Review Article

Osteonecrosis of the Femoral Head: Evaluation and Treatment Abstract Charalampos G. Zalavras, MD Jay R. Lieberman, MD

Osteonecrosis of the femoral head may lead to progressive destruction of the hip joint. Although the etiology of osteonecrosis has not been definitely delineated, risk factors include corticosteroid use, alcohol consumption, trauma, and coagulation abnormalities. Size and location of the lesion are prognostic factors for disease progression and are best assessed by MRI. The efficacy of medical management of osteonecrosis with pharmacologic agents and biophysical modalities requires further investigation. Surgical management is based on patient factors and lesion characteristics. Preservation of the femoral head may be attempted in younger patients without head collapse by core decompression with vascularized bone grafts, avascular grafts, bone morphogenetic proteins, stem cells, or combinations of the above or rotational osteotomies. The optimal treatment modality has not been identified. When the femoral head is collapsed, arthroplasty is the preferred option.

O

From the Keck School of Medicine of the University of Southern California, Los Angeles, CA. Dr. Lieberman or an immediate family member serves as a paid consultant to or is an employee of DePuy, has received research or institutional support from Amgen and Arthrex, and serves as a board member, owner, officer, or committee member of the American Academy of Orthopaedic Surgeons and the Hip Society. Neither Dr. Zalavras nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter. J Am Acad Orthop Surg 2014;22: 455-464 http://dx.doi.org/10.5435/ JAAOS-22-07-455 Copyright 2014 by the American Academy of Orthopaedic Surgeons.

July 2014, Vol 22, No 7

steonecrosis of the femoral head commonly affects patients in the third to fifth decades of life. In the United States, it is estimated that 20,000 to 30,000 new patients are diagnosed with osteonecrosis annually, and 5% to 12% of total hip arthroplasties (THAs) are performed based on this diagnosis.1,2 Although several risk factors have been identified, the pathogenesis of osteonecrosis has not been elucidated. The disease typically follows a progressive course leading to femoral head collapse and hip joint destruction. Nonsurgical modalities have been described, but surgical intervention is the most prominent therapeutic regimen. However, the optimal method to preserve the femoral head remains unclear, and in many patients, head sparing is not possible because of the extent of the pathologic process or the advanced stage of the disease on presentation.

Etiology and Pathogenesis Although risk factors for osteonecrosis have been identified (Table 1), the etiology and pathogenesis of osteonecrosis remain unclear. Death of bone cells is the end result of one or more pathogenic mechanisms, acting individually or synergistically, that include ischemia, direct cellular toxicity, and altered differentiation of mesenchymal stem cells (Table 2).

Ischemia Ischemia may result from vascular disruption, compression, constriction, or intravascular occlusion. Disruption of the vascular network around the femoral head results in traumatic osteonecrosis, thus causing complications in 15% to 50% of displaced femoral neck fractures and 10% to 25% of hip dislocations.1 Vascular compression may result from intraosseous hypertension secondary to

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Osteonecrosis of the Femoral Head: Evaluation and Treatment

Table 1 Risk Factors for Osteonecrosis Trauma Corticosteroid use Excessive alcohol consumption Coagulation disorders Hemoglobinopathies Dysbaric phenomena Autoimmune diseases Storage diseases Smoking Hyperlipidemia

fatty infiltration of the bone marrow following corticosteroid use or alcohol overuse. Vasoconstriction of femoral head epiphyseal arteries may be enhanced by corticosteroids. Intravascular occlusion may result from thrombosis, fat or gas embolization, or sickle cell aggregation. Thrombosis is the end of result of several coagulation disorders that result in an increased tendency for thrombosis (ie, thrombophilia) or a reduced ability to lyse thrombi (ie, hypofibrinolysis).3,4 Zalavras et al3 reported that coagulation abnormalities, such as low protein C, low protein S, high lipoprotein(a), and high von Willebrand factor levels, were present in a significantly higher proportion of patients with idiopathic osteonecrosis (10 of 17 patients [59%]) and secondary osteonecrosis (32 of 51 patients [63%]) compared with control subjects (3 of 36 patients [8%]). The identification of genetic predisposition to coagulation abnormalities generated interest in the influence of genetic factors on the development of osteonecrosis. Thrombophilic and hypofibrinolytic mutations have been associated with the disease.4,5 The thrombophilic G1691A mutation of factor V Leiden is significantly more common in patients with osteonecrosis (13 of 72 patients [18%]) compared with controls (14 of 300 patients [5%]).5

