Search tips
Search criteria 


Logo of hssjspringer.comThis journalToc AlertsSubmit OnlineOpen Choice
HSS J. 2009 September; 5(2): 99–113.
Published online 2009 March 18. doi:  10.1007/s11420-009-9107-x
PMCID: PMC2744745

SAS Weekly Rounds: Avascular Necrosis

Thomas W. Hamilton, MBChB, BSc,3 Susan M. Goodman, MD,corresponding author1 and Mark Figgie, MD2


Osteonecrosis of the femoral head is a condition that affects upwards of 10,000 individuals in the USA each year. The peak incidence is in the fourth decade of life, and overall, there is a male preponderance. The condition accounts for up to 12% of total hip arthroplasties performed in developed countries. The etiology can be traumatic or non-traumatic, with 90% of atraumatic cases attributed to corticosteroid therapy or excess alcohol consumption. Osteonecrosis of the femoral head reflects the final common pathway of a range of insults to the blood supply and ultimately results in femoral head collapse, acetabular involvement, and secondary osteoarthritis. Currently, conservative treatment options, which aim to correct pathophysiologic features allowing revascularization and new bone formation, appear to be able to delay but not halt the progression of this condition. As a consequence of femoral head osteonecrosis, many individuals undergo surgical treatments including: core decompression, osteotomy, non-vascularized bone matrix grafting, free vascularized fibular grafts, limited femoral resurfacing, total hip resurfacing, and total hip arthroplasty.

Keywords: osteonecrosis, avascular necrosis, femoral head

Case report

DM is a 56-year-old man with HIV/AIDS and osteonecrosis of the hip admitted for total hip arthroplasty.

The patient was initially evaluated by rheumatology for acute gouty arthritis of the ankle at the time of an admission to New York Presbyterian Hospital for pneumonia complicated by respiratory failure and Pseudomonas sepsis. After his extensive intensive care unit course, as he was mobilized, he developed pain in the left knee, left hip, and left thigh. His symptoms subsided then migrated to the right side. He had been walking independently, but progressed to require a cane, and subsequently a walker. The pain became progressively more severe, prompting him to seek surgical care. He was evaluated in the Surgical Arthritis Service (SAS) clinic.

His past medical history is significant for HIV. He has been on highly active anti-retroviral therapy (HAART) with Viracept 1250 BID and Epzicom 600/300 mg daily. At the time of this SAS evaluation, his CD 4 count was 473 and his viral load was undetectable. His nadir CD4 was six at the time of his admission for pneumonia and sepsis. In the past, he had been treated for hepatitis C with ribavirin, prednisone, and azathioprine. He has insulin-dependent diabetes managed with lispro and glargine insulin. He had a remote history of intravenous drug use and cocaine abuse. He has well-controlled hypertension. Medications at the time of his SAS evaluation included glargine and lispro insulin, Cozaar, Viracept, Epzicom, methadone, and Percocet.

The SAS evaluation revealed that he had difficulty walking due to pain and was using a walker. His pain was greater on the right than the left. Range of motion of the hips revealed limited flexion of the right hip to 40°. Internal rotation was absent, and he had 30° of external rotation. Flexion on the right was painful and restricted with flexion to 60°, absent internal rotation, and external rotation to 60. Distal strength was normal. X-rays were obtained and revealed avascular necrosis with subchondral fracture and collapse of both hips. Total hip arthroplasty was recommended.

He was admitted to the Hospital for Special Surgery for total hip arthroplasty, which he underwent without complication. The surgery was performed with a small postero-lateral approach. A Smith and Nephew non-cemented Reflection acetabular component with an elevated highly cross-linked polyethylene liner and an Anthology non-cemented femoral component with a 36-mm Oxinium femoral head were implanted. The femoral head had significant avascular changes with collapse and secondary arthritic changes. Viral load at the time of surgery was 7,000. He had a ConstaVac drain placed which was removed on postoperative day 1. He received vancomycin for antibiotic prophylaxis due to a penicillin allergy. He received Coumadin for DVT prophylaxis. Postoperatively, he was instructed to ambulate weight bearing as tolerated and was discharged home on postoperative day 5.

He was discharged home for follow-up in SAS clinic with the expectation of admission in 3 to 6 months for left hip arthroplasty.


Osteonecrosis of the femoral head, also known as aseptic or avascular necrosis, was first described in 1738 by Alexander Munro, a professor of anatomy at Edinburgh University. It was not until 1829 that Cruvilhier described how the femoral head pathology seen in this condition was secondary to impaired osseous blood flow [1]. Osteonecrosis affecting the femoral head frequently presents in the third, fourth, or fifth decade, with the mean age being 38 years [2]. With the exception of cases associated with systemic lupus erythematosus (SLE), there is a male preponderance and a male to female ratio of 7 to 3 [3]. The first series of 27 cases of femoral head osteonecrosis was described by Mankin and Brower [4] in 1962, and since then, there has been a steady increase in reported cases, in part due to better diagnostic techniques. Between 10,000 and 20,000 cases are reported annually in the USA with an estimated prevalence of up to 600,000 [2]. Overall, the diagnosis of osteonecrosis accounts for 5% to 12% of total hip arthroplasties (THA) performed each year [59].

