合人重组骨形态发生蛋白2的珊瑚能修复下颌骨节段性缺损;原位植入复合或未复合人重组骨形态发生蛋白2的脱钙冻干骨和单纯珊瑚不能修复下颌骨缺损。复合人重组骨形态发生蛋白2的脱钙冻干骨、珊瑚预制个性化、血管化组织工程骨瓣成功,转移后均能成功修复下颌骨缺损,而且修复下颌骨缺损的效果优于材料直接植入下颌骨缺损组。实验证实预制个性化骨瓣修复恒河猴下颌骨缺损模型是可行的。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

人骨形成蛋白7修饰骨髓间充质干细胞复合仿生型支架材料的体内成骨研究

目的 应用携带人骨形成蛋白7(hBMP7)基因的兔骨髓间充质干细胞(BMSC)与仿生型生物玻璃-胶原-透明质酸-磷脂酰丝氨酸(BG-COL-HYA-PS)支架材料复合培养,植入兔桡骨缺损模型中观察其在体内成骨的能力.方法 携带hBMP7基因或增强型绿色荧光蛋白(EGFP)基因的2型重组腺相关病毒(rAAV2)载体在体外分别转染兔BMSC,再将转染后和未转染的兔BMSC分别与BG-COL-HYA-PS支架材料复合培养7 d后植入3组兔桡骨缺损模型,每组6只兔.各组在分别术后8周、12周通过大体标本观察、影像学、组织学等方法观察骨缺损的修复情况.以正常兔桡骨为对照组(n=3),术后12周比较各组骨缺损修复组织生物力学差异.结果 rAAV2-hBMP7转染的兔BMSC与BG-COL-HYA-PS复合支架材料有良好的生物相容性,植入兔桡骨缺损模型内表现出明确的成骨能力和骨修复能力,而形成的新骨最大压力载荷值低于正常桡骨组织[(188.46±12.24)N比(203.25±19.29)N,P＜0.05].结论 用hBMP7修饰BMSC复合仿生型BG-COL-HYA-PS支架材料构建的组织工程骨具有较强的骨修复能力,但形成的新生骨组织与正常骨组织比较仍然有早期生物力学方面的不足.     

骨髓间充质干细胞与同种异体骨复合修复犬下颌骨缺损：成骨能力检测

 背景：同种异体骨与自体骨有相似解剖外形和生物学特性,是较佳的生物支架材料。自体骨髓来源的间充质干细胞具有多分化潜能,能向成骨、成软骨细胞分化,加速骨组织及软骨组织的形成。目的：探讨同种异体骨支架复合自体骨髓间充质干细胞促进犬下颌骨半侧缺损的新骨成骨能力。方法：拔出24只比格犬左侧下颌牙,伤口愈合后2个月,人为造成犬下颌骨缺损,对照组用单纯冻干同种异体骨修复,实验组用同种异体冻干骨加自体骨髓间充质干细胞修复。术后4,12,24周对下颌骨体部进行骨密度扫描以及Micro-CT检查。结果与结论：实验组移植后12周开始,下颌骨的骨密度显著高于对照组(P < 0.05),随着时间推移,实验组和对照组骨密度均增高,但实验组增高明显高于对照组。随时间推移,实验组骨结构参数成阶梯式递增或递减,对照组虽也有递增或递减,但不明显。术后24周实验组感兴趣区骨小梁分离度大于对照组(P < 0.05),骨体积分数、骨小梁数量、骨小梁厚度小于对照组(P < 0.05)。结果表明骨髓间充质干细胞能加速同种异体骨的骨改建速度。中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程全文链接：     

NaOH消蚀骨基质材料的研制及其修复骨缺损实验研究

目的:制备骨基质支架并与自体红骨髓联合移植修复兔桡骨节段性骨缺损,探讨该支架作为骨组织工程载体的可行性。方法:采用NaOH消蚀技术,制备出家兔骨细胞外基质支架,行扫描电镜观察及生物相容性实验,并与自体红骨髓联合移植于兔桡骨节段性骨缺损模型,通过X线、生物力学等检查,比较其联合红骨髓及单纯支架移植修复节段性骨缺损的疗效。结果:(1)经NaOH消蚀处理后,骨组织中的细胞成分被彻底清除,细胞外基质成分-胶原纤维仍维持三维立体网状结构;无明显排异反应且可降解吸收。(2)支架+自体红骨髓修复骨缺损,4周即出现成骨现象,8周可修复骨缺损;单纯支架移植,约在12周修复。生物力学测试结果,复合红骨髓组抗压强度大于对照组(P<0.05)。结论:此方法制备的骨基质材料与红骨髓联合,可有效地修复节段性骨缺损,是理想的骨组织工程天然载体。     