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Direct Cellular Toxicity and Altered Mesenchymal Stem Cell Differentiation Direct cellular insult may result from irradiation, chemotherapy, or oxidative stress. Lee et al6 observed that osteogenic differentiation of mesenchymal stem cells derived from the proximal femur was significantly reduced in patients with osteonecrosis compared with patients with osteoarthritis.

Multifactorial Process Predisposing risk factors may not be identified in every patient. Moreover, out of all patients exposed to a specific risk factor, only a small percentage develop the disease. For example, in two separate studies by Lieberman and colleagues7,8 that assessed the development of osteonecrosis after exposure to large corticosteroid doses, osteonecrosis was infrequently identified. In the first study, symptomatic hip osteonecrosis developed in only 3 of 203 patients (2%) who underwent liver transplantation. Similarly, in the second study, osteonecrosis of the hip or knee developed in only 6 of 204 patients (3%) following cardiac transplantation. This finding may be explained by the multifactorial process of osteonecrosis and suggests that additional genetic factors are necessary for a patient to develop symptomatic disease.

Diagnosis and Assessment Early diagnosis allows for treatment of the disease at an earlier stage, thereby potentially improving the outcome. A high index of suspicion is required, especially if the patient has predisposing risk factors.

Clinical Presentation Osteonecrosis may be asymptomatic in its early stages. When the disease becomes symptomatic, deep pain in

Table 2 Pathogenic Mechanisms for Osteonecrosis Ischemia Vascular disruption Femoral head fracture Hip dislocation Surgery Vascular compression or constriction Increased intraosseous pressure due to marrow fatty infiltration Corticosteroids, alcohol Vasoconstriction of arteries perfusing femoral head Corticosteroids, eNOS polymorphisms Intravascular occlusion Thrombosis Thrombophilia Low protein C and S Activated protein C resistance, factor V mutation High homocysteine eNOS polymorphisms Hypofibrinolysis High PAI activity, PAI-1 polymorphisms High lipoprotein(a) Embolization Fat, air Sickle cell occlusion Direct cellular toxicity Pharmacologic agents Irradiation Oxidative stress Altered differentiation of mesenchymal stem cells Increased adipogenesis and decreased osteogenesis Corticosteroids, alcohol eNOS = endothelial nitric oxide synthase, PAI = plasminogen activator inhibitor

the groin is the most common symptom, and pain may be referred to the ipsilateral buttock or knee. A detailed history may reveal the presence of risk factors. Physical examination may be normal or may reveal painful and limited hip motion, especially internal

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Charalampos G. Zalavras, MD and Jay R. Lieberman, MD

Figure 1

Figure 2

Lateral radiograph of the left hip (A) demonstrating presence of the crescent sign (arrows) and AP radiograph (B) demonstrating mild flattening of the femoral head (arrow).

rotation. A considerable loss of internal rotation may be associated with collapse of the femoral head.

Imaging Studies The diagnosis of osteonecrosis is based on plain AP and lateral frog-leg radiographs and MRI. Plain radiographs may be normal in the early stages. The first radiographic findings consist of cystic and sclerotic changes in the femoral head. The crescent sign most likely represents early delamination of the cartilage from the underlying bone and is a poor prognostic sign (Figure 1, A). Flattening of the femoral head initially is subtle and may be visible in only one view (Figure 1, B). Progressive flattening of the femoral head and degenerative changes of the hip joint are subsequently observed. MRI is 99% sensitive and specific and is the benchmark for diagnosing osteonecrosis.1 A single-density line on T1-weighted images delineates the necrotic–viable bone interface, and July 2014, Vol 22, No 7

a double-density line on T2-weighted images represents the hypervascular granulation tissue at the necrotic– viable bone interface (Figure 2).1,9 Transient osteoporosis of the hip should be included in the differential diagnosis when osteonecrosis is suspected. Transient osteoporosis of the hip, commonly affecting pregnant women and men in the fifth and sixth decades of life, presents with severe groin pain and an antalgic gait. MRI demonstrates bone marrow edema extending into the femoral neck and metaphysis. A differentiation between osteonecrosis and transient osteoporosis is essential because the latter is a self-limiting condition.