Neither the etiology nor natural history of osteonecrosis has been defined. Osteonecrosis can be associated with traumatic or non-traumatic insults to femoral head blood supply. The medial circumflex artery is the primary blood supply to the femoral head. Arising from the profunda femoris artery, its course is around the medial side of the femur, passing between pectineus and iliopsoas and then between the obturator externis and adductor brevis. The deep branch then runs close to the tendon of obturator externis before running under the posterior aspect of the hip capsule, the zona orbicularis before passing antro-medially along the neck until it reaches the posterior capsule. Here, the terminal branches, the lateral epiphysial arteries, enter the femoral head postero-superiorly supplying the epiphysis. In both sub-capital fractures and hip dislocation, the blood supply from deep branches of the medial circumflex artery is at risk of interruption.

Displaced fractures and dislocations of the hip are associated with mechanical interruption to the circulation of the femoral head. Fractures of the femoral neck have been associated with a 15% to 50% prevalence of osteonecrosis depending on fracture type, time until reduction, and accuracy of reduction [8, 1012]. The prevalence of osteonecrosis following hip dislocation ranges from 10% to 25% and is related to the duration of dislocation, with prompt reduction halving the prevalence seen if reduction is delayed for 12 h [13, 14].

Risk factors for osteonecrosis can also be classified into those that have a proven direct association where a cause effect relationship has been firmly established, those with a strong association, and those with a probable association (Table 1). Osteonecrosis can occur following a single insult such as a fracture or dislocation as previously described, but in most cases is the result of prolonged episodes of minor damage to the vascular supply to the femoral head.

Table 1
Risk factors for osteonecrosis [16]

The two most common risk factors of osteonecrosis are corticosteroid therapy and alcohol consumption, which account for as many as 90% of new cases of atraumatic osteonecrosis [2, 15, 17]. In cross-sectional studies, 10% to 30% of cases of osteonecrosis have been associated with corticosteroid therapy, and longitudinal studies indicate that 8% to 10% of individuals taking corticosteroids will develop osteonecrosis [18]. Doses of greater than 20 mg/day, even for a short period, have been associated with a higher risk. A meta-analysis by Felson and Anderson [18] revealed a 4.6-fold increase in the rate of osteonecrosis for every 10-mg/day increase in mean daily dose. The mechanism of steroid induced osteonecrosis still remains unclear. In 1964, Johnson proposed that lipocyte hypertrophy, induced by steroids, leads to increased pressure within the femoral head resulting in sinusoidal vascular collapse and ultimately necrosis [19, 20]. Others argue that the increased lipid content of the femoral head is a consequence of fat micro-emboli that disrupt the delicate blood supply to the femoral head [21, 22]. More recently, it has been shown that steroids may have a direct detrimental effect on endothelial and smooth muscle cells within the vasculature impeding venous drainage from the femoral head [23]. Lipocyte hypertrophy, fat emboli, and venous malfunction are all seen in osteonecrosis; however, it is still unclear how much each contributes to the pathophysiology of this condition.

Alcohol consumption has also been associated with increased rates of osteonecrosis [2]. A study by Matsuo et al. [17] demonstrated that an intake of greater than 400 ml alcohol per week, around three glasses of alcohol, 6 units, per day, increased the relative risk 9.8-fold compared to non-drinkers. Again, the pathophysiology of alcohol-induced osteonecrosis is not completely understood, but like corticosteroids, it is thought to be associated with changes in lipid metabolism within the femoral head [23, 24].

There is a large group of conditions where there is a probable association with osteonecrosis. The cause effect relationship is more difficult to establish in individual patients due to associated steroid use. Examples include connective tissue disorders including rheumatoid arthritis, SLE and ankylosing spondylitis, vascular disorders including giant cell arteritis, idiopathic thrombocytopenic purpura, and vasculitis orthopedic conditions including developmental dysplasia of the hip, congenital hip dislocation, hereditary dystosis, Legg–Calve–Perthes disease, and slipped capital femoral epiphysis have a likely but unproven association. Some 10% to 20% of cases of osteonecrosis are classified as idiopathic [1]. A study by Wheeless et al. [25] of the vascular anatomy of 99 hips with advanced osteonecrosis demonstrated that 94% had an abnormal vascular supply compared to 31% in the control group. Given that a reduction of femoral head blood supply by 1.6-fold reduces PO2 by a third, it is possible that individuals with anomalous femoral head blood supply are more susceptible to future insults that may lead to necrosis [26]. Alternatively, individuals carrying genetic mutations which lead to hypercoaguability may develop osteonecrosis when triggered by environmental stimulate.

Patients infected with HIV, such as our patient, have a higher incidence of osteonecrosis than the general population. Although the incidence of HIV-associated osteonecrosis has increased since the advent of HAART, cases have been reported prior to its use. No correlation has been seen with viral load, CD4 cell count, or age. HIV-infected patients with osteonecrosis are likely to have other well-defined risk factors for osteonecrosis. Hypercoagulability is common in the HIV-infected population, given a prevalence of anticardiolipin and antiphospholipid antibodies reported in up to 50% of patients. Corticosteroids are used for multiple indications in HIV-infected patients and have been implicated in the development of osteonecrosis in the HIV. Alcohol abuse and altered lipid metabolism are also seen in this population and may contribute to the increased incidence of osteonecrosis. The increase in osteonecrosis in the HIV-infected patients may simply reflect the increase in other risk factors in this population, as is demonstrated in this case [178, 179].

