Drescher W, Pufe T, Smeets R, Eisenhart-Rothe R V, Jäger M, Tingart M
Klinik für Orthopädie und Unfallchirurgie - Schwerpunkt Orthopädie, RWTH Universitätsklinikum Aachen.
Z Orthop Unfall. 2011 Apr;149(2):231-40; quiz 241-2. doi: 10.1055/s-0030-1270984. Epub 2011 Apr 5.
Femoral head necrosis is an ischaemic bone necrosis of traumatic or nontraumatic pathogenesis which can lead to hip joint destruction in young age. It is today the indication for 10 % of all the total hip joint replacements. Known aetiologies of nontraumatic femoral head necrosis are alcoholism, steroids, sickle cell anaemia, caisson, and Gaucher's disease. Further risk factors are chemotherapy, chronic inflammatory bowel disease, systemic lupus erythematosus, and multiple sclerosis, in which also steroids are involved. Gravidity is another risk factor, but still idiopathic pathogenesis is found. In diagnosis, the ARCO-classification of the Association for the Research of Osseous Circulation is essential. While stage 0 can only be found histologically, the reversible early stage 1 shows MR signal changes. In the irreversible early stage 2, first native x-ray changes are seen as lower radiolucency reflects new bone apposition on dead trabeculae. In stage 3, subchondral fracture follows, and in stage 4 secondary arthritis of the hip. Established therapy in stage 1 is core decompression, physiotherapy, and more and more also bisphosphonates. Sufficient data to support extracorporeal shock wave therapy are still lacking. Stem cell therapy seems to be a promising new therapy method in stage 2. In stage 2 and 3 mainly proximal femoral osteotomies and (non)vascularised bone transplantation are performed. In stage 4, depending on size and location of the necrotic zone and pathology of the adjacent bone, resurfacing or short stem hip arthroplasty can be performed. However, conventional THA is still golden standard. The problem and challenge, however, is the often young patient age in femoral head necrosis. Especially chemotherapy-associated osteonecrosis in leukaemia is found in patients in their second decade of life. Therefore, the hip should be preserved as long as possible.
股骨头坏死是一种由创伤性或非创伤性病因引起的缺血性骨坏死,可导致年轻人的髋关节破坏。如今,它占所有全髋关节置换手术的10%。非创伤性股骨头坏死的已知病因包括酗酒、使用类固醇、镰状细胞贫血、潜水病和戈谢病。其他风险因素还有化疗、慢性炎症性肠病、系统性红斑狼疮和多发性硬化症,这些疾病中也涉及类固醇。妊娠是另一个风险因素,但仍存在特发性病因。在诊断中,骨循环研究协会的ARCO分类至关重要。0期只能通过组织学发现,可逆的早期1期显示磁共振信号改变。在不可逆的早期2期,首次在X线平片上出现改变,表现为较低的透亮度,反映了死骨小梁上有新骨形成。3期会出现软骨下骨折,4期则会出现髋关节继发性关节炎。1期的既定治疗方法是髓芯减压、物理治疗,越来越多地还会使用双膦酸盐。目前仍缺乏支持体外冲击波治疗的充分数据。干细胞治疗在2期似乎是一种有前景的新治疗方法。2期和3期主要进行股骨近端截骨术和(带或不带)血管化骨移植。4期则根据坏死区域的大小和位置以及相邻骨骼情况,可进行表面置换或短柄髋关节置换术。然而,传统的全髋关节置换术仍然是金标准。然而,问题和挑战在于股骨头坏死患者往往较为年轻。尤其是白血病患者中与化疗相关的骨坏死多见于二十多岁的患者。因此,应尽可能长时间地保留髋关节。