Classification and Staging Several classification systems have been developed to stage osteonecrosis to provide information on prognosis and assist with treatment decisions (Table 3). The addition of MRI to the staging process and consideration of the extent and location of the necrotic

Coronal T1-weighted magnetic resonance image of the right hip demonstrating a single-density line (arrow) of low signal intensity that delineates the area of necrotic bone.

area are important advancements reflected in the University of Pennsylvania (ie, Steinberg) classification staging system.10

Natural History and Prognostic Factors Symptomatic femoral head osteonecrosis typically follows a progressive course. Prognostic factors for progression include the extent of the osteonecrotic lesion, location of the lesion within the femoral head, and the presence of bone marrow edema in the proximal femur. Imaging studies and particularly MRI are essential for evaluating these factors; these studies may help assess the risk for femoral head collapse and clarify the natural history of the disease. The extent of the osteonecrotic lesion is a prognostic factor for femoral head collapse; it can be assessed

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Osteonecrosis of the Femoral Head: Evaluation and Treatment

Table 3 Classification and Staging Systems for Osteonecrosis Ficat and Arlet Stage I Stage II

Normal Sclerotic or cystic lesions A No crescent sign B Subchondral collapse (crescent sign) without flattening of the femoral head Stage III Flattening of femoral head Stage IV Osteoarthritis with decreased joint space with articular collapse Steinberg University of Pennsylvania Stage 0 Normal or nondiagnostic radiograph, bone scan, and magnetic resonance imaging Stage I Normal radiograph; abnormal bone scan and/or magnetic resonance imaging A Mild (,15% of head affected) B Moderate (15% to 30% of head affected) C Severe (.30% of head affected) Stage II Lucent and sclerotic changes in femoral head A Mild (,15% of head affected) B Moderate (15% to 30% of head affected) C Severe (.30% of head affected) Stage III Subchondral collapse (crescent sign) without flattening of femoral head A Mild (,15% of articular surface) B Moderate (15% to 30% of articular surface) C Severe (.30% of articular surface) Stage IV Flattening of femoral head A Mild (,15% of surface and ,2-mm depression) B Moderate (15% to 30% of surface or 2- to 4-mm depression) C Severe (.30% of surface or .4-mm depression) Stage V Joint narrowing and/or acetabular changes A Mild B Moderate C Severe Stage VI Advanced degenerative changes

as a proportion of the cross-sectional area of the head or as the combined angle of the necrotic area in midsagittal and midcoronal MRI cuts (ie, modified Kerboul method). Ha et al11 prospectively evaluated 37 hips with precollapse osteonecrosis of the femoral head, of which 23 (62%) were symptomatic. The combined necrotic

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angle was determined on MRI using a modified Kerboul method (Figure 3), and hips were randomly assigned to either nonsurgical management or core decompression. Patient follow-up continued until collapse or for a minimum of 5 years when no collapse occurred. None of the 4 hips with a combined necrotic angle of