Aaron [27] proposed a mechanism that integrates these risk factors demonstrating that osteonecrosis is not a specific diagnostic entity but rather a final common pathway of a series of derangements that produce decreased blood flow leading to cellular death within the femoral head. Vascular interruption secondary to trauma as well as thrombotic occlusion and extravascular compression all result in decreased blood flow which in turn leads to ischemia, osteocyte necrosis, loss of structural integrity, and, ultimately, collapse of the femoral head.

Osteonecrosis can be clinically silent or can present with any number of manifestations. The chief complaint is often pain localized to the groin area but, occasionally, the ipsilateral buttock or knee. It has been described as deep, intermittent throbbing pain with an insidious onset that can be sudden. Physical examination reveals a coxalgic gait and pain with hip range of motion. Pain with internal rotation, clicking of the hip, and a reduced range of motion are often signs that the femoral head has already collapsed [6].

Histologically, in the early stages of the disease, examination of the femoral head shows bone marrow necrosis. Following the initial ischemic insult, the bone marrow cells die at different intervals. Hematopoietic cells die within 6 to 12 h followed by osteocytes at 12 to 48 h and marrow fat cells at day 5 [28]. When the repair process begins, the dead osteocytes are reabsorbed and empty lacunae are seen within the bone. Next, osteoblasts lay down new bone over the necrotic areas leading to the characteristic appearance termed “creeping substitution.” Histologically, this process of reabsorption and repair can be observed as early as 3 days following vascular insult. In small lesions, necrosis and repair continues simultaneously; however, in larger lesions, repair is impeded within the large necrotic avascular core, leading to marked thickening and increased density of its borders. This in turn leads to loss of structural integrity and subchondral collapse.

Important first-line investigations are anteroposterior and lateral hip x-rays; however, due to the relatively slow process of bone remodeling, it is important to note that there may initially be no radiographic changes visible [29, 30] (Fig. 1). Magnetic resonance imaging (MRI) is much more sensitive and can detect changes in femoral head fat content, which is seen as early as 5 days after vascular insult when adipocytes undergo necrosis. This is reflected as loss of the normal high intensity signal (Fig. 2). MRI is considered to be the gold standard diagnostic test with a sensitivity and specificity of 99% [6]. Bone scans have been used in high-risk groups to detect early remodeling but can be misleading, with high levels of false negative between 25% and 45% in cases subsequently confirmed by MRI or histological diagnosis [31, 32]. This is due to the transition period between the initial ischemic insult, seen as cold on bone scan, and the start of remodeling when the lesion is seen as hot lasting up to 14 days [28]. The most important differential diagnosis is that of transient osteoporosis which is seen in the third trimester of pregnancy and in men in the fifth and sixth decade of life. MRI in this condition demonstrates edema extending into the femoral neck which is uncommon in osteonecrosis [3335]. A thorough examination of the contralateral hip is essential, as a 40% to 80% incidence of bilaterality has been reported with transient osteoporosis [2, 36].

Fig. 1
Anteroposterior and lateral radiographs of a patient who presented with bilateral osteonecrosis secondary to HIV infection. The right hip demonstrates a reactive sclerotic rim surrounding a lytic necrotic area with segmental articular collapse in keeping ...
Fig. 2
Coronal T1 (a) and T2-weighted (b) magnetic resonance images of the right hip of another patient presenting with a pain on ambulation. A small osteonecrotic lesion is visible with the loss of the normally high signal intensity reflecting adipocyte necrosis ...

There are over 16 major classification systems used in osteonecrosis. The first, and most widely used system, was described by Ficat and Arlet [37] in the 1960s before the advent of MRI. Other systems have since been described taking into account MRI findings as well as the extent of involvement of the femoral head. These include the classification system of the University of Pennsylvania, described by Steinberg et al. [36], and the classification system of the Association Internationale de recherche sur la circulation Osseuse [38] (Table 2) Combined, these classification systems have been used in 95% of studies published [39].

Table 2
Classification of osteonecrosis

Early on in osteonecrosis, there are no changes visible on imaging studies, and this is referred to as stage 0 in all classification systems. This progresses to stage I where a decreased signal intensity is observed in T1-weighted MRI images. Increased uptake of tracer on bone scintigraphy may also be visible. Stage II represents the reparative stage, and radiographic changes are visible in subchondral bone. There may be evidence of osteosclerosis, cyst formation, or osteopenia. There is no evidence of subchondral fracture and the articular surface remains intact. Stage III is characterized by subchondral lucency, referred to as the crescent sign, which indicates subchondral collapse. After stage III, the different classifications diverge, but typically distinguish the amount of head depression, joint space narrowing, acetabular involvement, and advanced degenerative changes including loss of anatomical sphericity of the femoral head which ultimately leads to destruction of the integrity of the joint [1, 16].

Operative and non-operative approaches have been used in the management of osteonecrosis of the femoral head, and these will now be discussed in turn. Conservative treatments include the maintenance of non-weight-bearing status as well as pharmacological therapies. Weight-bearing modification has been proven ineffective except for the treatment of small asymptomatic lesions located outside the weight-bearing area [1]. Pharmacological treatments have been proposed for the early stages of the disease aiming to correct pathophysiologic features allowing revascularization and new bone formation. Non-operative management needs to be deployed early if it is to alter the physiology of the condition, and treating patients conservatively after the appearance of the crescent sign on x-ray, indicating subchondral collapse, is usually not successful.