脂肪基质细胞构建组织工程骨修复下颌骨缺损的实验研究

背景：以往实验认为,只有经过成骨诱导后的脂肪基质细胞才能作为骨组织工程的种子细胞。然而成骨诱导周期过程复杂,延长了细胞体外培养时间和花费。 目的：探讨未经过成骨诱导的犬脂肪基质细胞作为种子细胞,利用组织工程技术修复犬下颌骨缺损的可行性。 方法：取12个月龄犬背部皮下脂肪,经胶原酶消化法获得单个核细胞,将培养的第3代细胞与双相磷酸钙陶瓷形成支架复合物。在犬下颌骨两侧制备长20 mm、高10 mm的箱状缺损,拔除缺损区牙齿,分别植入细胞支架复合物和单纯双相磷酸钙陶瓷支架,不进行干预的区域作为空白对照。植入后4周及8周经组织学检测骨缺损修复情况。 结果与结论：支架植入后4周,部分支架材料降解,缺损区形成新生骨,双相磷酸钙陶瓷组成骨量明显少于细胞支架复合物组,形成少量新骨及部分新生血管。8周时,两组形成更多的新骨,广泛分布于骨缺损区域,但双相磷酸钙陶瓷组仍明显少于细胞支架复合物组,差异有显著性意义(P < 0.01)。提示脂肪基质细胞复合双相磷酸钙陶瓷可在体内成骨,不经过体外成骨诱导的脂肪基质细胞作为种子细胞,利用组织工程技术可修复下颌骨缺损。     

硼酸盐生物玻璃和自体髂骨移植对新西兰兔桡骨大段骨缺损修复的对比研究

目的比较硼酸盐生物玻璃和自体髂骨移植对新西兰兔桡骨大段骨缺损的修复效果。方法取38只新西兰兔,制作桡骨干15 mm骨缺损动物模型,并将其随机分为空白组(8只)、对照组(15只)和实验组(15只),对照组和实验组分别植入自体髂骨和硼酸盐生物玻璃(borate glass, BG)。术后4、8和12周行X线检查,观察材料的降解和新生骨生成情况。术后6周和9周分别腹腔注射茜素红和钙黄绿素。术后12周取材行组织学和Micro-CT检查。结果影像学和组织学结果显示对照组和实验组新骨生成明显优于空白组,12周后对照组和实验组新骨完全修复缺损;实验组材料降解与新骨生成协调进行;术后12周缺损处组织学切片显示,对照组和实验组缺损处有大量的新生骨组织。结论硼酸盐生物玻璃可完全修复兔桡骨干大段骨缺损,其修复效果与自体髂骨移植接近,在骨组织工程领域有广阔的应用前景。     

快速成型钛板结合自体骨移植修复犬下颌骨缺损

背景：近年来,快速成型技术被迅速的应用于医学重建领域,利用快速成型技术可为组织缺损患者制作个体化的植入物,可达到空间尺寸上的精确修复。 目的：利用快速成型技术制作个体化钛板,结合自体松质骨移植,修复犬下颌骨节段性缺损。 方法：9只杂种犬行螺旋CT扫描获取头颅骨骼数据,建立数字3D模型,在模型上模拟右侧下颌骨体部切除术,并制作个体化板状修复体,经快速成型加工制造,获得个体化的钛板。然后行动物实验,手术制造右侧下颌骨体部4 cm长节段性缺损,同期手术切取自体髂骨块固定于快速成型钛板的舌侧,修复下颌骨缺损。采用核医学、力学、影像学和组织学等方法评估骨移植后的转归。 结果与结论：应用快速成型支架重建了左右对称的下颌骨形态,自体髂骨移植后逐渐皮质化,植骨和钛板之间形成纤维结缔组织间隔层。在下颌骨缺损修复中,应用快速成型钛板能够达到形态和功能兼顾的效果。 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：     

