Retrieved human allografts - A clinicopathological study
Retrieved human allografts - A clinicopathological study
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DOI：
10.2106/00004623-200107000-00001
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发表时间：
2001-07-01
影响因子：
5.3
通讯作者：
Campanacci, DA
中科院分区：
文献类型：
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作者：
Enneking, WE;Campanacci, DA
背景资料：我们研究了73例大面积保存的人类同种异体移植物，从植入后2个月到156个月取出，以深入了解其修复机制。方法：通过放射学和组织学技术对标本进行研究，这些技术允许对愈合、皮质修复、软组织附着、骨折、结果：皮质-皮质连接处的愈合缓慢（约12个月），宿主来源的外部骨痂桥接连接处并填充相邻皮质之间的差距。差距中的骨即使在多年后也没有经历应力导向的重塑，并且，当故意破坏愈合时，在标志同种异体移植物-宿主连接的骨水泥线处发生失效。坏死移植物基质的修复是外部和内部的。外部修复包括在移植物的外表面上附着宿主骨的薄缝，第一年覆盖约40%的表面，第二年覆盖80%。内部修复仅限于皮质的末端和周边，渗透速度非常缓慢，5年后只有15%至20%的移植物得到修复，此后很少发生更深的修复。骨折后不久取出的标本中的移植物骨折仅显示骨折部位附近的坏死骨，而那些在骨折愈合后取出的标本显示骨折部位周围骨的内部修复显著增加。当使用骨水泥固定假体时，没有骨吸收或器械松动的证据。骨关节标本显示关节软骨中无软骨细胞存活。然而，脱细胞软骨的结构在两到三年后保留得很好，有时甚至长达五年。关节软骨的晚期退行性变化与软骨下血管重建和断裂同时发生，关节面被纤维血管修复组织的血管翳覆盖。与关节稳定的患者相比，关节不稳定患者的关节软骨发生退行性变化的时间更早，程度更深。结论：大块人体同种异体移植物的修复是一个缓慢的过程，在最初几年内遵循一个相当可预测的过程，并受到其他生物学活动的影响，如骨折修复，补充自体移植，临床相关性：这些观察结果提供了一个清晰，详细的图片的程度，时间，和缺陷的纳入和修复的大型人类同种异体移植物保存的传统银行技术。因此，它们为目前正在研究的最近开发的骨诱导物质的功效的比较研究提供了基础。
Background: We studied seventy-three massive preserved human allografts, retrieved from two to 156 months after implantation, to provide insight into the mechanisms of their repair.Methods: The specimens were studied with radiographic and histological techniques that permitted time-related quantitative analysis of the reparative mechanisms of union, cortical repair, soft-tissue attachment, fracture, and characteristics of the allograft-cement interface and the articular cartilage.Results: Union at cortical-cortical junctions occurred slowly (approximately twelve months) by host-derived external callus that bridged the junction and filled the gap between abutting cortices. The bone in the gap did not undergo stress-oriented remodeling even after many years, and, when the union was intentionally disrupted, failure occurred at the cement line that marked the allograft-host junction. Repair of the necrotic graft matrix was both external and internal. External repair consisted of the apposition of a thin seam of host bone on the outer surface of the graft, coating about 40% of the surface art one year and 80% at two years. Internal repair was confined to the ends and the periphery of the cortices and penetrated so slowly that only 15% to 20% of the graft was repaired by five years, after which deeper repair seldom occurred. Graft fractures in specimens retrieved soon after fracture showed only necrotic bone adjacent to the fracture site, whereas those retrieved after fracture-healing showed a marked increase in internal repair of the bone about the fracture site. When bone cement had been used to fix a prosthesis, there was no evidence of bone resorption or loosening of the device. The osteoarticular specimens showed no survival of chondrocytes in the articular cartilage. However, the architecture of the acellular cartilage was well preserved after two to three years and occasionally after as many as five years. Late degenerative changes in the articular cartilage coincided with subchondral revascularization and fragmentation, and the articulating surfaces became covered by a pannus of fibrovascular reparative tissue. Degenerative changes in articular cartilage occurred earlier and were more advanced in specimens retrieved from patients with an unstable joint than in those retrieved from patients with a stable joint.Conclusions: Repair of massive human allografts is an indolent process that follows a fairly predictable course during the first few years and is influenced by other biological activities, such as fracture repair, supplementary autografting, and tumor recurrence.Clinical Relevance: These observations provide a clear, detailed picture of the extent, timing, and deficiencies in the incorporation and repair of large human allografts preserved by conventional banking techniques. As such, they provide a basis for comparative studies of the efficacy of the recently developed osteoinductive substances currently under investigation.