As previously mentioned, many patients who have osteonecrosis have altered lipid metabolism leading to a hyperlipidemic state. In one study, 284 patients taking high-dose steroids were treated with lipid-lowering drugs and the incidence of osteonecrosis recorded. After a mean of 7.5 years, only 1% had developed osteonecrosis, which is much lower that the usual incidence of 3% to 20% in this patient group [40].

Bisphosphonates have also been used in the treatment of osteonecrosis. A study by Agarwalla et al. [41, 42] demonstrated a significant reduction in pain and disability scores in patients receiving bisphosphonates and a decrease in bone marrow edema on MRI. There was, however, no evidence of radigraphical regression. Lai et al. [43] conducted a small controlled trial comparing 29 osteonectotic hips with large lesions treated with alendronate to 25 hips that had not been treated. When followed up at 24 to 28 months, the treatment group had fewer incidences of collapse, 7% versus 76%, and the number requiring total hip arthroplasty was also reduced, 3% versus 64%.

Other drugs including anti-hypertensives have been used. The vasodilator Naftidrofuryl has been shown to reduce intraosseous pressure in a small case study; however, its clinical efficacy has yet to be demonstrated [44]. While there is a scientific basis for using some of these therapies, future prospective randomized trials are needed to determine their true efficacy. Some new therapies such as hyperbaric oxygen therapy [45, 46], electrical stimulation [4749], pulsed electromagnetic field therapy [5053], and extracorporeal shock wave therapy [54, 55] have shown promising results in animal studies, and early work suggests that they may have a role in the early stages of osteonecrosis. Further long-term outcome studies are needed to evaluate these treatments.

The surgical management of osteonecrosis can be divided into head-preserving procedures and arthroplasty. Patients with pre-collapse are generally treated with head-preserving procedures, whereas collapse of the femoral head and arthritis may require arthroplasty.

Core decompression has been used to reduce intraosseous pressure in the femoral head bone compartment (Table 3). The procedure was originally introduced as a diagnostic tool by Ficat and Arlet [37]. Typically, it is used to treat small to medium lesions and involves introducing an 8- to 12-mm cannulae into the lesion from just proximal to the level of the lesser trochanter to avoid the development of a stress fracture [56]. This technique can include augmentation with supplementary bone grafting [57, 58]. Numerous studies have been conducted to evaluate the effectiveness of this procedure. Mont et al. [59] conducted a meta-analysis of 23 studies published prior to 1995. This analysis of 1,026 hips revealed success rates of 84%, 65%, and 47% for stages 1, 2, and 3, respectively, giving an overall success rate of 63% compared to a 35% success rate in hips treated non-operatively, demonstrating that core decompression is more effective than conservative management. When taking into account the 23 studies published since 1995, the overall success rate of core decompression rises to 70%, with mean follow-up ranging from 2 to 10 years [56].

Table 3
Outcome after core decompression [56]

Core decompression has also been studied in conjunction with grafting of decalcified bone matrix. A study by Aaron et al. [58] analyzed 118 hips with Ficat stages 2 and 3 and compared the results of core decompression to core decompression augmented with decalcified bone matrix. They found no significant difference in outcome in Ficat stage 2 hips between augmented and control groups. However, in stage 3 hips at 24 months follow-up, there was a 47% success rate in the control group compared with an 88% success rate in those hips augmented with decalcified bone matrix, suggesting that augmentation with bone matrix may prove beneficial in more advanced disease.

Variations on this technique have also been described, including a percutaneous approach utilizing a 3.2-mm Steinmann pin that, in a study of 163 hips by Song et al. [83] with a minimum 5-year follow-up, had a 79% success rate in patients with stage I disease and 77% success rate in patients with stage II disease. The authors concluded that the results of multiple drilling with a small bore pin were comparable with other core decompression techniques. This technique needs further evaluation; however, it has the added benefit of being less invasive with low morbidity and fewer surgical complications. Overall core decompression is recommended for the treatment of early stage osteonecrosis of the hip and has the best results in pre-collapse lesions Ficat stages 1 and 2 that involve less than 30% of the femoral head [56].

Osteotomies have been used to realign the collapsing segment from the principal weight bearing area (Table 4). Two types are used: transtrochanteric rotational and intertrochanteric valgus varus which is combined with flexion or extension. Varying success rates between 56% and 79% have been reported as well as a range of technical difficulties of converting failed cases to THA. Benke and Barker [84], in a study of 105 THA after failed osteotomy, reported an infection rate of 8.6% and recorded technical difficulties including broken screws and femoral shaft fractures that occurred in 17.1% of cases. Ferguson et al. [85] reporting on 305 THA after failed osteotomy noted operating time to be significantly longer for the conversion compared to a standard hip, possibly explaining the increased infection rate as well as an increased blood loss. Infection rates were 9% in this study and the cumulative probability of failure at 10 years was 20.6%. As a result, femoral osteotomy is not widely accepted as a standard method of treatment.

Table 4
Outcome after rotational osteotomy

Non-vascularized bone grafting has also been described as a method of providing support to the articular cartilage surface, preventing joint collapse while promoting bone healing (Table 5). Grafting techniques can be via a core tract [98], trapdoor [99], or lightbulb technique [100]. Necrotic bone is removed and allogenic or autologous bone introduced. The overall clinical success is varied, and generally, this technique is reserved for individuals in which core decompression has been unsuccessful or individuals with post-collapse lesions of less than 2 mm, Pennsylvania stage IVA [99, 101103]. Several studies including one by Mont et al. [102] have demonstrated excellent outcomes in stage 3 disease, 83% at 5 years.