#190° collapsed; 4 of the 8 hips with a combined necrotic angle of between 190° and 240° collapsed; and all 25 hips with a combined necrotic angle of .240° collapsed. No difference was noted between untreated hips and hips undergoing core decompression.11 Nishii et al12 evaluated 54 osteonecrotic hips without collapse in 35 patients at a minimum follow-up of 5 years. Hips with extensive osteonecrotic lesions (ie, occupying more than two thirds of the weight-bearing area of the femoral head), compared with hips with smaller lesions, had a significantly higher rate of collapse and collapse progression to .2 mm. Interestingly, lack of collapse progression and improvement of symptoms were observed in eight of nine hips that had lesions occupying less than two thirds of the weight-bearing area of the femoral head.12 Bone marrow edema in the proximal femur appears to be a risk factor for collapse of the femoral head. Ito et al9 identified 83 asymptomatic or minimally symptomatic hips with MRI evidence of osteonecrosis and prospectively followed them until the hip became symptomatic or for a minimum of 2 years. Thirty-six of 83 hips (43%) became symptomatic and developed femoral head collapse. The presence of bone marrow edema on initial diagnostic MRI was significantly associated with progression to symptomatic disease with collapse of the head. All 21 hips with bone marrow edema on diagnosis were symptomatic at final follow-up, compared with 15 of 62 hips (24%) without bone marrow edema.9 Few studies with long-term followup have evaluated the fate of asymptomatic osteonecrosis. In a prospective study of 40 asymptomatic hips with small (,10% of femoral head volume) lesions, Hernigou et al13 reported that, after a minimum 10-year follow-up, 35 of 40 hips (88%) became symptomatic, and 29 of 40 hips (73%) collapsed. In contrast, Nam et al14

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Charalampos G. Zalavras, MD and Jay R. Lieberman, MD

Figure 3

Modified Kerboul method. The arc of the necrotic portion of the femoral head on both midcoronal (A) and midsagittal (B) magnetic resonance images is measured, and the sum of the two angles is then calculated. (Reproduced with permission from Ha YC, Jung WH, Kim JR, Seong NH, Kim SY, Koo KH: Prediction of collapse in femoral head osteonecrosis: A modified Kerboul method with use of magnetic resonance images. J Bone Joint Surg Am 2006;88[suppl 3]:35-40.)

reported that after a minimum 5-year follow-up, 43 of 105 hips (41%) remained asymptomatic, whereas 62 of 105 hips (59%) became painful and collapsed. The collapse rate was 5% in small lesions (,30% of the area of the femoral head) versus 46% in medium lesions (30% to 50%), and 83% in large (.50%) lesions.14 In both studies, pain consistently preceded the development of head collapse.13,14 A systematic review of nonsurgical management outcomes showed that at a mean follow-up of 53 months, only 28% of hips did not have radiographic progression, and 33% of hips did not require reoperation.15

Treatment Nonsurgical Management Nonsurgical management with observation or protected weight bearing has a very limited role in the treatment of femoral head osteonecrosis.13-15 The exception is follow-up of a small asymptomatic lesion until it becomes symptomatic. July 2014, Vol 22, No 7

Treatment With Biophysical Modalities and Pharmacologic Agents Biophysical modalities, such as extracorporeal shock waves and pulsed electromagnetic fields, have been used for treatment of osteonecrosis, but there is limited information in the literature. In a randomized trial, Wang et al16 compared extracorporeal shock waves to core decompression with nonvascularized fibula grafting; at a mean 25-month follow-up, both pain and Harris hip scores were significantly improved in the shock wave group. Pharmacologic agents, such as anticoagulants, lipid-lowering agents, diphosphonates, growth factors, antioxidants, vasoactive substances, and hormones, have been investigated for prevention and treatment of osteonecrosis; however, the few clinical studies of pharmacologic treatment of osteonecrosis have not yet established the usefulness of this approach.17-19 Enoxaparin may prevent progression of primary hip osteonecrosis in patients with thrombophilic or hypofibrinolytic disorders, but this

was not the case in osteonecrosis secondary to corticosteroid use.17 Alendronate for treatment of earlystage osteonecrosis was evaluated in two randomized trials, with conflicting results. Lai et al18 reported that, at a minimum follow-up of 24 months, alendronate significantly reduced disease progression and femoral head collapse (collapse of 2 of 29 hips [7%]) compared with the control group (collapse of 19 of 25 hips [76%]). In a study by Chen et al,19 these results were not corroborated; these authors reported no differences between the alendronate and placebo groups with respect to disease progression, the need for THA, and clinical outcome after 24 months. Successful pharmacologic treatment is complicated by our lack of understanding of the pathogenesis of osteonecrosis and the multifactorial nature of the disease.