生长因子缓释系统复合纳米支架材料修复犬下颌骨缺损

背景：支架材料联合细胞因子构建组织工程骨不受血管化和细胞培养因素的限制,这种构建模式可能诱导出较大体积的实用型组织工程骨。 目的：观察壳聚糖纳米微球/纳米羟基磷灰石/聚乳酸-羟基乙酸复合生长因子缓释支架修复犬下颌骨临界骨缺损的能力。 方法：取杂种犬12条,制作双侧下颌骨临界骨缺损模型,一侧植入复合生长因子骨形态发生蛋白2、转化生长因子β1及血管内皮生长因子165的壳聚糖纳米微球/纳米羟基磷灰石/聚乳酸-羟基乙酸缓释支架(实验组),另一侧植入壳聚糖纳米微球/纳米羟基磷灰石/聚乳酸-羟基乙酸缓释支架(对照组),术后4,8,12周取下颌骨标本行X 射线、组织学及免疫组织化学检查。 结果与结论：实验组术后不同时间点X射线灰度值及骨钙素积分吸光度值均高于对照组(P < 0.05),表明复合生长因子的支架材料修复骨缺损的成骨能力优于未复合生长因子的支架材料。组织学观察结果显示,实验组术后不同时间点成骨时间及效果均优于对照组,表明复合生长因子骨形态发生蛋白2、转化生长因子β1及血管内皮生长因子165的壳聚糖纳米微球/纳米羟基磷灰石/聚乳酸-羟基乙酸缓释支架可更快更有效地促进骨缺损修复。     

去抗原猪松质骨修复犬颌骨缺损的影像学分析

目前临床应用的异种骨多来源于牛,近年来许多学者对猪骨的临床应用进行了大量的探索。因此,本研究利用去抗原猪松质骨修复狗下颌骨缺损,并进行影像学评价,为后期利用组织工程修复颌骨缺损提供新的思路。本研究通过对4只中国杂种犬施行手术,构建了双侧下颌骨骨缺损动物模型,然后采取同体双侧对照原则,随机选取一侧用犬自体骨修复(设为对照组),对侧缺损处用去抗原猪松质骨修复(设为实验组),以钛板钛钉分别予以固定,于术后第12周、第24周进行锥形束电子计算机断层扫描(CBCT)、电子计算机断层扫描(CT)和单光子发射计算机断层成像术(SPECT)检查,以SPECT与CT进行图像异机融合。研究结果显示,去抗原猪松质骨改建速度虽然较自体骨为慢,但仍可作为支架材料修复颌骨缺损。通过以上研究,本文结果或可为临床修复大面积颌骨缺损所需材料提供一种新的选择。     

浓缩红骨髓/富血小板纤维蛋白复合载自体骨膜碎片修复下颌骨缺损

背景：富血小板纤维蛋白支架结构有利于红骨髓中间充质干细胞及各种生长因子的生长,促进最终成骨。 目的：探讨浓缩红骨髓/富血小板纤维蛋白复合载自体骨膜碎片支架材料修复兔下颌骨缺损的可行性。 方法：制备新西兰大白兔双侧下颌骨人工制备骨缺损模型,采用自身对照方法,左侧为实验侧,植入自体浓缩红骨髓/富血小板纤维蛋白复合载自体骨膜碎片与纳米羟基磷灰石支架材料;右侧为对照侧,植入自体骨膜碎片复合纳米羟基磷灰石支架材料。术后2,4,8,12周制备组织标本,行大体观察、影像学分析、苏木精-伊红染色、扫描电镜检测。 结果与结论：影像学检查及组织学染色显示,实验侧骨缺损处愈合程度、成骨速度及质量明显优于对照侧;扫描电镜显示实验侧复合材料与组织相容性好,无炎症刺激反应;牙CT分析数据及新骨形成情况分别证明实验侧骨密度CT值显著高于对照侧(P < 0.05),实验侧新生骨面积显著高于对照侧(P < 0.05)。表明浓缩红骨髓/富血小板纤维蛋白复合载自体骨膜碎片支架材料具有明显骨诱导作用,可望成为临床应用中修复颌骨缺损的新型材料。     

Repair of canine mandibular bone defects with bone marrow stromal cells and porous beta-tricalcium phosphate