Table 5
Outcome after non-vascuralized bone graft [56]

Free vascularized fibular grafts have the added advantage of supporting subchondral bone with a viable strong bone strut as well as providing revascularization to the femoral head aiding osteogenesis. The ipsilateral fibula is harvested with its peroneal artery with its two veins and inserted into the core tract and stabilized with a Kirschner wire. The ascending branches of the lateral circumflex artery and vein are then anastomosed to the peroneal vessels of the fibula using microvascular surgical techniques. Urbaniak et al. [107] reviewed the results of 1,523 hips treated with this technique between 1979 and 2000. A success rate of 91% was found at 6 months to 22 years follow-up in individuals with no preoperative evidence of collapse. In cases where there was evidence of collapse or joint space narrowing, success rates were found to be 85% and 73%, respectively [6]. In a small prospective study by Kane et al. [108] analyzing 39 hips followed for 2 years, the results of vascularized fibular grafts were better than that of core decompression 80% to 42%; however, as yet, no randomized control trials exist. Unfortunately, Vail and Urbaniak [109] have reported this technique to have a complication rate of 19%, which includes motor weakness, subjective discomfort in the ankle, as well as sensory abnormalities in the lower limb. Aluisio and Urbaniak [110] also noted the rate of fracture of the proximal femur to be 2.5% in one large series.

Once the femoral head has collapsed, alternative surgical options must be strongly considered. Limited femoral resurfacing can be used in late to mid collapse to salvage the femoral head provided there is no acetabular involvement. In younger patients, it has several potential advantages, including preservation of femoral bone stock, low dislocation rates, simplicity of revision, and deferral of total hip arthroplasty. Overall, the success of limited femoral resurfacing is approximately 84% at short-term follow-up (Table 6). Mont et al. [111] analyzed the functional outcome of limited femoral resurfacing. They found that at 7 years, there was a significant difference in the number of individuals playing sports when compared to age- and sex-matched subjects who underwent total hip arthroplasty. In this series, both groups had similar success rates of around 90%; however, continuing symptoms of groin pain were higher in the resurfacing group, 20% compared to 6%. Limited femoral resurfacing has the advantage of preserving femoral neck bone stock as well as leaving the femoral canal intact, facilitating future conversion to a total hip replacement. The results of these studies suggest that limited femoral resurfacing may be appropriate for younger patients presenting with more advanced osteonecrosis: Ficat stage 3 hips, lesions involving greater than 30% of the femoral head, and lesions with greater than 2 mm. There must be no evidence of acetabular cartilage involvement, and relative contraindications include large cysts in the femoral neck, osteopenia, and a body mass index greater than 35 [112, 113]. Limited femoral resurfacing should be considered, as an interim procedure as most will ultimately fail and require revision to total hip arthroplasty.

Table 6
Outcome after limited femoral resurfacing [113]

In more advanced disease where there is acetabular involvement, hip resurfacing can be considered. Like femoral resurfacing, it has the advantage of preserving femoral bone stock and has similar indications as limited femoral resurfacing. Overall, the success of total hip resurfacing is approximately 84% at early follow-up (Table 7). Studies have also demonstrated improved walking speeds and abductor and extensor movements showing superior hip kinematics when compared with standard hip replacements [123, 124]. As with limited femoral resurfacing, emerging clinical experience suggests that if involvement of the femoral head is greater than 30%, then the success of total hip resurfacing will be decreased.

Table 7
Outcome after total hip resurfacing [113]

Bipolar hemiarthroplasty has also been used in the treatment of osteonecrosis. Originally, it was designed to decrease acetabular shear forces by the use of an outer free acetabular cup that articulates with the prosthetic femoral head. Historically, it has always produced suboptimal results (Table 8) and does not circumvent the need for resection of the femoral neck and violation of the femoral canal which may complicate future revisions. The use of a thin polyethylene cup can also lead to extensive wear and subsequent osteolysis, particularly in active patients [130132]. As a result, bipolar hemiarthroplasty should largely be avoided as a treatment for osteonecrosis, particularly in young patients.

Table 8
Outcome after bipolar hemiarthroplasty [113]

Total hip replacement is the single treatment with the highest likelihood of providing excellent early pain relief and good functional outcome [6]. However, these advantages must be balanced against the fact that it sacrifices more host bone and narrows future operative options. The main indication is advanced osteonecrosis with secondary degenerative arthritis involving the acetabulum [1]. Relative contraindications to this procedure include the younger patient in which femoral-head-preserving options may be more appropriate or individuals who may be at risk of recurrent dislocation, such as alcoholics [142]. From the available data, it appears that cementless total hip arthroplasty has a better success rate than cemented systems, particularly over the last 10 years. Studies suggest that success rates are comparable with total hip arthroplasty performed for osteoarthritis [115, 143145], with some series reporting a 98% success rate 11 years postoperatively (Table 9) [146]. Seyler et al. [113] note that factors that contribute to high failure rates include young age, long life expectancy, increased body weight, and poor quality femoral bone.