Surgical Treatment Surgical treatment of osteonecrosis can be broadly divided into femoral head–preserving procedures and hip arthroplasty. Unfortunately, the optimal surgical treatment of osteonecrosis of the femoral head has not been identified. Femoral head–preserving procedures include core decompression; core decompression combined with supplemental nonvascularized bone grafting, vascularized bone grafting, concentrated stem cells, biologic adjuncts, or tantalum rods; and rotational osteotomies. Hip arthroplasty procedures include THA and resurfacing arthroplasty. Core Decompression Core decompression has been widely used for treatment of early-stage osteonecrosis intended to reduce intraosseous pressure in the femoral head, restore vascular flow, and improve pain. The procedure can be performed with a single core tract of varying size or with multiple small core tracts (Figure 4).

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Osteonecrosis of the Femoral Head: Evaluation and Treatment

Figure 4

Core decompression for a small osteonecrotic lesion seen on a coronal T1-weighted magnetic resonance image of the right hip (A). AP fluoroscopic images of the right hip show directing and centering the guidewire at the lesion (B), drilling over the guidewire to create a core tract (C), and removal of the necrotic bone with a burr (D). The femoral head is bone grafted with concentrated stem cells harvested from the iliac crest. The core tract is sealed with demineralized matrix.

Encouraging results have been reported when core decompression is performed at a precollapse stage in small lesions. Israelite et al20 conducted a study of core decompression with bone grafting in 276 hips with a minimum follow-up of 2 years and reported that THA was required in 38% of hips. In precollapse stages, small lesions (,15% of the femoral head) had a significantly better outcome (14% required arthroplasty) compared with intermediate lesions (15% to 30% of the femoral head) and large lesions (.30% of the femoral head), which required arthroplasty in 48% and 42% of hips, respectively.20 A systematic review by Marker et al15 showed that, of 1,268 hips treated since 1992, 70% did not require additional surgery and 63% had a successful radiographic outcome. Core Decompression With Nonvascularized Grafts, Stem Cells, or Biologic Adjuncts Core decompression has been supplemented with the insertion of allografts and nonvascularized autografts to provide mechanical support of the osteonecrotic lesion and prevent collapse. Grafting can be performed with the Phemister technique (ie, through the core tract), the light bulb technique (ie, through a cortical window at the

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junction of cartilage and the femoral neck), or the trap door technique (ie, through a cartilage window). Given the decreased osteogenic differentiation ability of mesenchymal stem cells from the proximal femur of patients with osteonecrosis,6 recent studies have focused on the promotion of bone formation and enhancement of the repair process by introducing bone morphogenetic proteins or bone marrow cells.21-23 Lieberman et al21 treated 17 hips in 15 patients with core decompression, autogenous bone graft, and a fibular allograft perfused with human bone morphogenetic protein and noncollagenous proteins. At a mean follow-up of 53 months, 14 of 15 hips (93%) with Ficat-Arlet stage IIA disease had relief of pain and no radiographic progression. Hernigou and Beaujean22 prospectively evaluated core decompression and injection of concentrated autologous bone marrow cells in 189 hips of 116 patients. At a minimum follow-up of 5 years, arthroplasty was required in only 9 of the 145 Steinberg stage I and II hips (6%), compared with 25 of the 44 hips (57%) that were in stages III and IV. A lower number of progenitor cells were harvested from patients with steroid- or alcohol-induced osteonecrosis, and these patients had a greater risk of

failure than did patients with other diagnoses. A recent small prospective study conducted by Gangji et al23 compared core decompression with implantation of autogenous bone marrow cells with core decompression alone. Bone marrow implantation significantly reduced pain and disease progression at a 5-year follow-up. In the bone marrow group, 3 of 13 hips (23%) progressed, compared with 8 of 11 hips (73%) in the control core decompression group. However, the need for THA was not significantly reduced in the bone marrow group (2 of 13 hips [15%]) versus the control group (3 of 11 hips [27%]). In the future, bone grafting procedures combined with systemic agents that promote bone repair may be the best regimen to optimize results. Vascularized Bone Grafting The goal of vascularized bone grafting using fibula or iliac crest grafts is to support the subchondral bone with a viable strong bone strut and enhance revascularization of the femoral head (Figure 5). A comparison of vascularized to nonvascularized fibula grafting demonstrated that vascularized fibular graft (VFG) significantly improved survival of precollapse hips (86% versus 30%) at 7 years postoperatively.24 Soucacos et al25 reported that, at