Tissue engineering has become a new approach for repairing bone defects. Previous studies have been limited to the use of slow-degradable scaffolds with bone marrow stromal cells (BMSCs) in mandibular reconstruction. In this study, a 30 mm long mandibular segmental defect was repaired by engineered bone graft using osteogenically induced autologous BMSCs seeded on porous beta-tricalcium phosphate (beta-TCP, n=5). The repair of defects was compared with those treated with beta-TCP alone (n=6) or with autologous mandibular segment (n=4). In the BMSCs/beta-TCP group, new bone formation was observed from 4 weeks post-operation, and bony-union was achieved after 32 weeks, which was detected by radiographic and histological examination. In contrast, minimal bone formation with almost fibrous connection was observed in the group treated with beta-TCP alone. More importantly, the engineered bone with BMSCs/beta-TCP achieved a satisfactory biomechanical property in terms of bending load strength, bending displacement, bending stress and Young's modulus at 32 weeks post-operation, which was very close to those of contralateral edentulous mandible and autograft bone (p>0.05). Based on these results, we conclude that engineered bone from osteogenically induced BMSCs and biodegradable beta-TCP can well repair the critical-sized segmental mandibular defects in canines.     

表面修饰羟基磷灰石修复骨缺损骨形态发生蛋白-2的表达

目的了解精氨酸-甘氨酸-天冬氨酸多肽表面修饰的羟基磷灰石（hydroxyapatite,HA）修复节段性骨缺损局部骨形态发生蛋白-2（bone morphogenefic protein-2，BMP-）的表达。方法以骨髓基质干细胞（marrow stromal cels，MSCs）复合Arg-Gly-Asp（RGD）多肽表面修饰的HA或单纯材料培养制备组织工程骨，选择60只新西兰白兔。制作15mm长的桡骨节段性骨缺损模型，根据植入不同的材料分为A、B、C、D组。A组：骨缺损区植入MSCs复合RGD多肽表面修饰的HA培养制备的组织工程骨；B组：骨缺损区植入MSCs复合HA培养制备的组织工程骨；C组：骨缺损区植入RGD多肽表面修饰的HA；D组：骨缺损区植入HA。术后4周取材，行修复区局部BMP-2免疫组化分析。结果术后4周各组骨缺损区均有新骨生成，修复区局部BMP-2表达水平依次为：A〉B〉C〉D（P〈0．05）。结论RGD多肽表面修饰对以HA为支架材料组织工程骨的修复作用有明显优化作用。     

Repair of experimental alveolar bone defects by tissue-engineered bone

Alveolar bone resorption caused by periodontal diseases remains a difficult clinical problem to treat. Our purpose here was to develop protocols for repairing experimental horizontal alveolar bone defects. The procedure entailed isolating bone marrow stromal cells (BMSC). They were expanded and induced in vitro into osteogenic cells in a defined medium. Induced BMSCs were mixed with calcium alginate to form a gel form of cell-scaffold construct for developing engineered bone. A horizontal alveolar bone defect was created in 15 mongrel dogs, which was 5 mm high on each of two buccal sides at the location of mandibular premolar 3, 4, and molar 1. Without bias, the animals were separated into the following groups: (1) cell-scaffold construct as the experimental group; (2) calcium alginate alone as the control group A; (3) untreated as the control group B. Block sections of the defects were collected at 4, 12, and 24 weeks postsurgery, respectively, and processed for gross and histological observation as well as x-ray examination. The results showed that in vitro induced BMSCs exhibited an osteogenic phenotype. Histologically, bone nodule structure was observed in the tissue of the experimental group at 4 weeks postsurgery and the engineered bone became more mature after 12 weeks, which was similar to normal bone. At 12 weeks postsurgery, the height of repaired alveolar bone reached 2.43 +/- 0.93 mm, 0.98 +/- 0.87 mm, 0.78 +/- 0.75 mm for the experimental group, control groups A and B, respectively, with a significant difference between the experimental and control groups (p < 0.01). The average level of buccal alveolar ridge in experimental group, control groups A and B reached 48.59%, 19.74%, and 15.76% of the height of normal alveolus, respectively, with a significant difference between the experimental group and two control groups (p < 0.01). We thus conclude that BMSCs can be induced to become osteogenic and can be used as seed cells to engineer bone tissue and repair experimental alveolar bone defects.     

