Greksa Ferenc, Tóth Kálmán, Boros Mihály, Szabó Andrea
Department of Orthopedics, University of Szeged, Szeged, Hungary.
J Orthop Sci. 2012 Jul;17(4):477-83. doi: 10.1007/s00776-012-0222-z. Epub 2012 Apr 5.
Intramedullary reaming and nailing of long bones impairs the endosteal circulation, often causing necrosis of the inner region of the bone cortex. We hypothesized that compensatory hypertrophy of the periosteal microcirculation may develop in response to mechanical destruction of the endosteum, and that this may affect bone survival in these circumstances. In these studies, nailing was performed with materials that affect regeneration of the endosteum differently, and the effects on the tibial periosteal microvasculatory organization were examined.
In male Wistar rats, the right tibia was reamed and implanted with an inert titanium nail or a less osseointegrative polyethylene nail; the contralateral tibial endosteum was destroyed by reaming. Reaming without nailing or sham operation was performed on both extremities in two other groups of rats. Twelve weeks later, the anteromedial and anterolateral surfaces of the tibias were exposed by a microsurgical technique. The structural characteristics of the periosteal microcirculation (vessel density and distribution of vessel diameters) were determined by intravital videomicroscopy and computer-assisted analysis. The stability of the implants was assessed on the basis of grades 0-2 on a qualitative scale.
Tibial reaming alone caused significant increases in overall blood vessel and capillary densities in the periosteum compared with those of the intact tibias. Implantation with a titanium nail resulted in firm embedding of the nail and caused changes in the periosteal vasculature similar to those after reaming alone. In contrast, implantation of a polyethylene nail was followed by the development of marked instability of the endomedullary implant and significant increases in the percentage of capillaries and the vessel density in the periosteum.
Destruction of the endosteal microcirculation per se brings about an increase in periosteal vascular density, which is further augmented if implantation is performed with a material which delays regeneration of the endosteal circulation.
长骨的髓内扩髓和髓内钉固定会损害骨内膜循环，常导致骨皮质内部区域坏死。我们推测，骨内膜的机械性破坏可能会引发骨膜微循环的代偿性肥大，并且在这种情况下这可能会影响骨的存活。在这些研究中，使用对骨内膜再生影响不同的材料进行髓内钉固定，并检查其对胫骨骨膜微血管组织的影响。
在雄性Wistar大鼠中，对右胫骨进行扩髓并植入惰性钛钉或骨整合性较差的聚乙烯钉；对侧胫骨骨内膜通过扩髓破坏。另外两组大鼠的双下肢均进行单纯扩髓而不植入髓内钉或假手术。12周后，通过显微外科技术暴露胫骨的前内侧和前外侧表面。通过活体显微镜检查和计算机辅助分析确定骨膜微循环的结构特征（血管密度和血管直径分布）。根据0-2级的定性标准评估植入物的稳定性。
与完整胫骨相比，单纯胫骨扩髓导致骨膜中总体血管和毛细血管密度显著增加。植入钛钉导致钉子牢固嵌入，并引起与单纯扩髓后相似的骨膜脉管系统变化。相比之下，植入聚乙烯钉后，髓内植入物出现明显不稳定，骨膜中毛细血管百分比和血管密度显著增加。
骨内膜微循环的破坏本身会导致骨膜血管密度增加，如果使用延迟骨内膜循环再生的材料进行植入，这种增加会进一步加剧。