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Charalampos G. Zalavras, MD and Jay R. Lieberman, MD

Figure 5

Vascularized fibula graft. The fibular graft is inserted into the core tract and stabilized with a Kirschner wire (K). The peroneal veins and artery are anastomosed to the ascending branches of the lateral femoral circumflex artery (LFCA) and vein.

a mean follow-up of 4.7 years, osteonecrosis progressed radiographically in only 5% of Steinberg stage II hips treated with VFG compared with 44% of stage IV hips. Berend et al26 evaluated VFG for postcollapse osteonecrosis of the femoral head and found that, despite the advanced stage of the disease, 64.5% of hips with a minimum follow-up of 5 years did not require conversion to THA. Unfortunately, no level I studies are available to compare the efficacy of vascularized and nonvascularized grafts. The long-term outcome of VFG has been investigated.27,28 Yoo et al27 reported that, at a mean follow-up of 13.9 years, 13 of 124 hips (11%) failed and underwent THA. No difference in hip survival was observed between Ficat-Arlet stage II and III hips. Hip survival was significantly associated with patient age and size and with location of the lesion.27 Edward et al28 followed 65 FicatArlet stage I and II hips for a mean of 14.4 years. The survival rate was 60% (39 of 65 hips), and the 39 July 2014, Vol 22, No 7

surviving hips had a mean Harris hip score of 89. Free vascularized bone grafting is technically demanding, requires expertise in microsurgery, and is associated with donor site morbidity (ie, motor weakness, contracture of the flexor hallucis longus, sensory abnormalities) in approximately 20% of patients. In general, this procedure should be reserved for patients without collapse of the femoral head.

Tantalum Rod Insertion A tantalum implant has been used as an alternative to bone grafting following core decompression. The tantalum implant aims to provide mechanical structural support to the necrotic area and may enhance bone ingrowth because of its high porosity and osteoconductive microtexture. In a study by Veillete et al,29 early results at a mean follow-up of 24 months showed radiographic progression in 16 of 58 hips (28%) and conversion to arthroplasty in 9 of 58 hips (16%). In a study by Tanzer et al30 of 113 osteonecrotic hips treated with a tantalum rod, the failure rate was 15% (17 hips), and the mean interval between implantation and failure was 13.4 months. Histologic analysis of specimens retrieved at the time of conversion to a THA demonstrated little bone ingrowth and insufficient mechanical support of the subchondral bone.30 Based on the available data, we cannot recommend that this technology be used until longterm follow-up results are published.

Rotational Osteotomies Osteotomies aim to prevent femoral head collapse by transposing the osteonecrotic area from a weight-bearing to a non–weight-bearing area of the hip joint, thereby diverting mechanical stress from the lesion to healthy bone. Two types of osteotomies have been used: transtrochanteric rota-

