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在绵羊模型中,骨膜可刺激自体软骨细胞移植中的软骨下骨致密化。

Periosteum stimulates subchondral bone densification in autologous chondrocyte transplantation in a sheep model.

作者信息

Russlies Martin, Behrens Peter, Ehlers Eva-Maria, Bröhl Christin, Vindigni Christina, Spector Myron, Kurz Bodo

机构信息

Department of Orthopaedic Surgery, University Hospital Lübeck, 23538 Lübeck, Germany.

出版信息

Cell Tissue Res. 2005 Jan;319(1):133-42. doi: 10.1007/s00441-004-1001-8. Epub 2004 Oct 27.

DOI:10.1007/s00441-004-1001-8
PMID:15517404
Abstract

In this sheep study, we have tested the hypothesis that an osteogenic response is triggered in the subchondral bone by periosteum implanted in full thickness cartilage defects and can be prevented by replacing the periosteum by a cell-free collagen type I/III membrane. Two 7-mm diameter osteochondral defects were made in the trochlea groove and in the medial femoral condyle of one of the knees in each of 15 adult sheep. The animals were divided into three groups (n=5): a control group with untreated cartilage defects, a group treated with autologous chondrocyte transplantation (ACT) and periosteum, and a group treated with ACT in combination with a collagen I/III membrane cover. Histological examination was performed 1 year later. The optical density of the subchondral bone in the histological sections was measured with digital imaging software. There was a dramatic, statistically significant (P<0.0001; power=1) increase in bone density of 45%-70% under defects that were treated with the periosteal cover, compared with the collagen membrane and control groups, which displayed the same bone density. There was no difference in the cartilaginous reparative tissue in the defects in the three groups. Periosteum thus stimulates the remodelling process in subchondral bone. Stiffening of the subchondral bone can lead to degeneration of the overlying reparative cartilaginous tissue because of an increase in the mechanical stress in the tissue. These findings warrant evaluation of subchondral bone changes in patients treated by ACT and the correlation of these changes with clinical outcome.

摘要

在这项绵羊研究中,我们验证了以下假设:植入全层软骨缺损处的骨膜会在软骨下骨引发成骨反应,而用无细胞I/III型胶原膜替代骨膜可预防这种反应。在15只成年绵羊的每只羊的一个膝关节的滑车沟和股骨内侧髁制作两个直径7毫米的骨软骨缺损。将动物分为三组(n = 5):一组为未治疗软骨缺损的对照组,一组接受自体软骨细胞移植(ACT)和骨膜治疗,另一组接受ACT联合I/III型胶原膜覆盖治疗。1年后进行组织学检查。用数字成像软件测量组织学切片中软骨下骨的光密度。与胶原膜组和对照组相比,接受骨膜覆盖治疗的缺损下方骨密度显著增加45% - 70%,差异具有统计学意义(P < 0.0001;检验效能 = 1),而胶原膜组和对照组的骨密度相同。三组缺损处的软骨修复组织无差异。因此,骨膜可刺激软骨下骨的重塑过程。软骨下骨硬化会导致上方修复性软骨组织退变,因为组织中的机械应力增加。这些发现值得评估接受ACT治疗的患者的软骨下骨变化以及这些变化与临床结果的相关性。

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