首页> 外文期刊>The Journal of Bone and Joint Surgery. American Volume >Spontaneous repair of full-thickness defects of articular cartilage in a goat model. A preliminary study.
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Spontaneous repair of full-thickness defects of articular cartilage in a goat model. A preliminary study.

机译:自发修复山羊模型中关节软骨的全层缺损。初步研究。

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BACKGROUND: Full-thickness defects measuring 3 mm in diameter have been commonly used in studies of rabbits to evaluate new procedures designed to improve the quality of articular cartilage repair. These defects initially heal spontaneously. However, little information is available on the characteristics of repair of larger defects. The objective of the present study was to define the characteristics of repair of 6-mm full-thickness osteochondral defects in the adult Spanish goat. METHODS: Full-thickness osteochondral defects measuring 6 x 6 mm were created in the medial femoral condyle of the knee joint of adult female Spanish goats. The untreated defects were allowed to heal spontaneously. The knee joints were removed, and the defects were examined at ten time-intervals, ranging from time zero (immediately after creation of the defect) to one year postoperatively. The defects were examined grossly, microradiographically, histologically, and with magnetic resonance imaging and computed tomography. RESULTS: The 6-mm osteochondral defects did not heal. Moreover, heretofore undescribed progressive, deleterious changes occurred in the osseous walls of the defect and the articular cartilage surrounding the defect. These changes resulted in a progressive increase in the size of the defect, the formation of a large cavitary lesion, and the collapse of both the surrounding subchondral bone and the articular cartilage into the periphery of the defect. Resorption of the osseous walls of the defect was first noted by one week, and it was associated with extensive osteoclastic activity in the trabecular bone of the walls of the defect. Flattening and deformation of the articular cartilage at the edges of the defect was also observed at this time. By twelve weeks, bone resorption had transformed the surgically created defect into a larger cavitary lesion, and the articular cartilage and subchondral bone surrounding the defect had collapsed into the periphery of the defect. By twenty-six weeks, bone resorption had ceased and the osseous walls of the lesion had become sclerotic. The cavitary lesion did not become filled in with fibrocartilage. Instead, a cystic lesion was found in the center of most of the cavitary lesions. Only a thin layer of fibrocartilage was present on the sclerotic osseous walls of the defect. Specimens examined at one year postoperatively showed similar characteristics. CONCLUSIONS: Full-thickness osteochondral defects, measuring 6 mm in both diameter and depth, that are created in the medial femoral condyle of the knee joint of adult Spanish goats do not heal spontaneously. Instead, they undergo progressive changes resulting in resorption of the osseous walls of the defect, the formation of a large cavitary lesion, and the collapse of the surrounding articular cartilage and subchondral bone. CLINICAL RELEVANCE: As surgeons apply new reparative procedures to larger areas of full-thickness articular cartilage loss, we believe that it is important to consider the potential deleterious effects of a "zone of influence" secondary to the creation of a large defect in the subchondral bone. When biologic and synthetic matrices with or without cells or bioactive factors are placed into surgically created osseous defects, the osseous walls serve as shoulders to protect and stabilize the preliminary repair process. It is important to protect the repair process until biologic incorporation occurs and the chondrogenic switch turns the cells on to synthesize an articular-cartilage-like matrix. It takes a varying period of time to fill a large, surgically created bone defect underlying a chondral surface. The repair of such a defect requires bone synthesis and the reestablishment of a subchondral plate with a tidemark transition to the new overlying articular surface. The prevention of secondary changes in the surrounding bone and articular cartilage and the durability of the new reparative tissue making up the articulating surface
机译:背景:在兔子的研究中,通常使用直径3毫米的全厚度缺损来评估旨在改善关节软骨修复质量的新方法。这些缺陷最初可以自愈。但是,有关大缺陷修复特性的信息很少。本研究的目的是确定西班牙成年山羊6毫米全厚度骨软骨缺损的修复特征。方法:在成年雌性西班牙山羊膝关节的内侧股骨con内创建了6 x 6 mm的全厚度骨软骨缺损。未经处理的缺损可以自愈。从十个时间间隔(缺陷产生后立即)到术后一年,从十个时间间隔中取出膝关节,并检查缺陷。对缺陷进行了全面,微观,组织学检查,并通过磁共振成像和计算机断层扫描进行了检查。结果:6毫米骨软骨缺损未愈合。而且,迄今未描述的进行性的,有害的改变发生在缺损的骨壁和缺损周围的关节软骨中。这些变化导致缺损的大小逐渐增加,形成大的空洞病变,周围的软骨下骨和关节软骨都塌陷到缺损的周围。缺陷的骨壁的吸收最初在一周内被发现,并且与缺陷壁的小梁骨中广泛的破骨细胞活性有关。此时也观察到了缺损边缘的关节软骨变平和变形。到十二周时,骨吸收已将手术产生的缺损转变为较大的空洞病变,缺损周围的关节软骨和软骨下骨塌陷到缺损的周围。到第二十六周,骨吸收停止,病变的骨壁硬化。空洞病变未充满纤维软骨。相反,在大多数空洞病变的中心发现了一个囊性病变。在缺损的硬化性骨壁上仅存在一层纤维软骨。术后一年检查的标本显示出相似的特征。结论:成年西班牙山羊膝关节内侧股骨created内形成的直径和深度均为6毫米的全厚度骨软骨缺损不能自愈。相反,它们会进行性变化,导致缺损的骨壁吸收,形成大的空洞病变,以及周围的关节软骨和软骨下骨塌陷。临床相关性:由于外科医师将新的修复程序应用于全厚度关节软骨丧失的较大区域,因此我们认为,重要的是考虑继发于软骨下大缺陷的“影响区”的潜在有害作用骨。当将具有或没有细胞或生物活性因子的生物和合成基质放入手术产生的骨缺损中时,骨壁可作为肩部保护和稳定初步修复过程。重要的是保护修复过程,直到发生生物掺入并且软骨形成开关打开细胞以合成关节软骨样基质为止。填充在软骨表面下的由手术产生的大骨缺损需要花费不同的时间。要修复此类缺损,需要进行骨合成,并且需要重新进行软骨下板的重建,并在潮间带过渡到新的上覆关节表面。防止周围骨骼和关节软骨的继发性变化以及构成关节表面的新修复组织的耐久性

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