tional osteotomies (anterior or posterior) and intertrochanteric varus or valgus osteotomies (usually combined with flexion or extension). Transtrochanteric rotational osteotomies have been popularized in Japan. Sugioka and Yamamoto31 reported survival of 43 of 46 hips (93%) at a mean 12-year follow-up after a posterior rotational osteotomy. However, these results have not been replicated in the United States or Europe, and intertrochanteric varus or valgus osteotomies have been preferred instead. Mont et al32 reported good or excellent clinical outcomes without need for arthroplasty in 28 of 37 hips (76%) at a mean follow-up of 11.5 years following intertrochanteric varus osteotomy. Success of an osteotomy procedure depends on the size of the osteonecrotic lesion and requires careful preoperative evaluation to assess whether a sufficiently large area of healthy bone can be transposed to the weightbearing area of the acetabulum. The outcome is improved when the intact area of the transposed femoral head is at least one third of the weight-bearing area of the acetabulum and the combined necrotic angle is ,200°. Osteotomies are technically demanding, and conversion of failed cases to THA may be difficult. Total Hip Arthroplasty Collapse of the femoral head or the presence of a large osteonecrotic lesion in the precollapse stages compromises the outcome of headsparing procedures. THA is the surgical treatment that can most reliably achieve pain relief and provide prompt functional return with a single procedure in patients with femoral head collapse, especially when painful degenerative changes of the hip joint are present. The durability of THA in patients with osteonecrosis compared with that in patients with osteoarthritis has

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Osteonecrosis of the Femoral Head: Evaluation and Treatment

Table 4 Outcome of Noncemented Total Hip Arthroplasty in Patients with Osteonecrosis

Study Kim et al34

Hips With ON (patients)

Patient Age in Years: Mean (range)

Body Mass Index in kg/ m2: Mean (range)

64 (55)

40.2 (25-49)

23.1 (17-32)

Noncemented Arthroplasty Details Modular stem: all

Femoral Stem Acetabular Revision Cup Rate Revision due to Rate due to Aseptic Aseptic Loosening Loosening

Follow-up in Years: Mean (range)

HHS: Mean (range)

15.8 (15-16.8)

92.7 (72-100)

0%

14%

12.6 (10-16)

80.3 (5-100)

2%

0%

5%

5%

Ceramic on poly: 45 Metal on poly: 19 Bedard et al35

60 (50)

43.3 (22-63)

30.6 (18-51)

Chrome-cobaltcoated stem: all

Issa et al36

42 (32)a

37 (18-58)

N/A

Hydroxyapatitecoated stem: all

7.5 (5-11)

87 (78-100)

Issa et al36

102 (87)a

43 (18-71)

N/A

N/A

7 (3-10.5)

88 (70-100)

3%

3%

Kim et al37

69 (N/A)b

24 (19-30)

26 (22-36)

Anatomic metaphysealfitting stem: all

14.6 (10-16)

95(71-100)

0%

0%

17.3 (16-18)

93 (75-100)

0%

0%

Metal on poly: all

Ceramic on ceramic: all Kim et al38

94 (94)c

47 (26-58)

N/A

Anatomic metaphysealfitting stem: all Metal on poly: all

HHS = Harris hip score, ON = osteonecrosis, N/A = nonavailable, poly = polyethylene a Forty-two hips with ON due to sickle cell anemia were compared with 102 hips with ON due to other etiologies. b Osteonecrosis was the diagnosis in 69 of 127 hips in this study. Patient data and outcome data are derived from all 127 hips in 96 patients. c Noncemented THA was performed in 94 of 142 hips in this study. Patient data and outcome data are derived from these 94 hips in 94 patients.

been questioned based on the younger age and increased activity of patients with osteonecrosis. Ortiguera et al33 reported that, at a mean follow-up of 17.8 years, patients with osteonecrosis had a significantly higher dislocation rate than did patients with osteoarthritis. Patients with osteonecrosis may have higher dislocation rates because, in many cases, the patient has better preoperative range of motion compared with a patient who has long-standing osteoarthritis. In addition, the revision rate in patients younger than 50 years with osteonecrosis was significantly higher compared with that in patients in the same age group with osteoarthritis.33 Over the past 15 years, the results of THA have considerably improved. Noncemented fixation can reliably be achieved in most patients with osteonecrosis of the hip; recent studies have