Table 9
Outcome after total hip arthroplasty [113]

Despite improved outcomes after total hip arthroplasty, there still are some subpopulations of patients including those with SLE, sickle cell disease and those individuals taking high-dose steroids after undergoing renal transplantation that have less than optimal results (Table 10) [142, 166]. This may reflect the ongoing pathology of these conditions with continuing insults to the vasculature of the bone, delaying bone ingrowth following implantation. Other factors that may influence the failure rates include decreased immune status leading to higher infection rates and steroid use which increases infection rates and may result in poorer quality bone and healing ability.

Table 10
Total hip arthroplasty after specific etiologies [113]

There a few randomized controlled trials in advanced osteonecrosis. One by Grecula et al. [120] in 1995 compared the outcomes of patients aged under 50 treated with either standard cemented arthroplasty, limited femoral resurfacing, or total hip resurfacing. When followed up at 96 months, results were found to be 80%, 70%, and 15%, respectively.

As previously mentioned, it is important to evaluate the contralateral hip, as bilateral involvement has been reported to be between 40% and 80%. A recent study by Nam et al. [176] investigated the progression of asymptomatic osteonecrosis. Three hundred twelve patients presented with bilateral non-traumatic osteonecrosis, of which 128 underwent joint-preserving procedures and 184 received no treatment for their asymptomatic hip. Sixty-two (59%) hips were classified stage I and 43 (31%) stage II. Fifty-one percent of cases were related to alcohol abuse, 19% corticosteroid-related, and 30% were idiopathic. At 5 years follow-up, 59% of the asymptomatic hips had progressed to collapse, of these 5% involved less than 30% of the femoral head area, 46% involving 30% to 50%, and 83% involving more than 50%, again demonstrating the importance of the size of the lesion in relation to risk of collapse. Forty-one percent of hips remained asymptomatic without signs of collapse, with 30% progressing from stage I to stage II. These results suggest that in early stage asymptomatic osteonecrosis, regular observation in conjunction with pharmacological therapy may be the most appropriate management.


The pathophysiology and management of osteonecrosis is complex and controversial. A better understanding of the biology behind this condition as well as the factors that put some individuals at a higher risk than others will hopefully lead to earlier diagnosis. This in turn may lead to more effective therapies to correct pathophysiological features. The primary goal of treatment should be to relieve pain, maintain a congruent hip joint, and delay the need for total hip arthroplasty for as long as possible. Four main radiographic features are useful in determining the extent of the disease and selecting the appropriate surgical intervention. First is to assess if there has been collapse of the femoral head, demonstrated by the crescent sign on x-ray. If the head has collapsed, then the success rate of head-preserving procedures decreased significantly [6]. Second is the size and location of the lesion. If the involvement is greater that 30% of the femoral head, or the entire weight-bearing surface is involved, then the success of head-saving procedures will be decreased [102, 177]. The third evaluation is to assess the extent of head depression. Collapse of greater than 2 mm likely requires arthroplasty, although the effect of bone grafting when collapse is present is an area of some debate. If the acetabulum is involved, then total hip arthroplasty is the only surgical option. Ultimately, the final decision is made following interoperative inspection of the femoral cartilage and acetabulum. A suggested algorithm is presented in Table 11 [6]. Total hip arthroplasty was indicated in our patient due to collapse of the femoral head.

Table 11
Treatment algorithm for osteonecrosis of the femoral head [6]

While current conservative treatment options appear hopeful, it has not been demonstrated that any of these therapies halt progression of this condition and larger randomized control trials are needed to fully evaluate effectiveness [5]. In terms of more conservative surgical management strategies, there may be potential for head-preserving surgery such as percutaneous core decompression combined with the use of novel adjuvants such as growth factors and cytokines which may help augment repair prior to collapse. Further controlled trials are needed to evaluate the role of limited femoral resurfacing and total hip arthroplasty in the younger population as well as in subgroups of patients in whom total hip arthroplasty has proven less than optimal.


Many thanks to Frank Henn and Amar Rayadhyaksha for critically appraising as well as providing images for the manuscript.