Autogenous bone marrow stromal cell sheets-loaded mPCL/TCP scaffolds induced osteogenesis in a porcine model of spinal interbody fusion

This study was designed to investigate whether a tissue-engineered construct composed of autogenous cell sheets and a polycaprolactone-based bioresorbable scaffold would enhance bone regeneration and spinal interbody fusion in a large animal model. Porcine-derived autogenous bone marrow stromal cells (BMSCs) cultured into multilayered cell sheets were induced into osteogenic differentiation with dexamethasone, l-ascorbic acid, and β-glycerol phosphate. These cell sheets were assembled with bioresorbable scaffolds made from medical-grade poly(epsilon-caprolactone) incorporating 20% β-tricalcium phosphate (mPCL/TCP) as tissue-engineered BMSC constructs. L2/3, L4/5 discectomies and decortication of the vertebral end plates were performed on 16 SPF Yorkshire pigs through an anterolateral approach. The tissue-engineered BMSC constructs were transplanted into the prepared intervertebral disc spaces of half of the pigs (n?=?8), whereas cell-free mPCL/TCP served as controls in the remaining pigs. New bone formation and spinal fusion were evaluated at 3 and 6 months using microcomputed tomography, histology, fluorochrome bone labeling, and biomechanical testing. New bone formation was evident as early as 3 months in the BMSC group. At 6 months, bony fusion was observed in >60% (5/8) of segments in the BMSC group. None of the control animals with cell-free scaffold showed fusion at both time points. Biomechanical evaluation further revealed a significantly increased segmental stability in the BMSC group compared with the cell-free group at 6 months postimplantation (p?相似文献   

组织工程化肌腱修复鸡趾屈肌腱缺损的生物力学特性研究

组织工程化肌腱植入体内修复的肌腱其抗拉强度达不到正常肌腱的数值。为探讨这一问题的原因，我们选择罗曼雏鸡足趾屈肌腱细胞与可降解聚羟基乙酸筛网体外复合培养构建组织工程化肌腱。用此工程化肌腱修复20只罗曼鸡第二趾深屈肌腱0．5～0．8cm缺损。术后第2、4、6、8周取材，测定样品中材料的重量、羟脯氨酸含量及抗拉强度等力学特性指标。结果显示，植入2、4、6、8周，支架材料重量下降很快，至第8周基本降解；修复的肌腱中代表胶原合成总量的羟脯氨酸含量随时间增加，但变化不明显；修复的肌腱断裂能量和抗拉强度均随时间呈一先降低后逐渐增大的变化，抗拉强度在第8周才达到正常肌腱的23％。结果提示，植入的组织工程化肌腱在其材料迅速降解的同时，胶原生成量并不多，二者出现明显的不匹配，导致修复的肌腱抗拉强度低。     

The performance of a bone-derived scaffold material in the repair of critical bone defects in a rhesus monkey model

The efficacy and safety of a material derived from human bones in the repair of critical segmental bone defects are evaluated in a rhesus monkey model. Frozen human bones were chemically and physically processed into a partially demineralized and deproteinized material in blocks. The complete tissue-engineered (TE) bone was constructed of the material preseeded with allogeneic bone marrow mesenchymal stem cells (MSCs). The material alone and the TE bone were, respectively, implanted to bridge 2.5cm-long critical defects in right and left radii of 15 monkeys. At weeks 1, 2, 3, 6 and 12 post-implantation, the grafts were collected from three animals and assessed for the local expression of osteogenic markers, histological and roentgenographic features, and immune reactions. It was shown that defects were well repaired with both treatments whereas the bone defects in 2 additional untreated animals remained the same size after 12 weeks. In radii implanted with the TE bones, the repair processes were approximately 3 weeks faster and new bones were formed in a multipoint way. There was neither observable toxic effect nor overt immune rejection in any animals. Taken together, these observations suggest that the TE bone blocks composited of the allogeneic or xenogeneic bone-derived scaffold and allogeneic MSCs may provide an ideal method for repairing large segmental bone defects.     

