Pathophysiology and risk factors for osteonecrosis

被引：188
作者：
Shah K.N. [1 ]
Racine J. [1 ]
Jones L.C. [2 ]
Aaron R.K. [1 ]
机构：
[1] Department of Orthopaedics, Warren Alpert Medical School of Brown University, 100 Butler Drive, Providence, 02906, RI
[2] Department of Orthopaedic Surgery, Johns Hopkins Medical Institutions, 601 N. Caroline Street, 5245, Baltimore, 21287, MD
来源：
Current Reviews in Musculoskeletal Medicine | 2015年 / 8卷 / 3期
关键词：
Intraosseous extravascular compression; Intravascular occlusion; Microcirculation; Osteonecrosis; Subchondral bone resorption; Vascular interruption;
D O I：
10.1007/s12178-015-9277-8
中图分类号：
学科分类号：
摘要：
Osteonecrosis, also known as avascular necrosis or AVN, is characterized by a stereotypical pattern of cell death and a complex repair process of bone resorption and formation. It is not the necrosis itself but rather the resorptive component of the repair process that results in loss of structural integrity and subchondral fracture. Most likely, a common pathophysiological pathway exists involving compromised subchondral microcirculation. Decreased femoral head blood flow can occur through three mechanisms: vascular interruption by fractures or dislocation, intravascular occlusion from thrombi or embolic fat, or intraosseous extravascular compression from lipocyte hypertrophy or Gaucher cells. In this review, we emphasize etiologic relationships derived mostly from longitudinal cohort studies or meta-analyses whose causal relationships to osteonecrosis can be estimated with confidence. Understanding risk factors and pathophysiology has therapeutic implications since several treatment regimens are available to optimize femoral head circulation, interrupt bone resorption, and preserve the subchondral bone. © 2015, Springer Science+Business Media New York.
引用
收藏
页码：201 / 209
页数：8
相关论文
共 89 条
[21]  
Learmonth I.D., Maloon S., Dall G., Core decompression for early atraumatic osteonecrosis of the femoral head, J Bone Joint Surg, 72B, (1990)
[22]  
Welch R.D., Et al., Bone changes associated with intraosseous hypertension in the caprine tibia, J Bone Joint Surg Am, 75, 1, pp. 53-60, (1993)
[23]  
Arnoldi C.C., The relationship between intraosseous and intra-articular pressure, Bone circulation, pp. 213-221, (1984)
[24]  
Downey D.J., Simkin P.A., Taggart R., The effect of compressive loading on intraosseous pressure in the femoral head in vitro, J Bone Joint Surg, 70A, (1988)
[25]  
Kiaer T., Gronlund J., Sorensen K.H., Subchondral pO2, pCO2, pressure, pH, and lactate in human osteoarthritis of the hip, Clin Orthop Relat Res, 229, pp. 149-155, (1988)
[26]  
Jones J.P., Concepts of etiology and early pathogenesis of osteonecrosis, Instr Course Lect, 43, pp. 499-512, (1994)
[27]  
Jones J.P., Etiology and pathogenesis of osteonecrosis, Semin Arthroplast, 2, pp. 160-168, (1991)
[28]  
Spitzer W.O., Horwitz S.M., Et al., Selected nonexperimental methods: An orientation, Principles and practice of research, pp. 104-113, (1991)
[29]  
Johnson E.O., Soultanis K., Soucacos P.N., Vascular anatomy and microcirculation of skeletal zones vulnerable to osteonecrosis: Vascularization of the femoral head, Orthop Clin N Am, 35, 3, pp. 285-291, (2004)
[30]  
Zlotorowicz M., Et al., The blood supply to the femoral head after posterior fracture/dislocation of the hip, assessed by CT angiography, Bone Joint J, 95-B, 11, pp. 1453-1457, (2013)
123456789