Pericollapse Stage of Osteonecrosis of the Femoral Head: A Last Chance for Joint Preservation

Zhang, Qing-Yu; Li, Zi-Rong; Gao, Fu-Qiang; Sun, Wei

With the development of ONFH, mechanical strength decreases in the necrotic and cystic zone due to accumulated fatigue fractures of necrotic trabeculae after sustained loads and increased trabecular fragility; meanwhile, shear stress concentrates at the junctional zone between the normal bone and sclerotic zone and the necrotic area, which causes a loss of structural stability of the femoral head. [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] 32] In these processes, the subchondral fracture impairs the immobilization function of subchondral bone to articular cartilage and initiates head collapse. [15, 24, 26, 32, 36] Focal resorption of the broken subchondral plate and secondary compaction of necrotic cancellous bone result in the formation of a cavum below the subchondral plate, which appears as a crescent sign or radiolucent line on X-ray radiographs and joint effusion and closely correlates with the occurrence of BME and hip pain. [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] Primary BME of the hip in most cases runs a self-limiting and transient course; however, ONFH accompanied by BME tends to have a larger necrotic volume compared with ONFH without BME, and it was suggested that BME was the most significant risk factor for aggravated pain of osteonecrotic hips. [21, 26] In Theruvath et al.'s [18] report about pediatric and adolescent leukemia patients with glucocorticoid-induced ONFH, during follow-up, 70% of patients with BME eventually progressed to head collapse, even though edema might completely resolve later during follow-up; surprisingly, however, of 24 patients without BME, only one collapse was observed. Multiple theories such as disruption of sensory nerves within the bone marrow, venous hypertension, regional acceleratory phenomena (acceleratory rapidity of the ordinary biological regional processes after fracture, arthrodesis, or osteotomy), and trauma have been proposed, but no one mechanism has been authenticated for the development of BME. [33, 34] Given the former findings, it is also rational to assume that BME in ONFH might be an inflammatory change to mechanical stress of subchondral fractures or to tissue ischemia around the necrotic area. [18, 26, 34] Causes and severity of pain in patients with ONFH are varied and multifactorial in different stages. Most ARCO Stage I/II cases are asymptomatic, but with the aggravation of bone mass loss, bone marrow necrosis, and bone infarction, intermedullary pressure rises and dull pain may occur at the hips, groin, thighs, or knees in a few cases. [15, 37] While at a later stage, due to the degenerative osteoarthritic changes, severe pain persistently exists during either physical activity or resting. In the observation of the natural progression of asymptomatic ONFH, obvious pain and other suddenly aggravated symptoms are normally related to the occurrence of femoral head collapse. [10, [37] [38] [39] Min et al. [38] reported that after the pain developed, all 62 hips had progressed to Steinberg III or later stages, and of them, 44 cases continued to deteriorate sufficiently to accept hip arthroplasty in 1 year. Possible conjectures for the aggravation of clinical symptoms in the pericollapse stage include deteriorative structural instability of the femoral head, enhanced secretion of inflammatory mediators, elevated intramedullary pressure, and increase in hyperstatic pressure caused by joint effusion, etc. [18] [19] [20] 22, 33, 35] There are, of course, excepti