1. Lavernia CJ, Sierra RJ, Grieco FR (1999) Osteonecrosis of the femoral head. J Am Acad Orthop Surg 7(4):250–261 (Jul–Aug) [PubMed]
2. Mont MA, Hungerford DS (1995) Non-traumatic avascular necrosis of the femoral head. J Bone Jt Surg Am 77(3):459–474 (Mar) [PubMed]
3. Koo KH, Kim R (1995) Quantifying the extent of osteonecrosis of the femoral head. A new method using MRI. J Bone Jt Surg Br 77(6):875–880 (Nov) [PubMed]
4. Mankin HJ, Brower TD (1962) Bilateral idiopathic aseptic necrosis of the femur in adults: “Chandler’s disease”. Bull Hosp Joint Dis 23:42–57 [PubMed]
5. Urbaniak JR, Harvey EJ (1998) Revascularization of the femoral head in osteonecrosis. J Am Acad Orthop Surg 6(1):44–54 (Jan–Feb) [PubMed]
6. Lieberman JR, Berry DJ, Mont MA, Aaron RK, Callaghan JJ, Rajadhyaksha AD et al (2003) Osteonecrosis of the hip: management in the 21st century. Instr Course Lect 52:337–355 [PubMed]
7. Mankin HJ (1992) Nontraumatic necrosis of bone (osteonecrosis). N Engl J Med 326(22):1473–1479 (May 28) [PubMed]
8. Jacobs B (1978) Epidemiology of traumatic and nontraumatic osteonecrosis. Clin Orthop Relat Res (130):51–67 (Jan–Feb) [PubMed]
9. Coventry MB (1974) The treatment of fracture–dislocation of the hip by total hip arthroplasty. J Bone Jt Surg Am 56(6):1128–1134 (Sep) [PubMed]
10. Barnes R, Brown JT, Garden RS, Nicoll EA (1976) Subcapital fractures of the femur. A prospective review. J Bone Jt Surg Br 58(1):2–24 (Feb) [PubMed]
11. Garden RS (1971) Malreduction and avascular necrosis in subcapital fractures of the femur. J Bone Jt Surg Br 53(2):183–197 (May) [PubMed]
12. Brav EA (1962) Traumatic dislocation of the hip: army experience and results over a twelve-year period. J Bone Jt Surg Am 44:1115–134
13. Cruess RL (1981) Steroid-induced osteonecrosis. J R Coll Surg Edinb 26(2):69–77 (Mar) [PubMed]
14. Upadhyay SS, Moulton A, Srikrishnamurthy K (1983) An analysis of the late effects of traumatic posterior dislocation of the hip without fractures. J Bone Jt Surg Br 65(2):150–152 (Mar) [PubMed]
15. Hungerford DS, Zizic TM (1978) Alcoholism associated ischemic necrosis of the femoral head. Early diagnosis and treatment. Clin Orthop Relat Res (130):144–153 (Jan–Feb) [PubMed]
16. Jones LC, Hungerford DS (2007) The pathogenesis of osteonecrosis. Instr Course Lect 56:179–196 [PubMed]
17. Matsuo K, Hirohata T, Sugioka Y, Ikeda M, Fukuda A (1988) Influence of alcohol intake, cigarette smoking, and occupational status on idiopathic osteonecrosis of the femoral head. Clin Orthop Relat Res (234):115–123 (Sep) [PubMed]
18. Felson DT, Anderson JJ (1987) Across-study evaluation of association between steroid dose and bolus steroids and avascular necrosis of bone. Lancet 1(8538):902–906 (Apr 18) [PubMed]
19. Johnson LC (1964) Histogenesis of avascular necrosis. In: Proceedings of the conference on aseptic necrosis of the femoral head. Washington, D. C., U. S. Public Health Service pp. 55–79
20. Solomon L (1981) Idiopathic necrosis of the femoral head: pathogenesis and treatment. Can J Surg 24(6):573–578 (Nov) [PubMed]
21. Jaffe WL, Epstein M, Heyman N, Mankin HJ (1972) The effect of cortisone on femoral and humeral heads in rabbits. An experimental study. Clin Orthop Relat Res 82:221–228 (Jan–Feb) [PubMed]
22. Jones JP Jr (1993) Fat embolism, intravascular coagulation, and osteonecrosis. Clin Orthop Relat Res (292):294–308, Jul [PubMed]
23. Nishimura T, Matsumoto T, Nishino M, Tomita K (1997) Histopathologic study of veins in steroid treated rabbits. Clin Orthop Relat Res (334):37–42 (Jan) [PubMed]
24. Kenzora JE, Glimcher MJ (1985) Pathogenesis of idiopathic osteonecrosis: the ubiquitous crescent sign. Orthop Clin North Am 16(4):681–696 (Oct) [PubMed]
25. Wheeless CR, Lins RE, Knelson MH, Urbaniak JR (1997) Digital subtraction angiography in patients with osteonecrosis of the femoral head. In: Urbaniak JR, Jones JP Jr (eds) Osteonecrosis: etiology, diagnosis and treatment. American Academy of Orthopaedic Surgeons, Rosemont, IL, pp 241–245
26. Kiaer T, Pedersen NW, Kristensen KD, Starklint H (1990) Intra-osseous pressure and oxygen tension in avascular necrosis and osteoarthritis of the hip. J Bone Jt Surg Br 72(6):1023–1030 (Nov) [PubMed]
27. Aaron RK (1998) Osteonecrosis: etiology, pathophysiology and diagnosis. In: Campbell P, Rosenberg AG, Rubash HE (eds) The adult hip. Lippincott, Philadelphia, pp 451–466
28. Conway WF, Totty WG, McEnery KW (1996) CT and MR imaging of the hip. Radiology 198(2):297–307 (Feb) [PubMed]
29. Totty WG, Murphy WA, Ganz WI, Kumar B, Daum WJ, Siegel BA (1984) Magnetic resonance imaging of the normal and ischemic femoral head. AJR Am J Roentgenol 143(6):1273–1280 (Dec) [PubMed]
30. Steinberg ME, Steinberg DR (1991) Avascular necrosis of the femoral head. In: Steinberg ME (ed) The hip and its disorders. Saunders, Philadelphia, pp 623–647