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reported satisfactory midterm outcomes of noncemented arthroplasty in patients with osteonecrosis34-38 (Table 4). Kim et al34 demonstrated that, after a minimum 15-year followup in patients with osteonecrosis younger than 50 years, no noncemented femoral stems and 14% of noncemented acetabular cups required revision because of aseptic loosening. Bedard et al35 reported that, after a minimum 10-year follow-up, the reoperation rate for aseptic loosening was 2% and zero for noncemented femoral and acetabular components, respectively. When preparing an acetabulum in an osteonecrotic hip, the surgeon must remember that the bone quality may be poor secondary to corticosteroid use, lack of weight bearing, or the underlying disease (ie, rheumatoid arthritis). In addition, the subchondral

sclerosis typically associated with osteoarthritis may not be present, so it is prudent to gently ream the acetabulum and use care when impacting the acetabular component. The surgeon should be aware of any alterations of femoral anatomy resulting from previous osteotomy, core decompression, or bone graft. An intraoperative plain radiograph may be useful to help verify appropriate seating and alignment of the femoral broach. Moreover, careful perioperative management and optimization of the patient’s medical conditions may reduce complications and improve outcomes. Hip Resurfacing Arthroplasty Resurfacing arthroplasty preserves bone and does not compromise subsequent conversion to THA; therefore, it has been considered a viable option in the management of

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postcollapse osteonecrosis in young patients with good bone stock. However, a femoral neck fracture may complicate the procedure, and the outcome may be compromised in women, obese patients, and patients with extensive necrotic lesions, poor bone stock, or narrow femoral necks. In a series of 550 resurfacing procedures, 71 of which were performed for osteonecrosis, the prevalence of femoral neck fractures was 2.5% (14 of 550).39 Obesity, female gender, and femoral head/neck cysts were significantly associated with this complication. Interestingly, the prevalence of femoral neck fractures was 17% in the first 69 procedures compared with 0.4% in the 481 subsequent procedures, indicating the importance of patient selection and surgical technique in the early learning curve of this technically difficult procedure.39 Furthermore, concerns with the generation of metallic wear debris associated with the metal-on-metal bearing and the quality of bone in the femoral head have limited the use of hip resurfacing in patients with osteonecrosis of the hip. Selection of Treatment Options Because there is no level I evidence with long-term follow-up, it is difficult to identify the optimal treatment protocol to manage patients with precollapse lesions. Moreover, the existing retrospective studies use different staging systems and report on patients with different underlying diagnoses. In a recent systematic review, Lieberman et al40 concluded that the optimal head-sparing procedure is difficult to determine because of limitations in the current literature. These authors also found that the outcome of headsparing procedures is compromised when collapse has already occurred. Radiographic progression of the disease was observed in 31% of precollapse hips (264 of 864 hips with available data) treated with a headsparing procedure compared with July 2014, Vol 22, No 7

49% of postcollapse hips (419 of 850 hips). Conversion to THA was required in 19% of precollapse hips (409 of 2,163) compared with 30% of postcollapse hips (442 of 1,463).40 In the absence of level I evidence, it is not possible to make definitive treatment recommendations. However, based on the available data, our treatment recommendations can be summarized as follows: patients with symptomatic osteonecrosis with small lesions in precollapse hips should be treated with a head-sparing procedure; large lesions in precollapse hips may be treated with a head-sparing procedure in younger patients, but it is reasonable to consider THA in older patients; and the great majority of patients with collapse of the femoral head should not have a femoral head-saving procedure. THA is the most reliable option for these patients.

Summary Osteonecrosis of the femoral head commonly affects patients in the third to fifth decades of life and follows a progressive course resulting in femoral head collapse and hip joint degeneration. The major risk factors include corticosteroid use, excessive alcohol intake, trauma, and coagulation abnormalities. Diagnosis is based on radiographs and MRI. Imaging findings, such as head collapse and the size and location of the lesion, should be considered in the selection of a treatment method. Pharmacologic agents and biophysical modalities require further study. Surgical treatment consists of either femoral head-sparing procedures or arthroplasty. Preservation of the femoral head is preferable in younger patients without head collapse. In the presence of collapse, arthroplasty reliably achieves prompt pain relief and functional return with a single procedure.

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Osteonecrosis of the femoral head: evaluation and treatment.

Osteonecrosis of the femoral head may lead to progressive destruction of the hip joint. Although the etiology of osteonecrosis has not been definitely...
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