纳米羟基磷灰石纤维蛋白凝胶复合重组人成骨蛋白1修复骨缺损

背景：纳米级的羟基磷灰石纤维蛋白凝胶材料与人体内组织成分更为相似,具有良好的生物与力学性能,但缺乏骨诱导作用。 目的：观察纳米羟基磷灰石纤维蛋白凝胶/重组人成骨蛋白1复合人工骨的骨缺损修复能力。 方法：制备新西兰大白兔单侧桡骨缺损模型后,以数字表法随机分为3组,分别植入不同材料行骨缺损修复：纳米羟基磷灰石纤维蛋白凝胶/重组人成骨蛋白1人工骨组、纳米羟基磷灰石/纤维蛋白凝胶组、空白对照组(未植入任何材料)。术后4,8,12周行大体标本观察、X射线、扫描电镜、放射性核素骨扫描及生物力学测试,比较各组材料修复骨缺损的能力。 结果与结论：术后4,8,12周,纳米羟基磷灰石纤维蛋白凝胶/重组人成骨蛋白1人工骨组X射线评分、成骨效果、放射性核素聚集强度、生物力学强度均高于纳米羟基磷灰石/纤维蛋白凝胶组(P < 0.05)。空白对照组骨缺损区无骨性连接,骨端硬化,骨缺损未能修复。说明纳米羟基磷灰石纤维蛋白凝胶/重组人成骨蛋白1复合人工骨具有良好的骨缺损修复能力,有望成为一种理想的骨缺损修复材料。     

Segmental bone regeneration using a load-bearing biodegradable carrier of bone morphogenetic protein-2

Segmental defect regeneration has been a clinical challenge. Current tissue-engineering approach using porous biodegradable scaffolds to delivery osteogenic cells and growth factors demonstrated success in facilitating bone regeneration in these cases. However, due to the lack of mechanical property, the porous scaffolds were evaluated in non-load bearing area or were stabilized with stress-shielding devices (bone plate or external fixation). In this paper, we tested a scaffold that does not require a bone plate because it has sufficient biomechanical strength. The tube-shaped scaffolds were manufactured from poly(propylene) fumarate/tricalcium phosphate (PPF/TCP) composites. Dicalcium phosphate dehydrate (DCPD) were used as bone morphogenetic protein-2 (BMP-2) carrier. Twenty-two scaffolds were implanted in 5mm segmental defects in rat femurs stabilized with K-wire for 6 and 15 weeks with and without 10 microg of rhBMP-2. Bridging of the segmental defect was evaluated first radiographically and was confirmed by histology and micro-computer tomography (microCT) imaging. The scaffolds in the BMP group maintained the bone length throughout the duration of the study and allow for bridging. The scaffolds in the control group failed to induce bridging and collapsed at 15 weeks. Peripheral computed tomography (pQCT) showed that BMP-2 does not increase the bone mineral density in the callus. Finally, the scaffold in BMP group was found to restore the mechanical property of the rat femur after 15 weeks. Our results demonstrated that the load-bearing BMP-2 scaffold can maintain bone length and allow successfully regeneration in segmental defects.     

Repairing large porcine full-thickness defects of articular cartilage using autologous chondrocyte-engineered cartilage

Large full-thickness defects of articular cartilage remain a major challenge to orthopedic surgeons because of unsatisfactory results of current therapy. Many methods, such as chondrectomy, drilling, cartilage scraping, arthroplasty, transplantation of chondrocytes, periosteum, perichondrium, as well as cartilage and bone, have been tried to repair articular cartilage defects. However, the results are far from satisfactory. In this study, we applied a tissue-engineering approach to the repair of articular cartilage defects of knee joints in a porcine model. Using isolated autologous chondrocytes, polyglycolic acid (PGA), and Pluronic, we have successfully in vivo-engineered hyaline cartilage and repaired articular cartilage defects. The surface of the repaired defects appeared smooth at 24 weeks postrepair. Histological examination demonstrated a typical hyaline cartilage structure with ideal interface healing between the engineered cartilage and the adjacent normal cartilage and underlying cancellous bone. In addition, glycosaminoglycan (GAG) levels in the engineered cartilage reached 80% of that found in native cartilage at 24 weeks postrepair. Biomechanical analysis at 24 weeks demonstrated that the biomechanical properties of the tissue-engineered cartilage were improved compared with those at an earlier stage. Thus, the results of this study may provide insight into the clinical repair of articular cartilage defects.