31. Beltran J, Herman LJ, Burk JM, Zuelzer WA, Clark RN, Lucas JG et al (1988) Femoral head avascular necrosis: MR imaging with clinical-pathologic and radionuclide correlation. Radiology 166(1 Pt 1):215–220 (Jan) [PubMed]
32. Markisz JA, Knowles RJ, Altchek DW, Schneider R, Whalen JP, Cahill PT (1987) Segmental patterns of avascular necrosis of the femoral heads: early detection with MR imaging. Radiology 162(3):717–720 (Mar) [PubMed]
33. Bramlett KW, Killian JT, Nasca RJ, Daniel WW (1987) Transient osteoporosis. Clin Orthop Relat Res (222):197–202 (Sep) [PubMed]
34. Kaplan SS, Stegman CJ (1985) Transient osteoporosis of the hip. A case report and review of the literature. J Bone Jt Surg Am 67(3):490–493 (Mar) [PubMed]
35. Potter H, Moran M, Schneider R, Bansal M, Sherman C, Markisz J (1992) Magnetic resonance imaging in diagnosis of transient osteoporosis of the hip. Clin Orthop Relat Res (280):223–229 (Jul) [PubMed]
36. Steinberg ME, Hayken GD, Steinberg DR (1995) A quantitative system for staging avascular necrosis. J Bone Jt Surg Br 77(1):34–41 (Jan) [PubMed]
37. Ficat RP, Arlet J (1980) Functional investigation of bone under normal circumstances. In: Hungerford DS (ed) Ischemia and necrosis of the bone. Williams and Wilkins, Baltimore, pp 29–52
38. Committee on Terminology and Classification (1992) Association Research Circulation Osseous (ARCO) news, vol 4, pp 41–46
39. Mont MA, Marulanda GA, Jones LC, Saleh KJ, Gordon N, Hungerford DS et al (2006) Systematic analysis of classification systems for osteonecrosis of the femoral head. J Bone Jt Surg Am 88(Suppl 3):16–26 (Nov) [PubMed]
40. Pritchett JW (2001) Statin therapy decreases the risk of osteonecrosis in patients receiving steroids. Clin Orthop Relat Res (386):173–178 (May) [PubMed]
41. Agarwala S, Sule A, Pai BU, Joshi VR (2002) Alendronate in the treatment of avascular necrosis of the hip. Rheumatology (Oxford) 41(3):346–347 (Mar) [PubMed]
42. Agarwala S, Jain D, Joshi VR, Sule A (2005) Efficacy of alendronate, a bisphosphonate, in the treatment of AVN of the hip. A prospective open-label study. Rheumatology (Oxford) 44(3):352–359 (Mar) [PubMed]
43. Lai KA, Shen WJ, Yang CY, Shao CJ, Hsu JT, Lin RM (2005) The use of alendronate to prevent early collapse of the femoral head in patients with nontraumatic osteonecrosis. A randomized clinical study. J Bone Jt Surg Am 87(10):2155–2159 (Oct) [PubMed]
44. Arlet J, Mazieres B, Thiechert M, Vallieres G (1990) The effcts of IV injection of Naftidofuryl (praxilene) on intramedullary pressure in patients with osteonecrosis of the femoral head. In: Arlet J, Mazieres B (eds) Bone circulation and bone necrosis. Springer, Berlin, Germany, pp 405–406
45. Reis ND, Schwartz O, Militianu D, Ramon Y, Levin D, Norman D et al (2003) Hyperbaric oxygen therapy as a treatment for stage-I avascular necrosis of the femoral head. J Bone Jt Surg Br 85(3):371–375 (Apr) [PubMed]
46. Peskin B, Shupak A, Levin D, Norman D, Jacob Z, Boss JF et al (2001) Effects of non-weight bearing and hyperbaric oxygen therapy in vascular deprivation-induced osteonecrosis of the rat femoral head. Undersea Hyperb Med 28(4):187–194 (Fall) [PubMed]
47. Aaron RK, Steinberg ME (1991) Electrical stimulation of osteonecrosis of the femoral head. Semin Arthroplasty 2(3):214–221 (Jul) [PubMed]
48. Trancik T, Lunceford E, Strum D (1990) The effect of electrical stimulation on osteonecrosis of the femoral head. Clin Orthop Relat Res (256):120–124 (Jul) [PubMed]
49. Steinberg ME, Brighton CT, Hayken GD, Tooze SE, Steinberg DR (1985) Electrical stimulation in the treatment of osteonecrosis of the femoral head—a 1-year follow-up. Orthop Clin North Am 16(4):747–756 (Oct) [PubMed]
50. Seber S, Omeroglu H, Cetinkanat H, Kose N (2003) The efficacy of pulsed electromagnetic fields used alone in the treatment of femoral head osteonecrosis: a report of two cases. Acta Orthop Traumatol Turc 37(5):410–413 [PubMed]
51. Hofmann S, Mazieres B (2000) Osteonecrosis: natural course and conservative therapy. Orthopade 29(5):403–410 (May) [PubMed]
52. Walter TH (1985) Bioelectrical osteogenesis: acceleration of fracture repair and bone growth. An alternative to bone grafting in nonunions. Clin Podiatry 2(1):41–57 (Jan) [PubMed]
53. Brighton CT, Friedenberg ZB, Black J, Esterhai JL, Jr, Mitchell JE, Montique F, Jr (1981) Electrically induced osteogenesis: relationship between charge, current density, and the amount of bone formed: introduction of a new cathode concept. Clin Orthop Relat Res (161):122–132 (Nov–Dec) [PubMed]
54. Wang CJ, Wang FS, Huang CC, Yang KD, Weng LH, Huang HY (2005) Treatment for osteonecrosis of the femoral head: comparison of extracorporeal shock waves with core decompression and bone-grafting. J Bone Jt Surg Am 87(11):2380–2387 (Nov) [PubMed]
55. Ludwig J, Lauber S, Lauber HJ, Dreisilker U, