Tudisco Cosimo, Botti Flavia, Bisicchia Salvatore, Ippolito Ernesto
Department of Orthopaedic Surgery - University of Rome "Tor Vergata" - Viale Oxford 81, 00133, Rome, Italy.
J Orthop Res. 2015 Apr;33(4):535-41. doi: 10.1002/jor.22788. Epub 2015 Jan 21.
To describe the morphology of the proximal femoral epiphysis in a rabbit model from the ischemic insult to the end of the revascularization process. Ischemia of the femoral head was induced in 32 rabbits at the 8th day of life, by sectioning the joint capsule and the ligamentum teres and dislocating the femoral head. Rabbits were sacrificed at 4, 8, 12, 18, 21, 26, 34, and 48 days after surgery and femoral heads were observed histologically. During the first days following the ischemic injury, large areas underwent necrotic changes. Both epiphyseal and physeal cartilage were thicker than normal and less trabecular bone formation was evident. Bone marrow was also diffusely necrotic within the secondary center of ossification. After day 12th, reparative process started with formation of extensive areas of fibrocartilage and several secondary centers of ossifications. At that stage femoral head deformity was already evident. In the following days the secondary centers of ossification cohalesced and epiphyseal and physeal cartilage resumed a normal appearance, but the femur showed a permanent deformity. In newborn rabbits, the ischemic injury to the femoral head blocked the ossification of the epiphyseal and physeal cartilage associated to necrotic bone marrow within the secondary center of ossification of the femoral head as well as to extensive areas of necrosis of epiphyseal and physeal cartilage. Extensive areas of fibrocartilage and small newly formed ossification centers within the femoral epiphysis were the results of the revascularization process, and femoral head deformity became stable afterward.
描述兔模型中从股骨头缺血损伤到血管再通结束阶段股骨近端骨骺的形态学变化。在32只出生第8天的兔子中,通过切断关节囊和圆韧带并使股骨头脱位诱导股骨头缺血。在术后4、8、12、18、21、26、34和48天处死兔子,对股骨头进行组织学观察。在缺血损伤后的最初几天,大片区域发生坏死性改变。骨骺软骨和生长板软骨均比正常厚,小梁骨形成明显减少。在继发骨化中心内骨髓也呈弥漫性坏死。第12天后,修复过程开始,形成广泛的纤维软骨区域和几个继发骨化中心。在那个阶段,股骨头畸形已经明显。在接下来的几天里,继发骨化中心融合,骨骺软骨和生长板软骨恢复正常外观,但股骨显示出永久性畸形。在新生兔中,股骨头缺血损伤阻碍了与股骨头继发骨化中心内坏死骨髓相关的骨骺软骨和生长板软骨的骨化,以及骨骺软骨和生长板软骨的广泛坏死区域。股骨骨骺内广泛的纤维软骨区域和新形成的小骨化中心是血管再通过程的结果,此后股骨头畸形变得稳定。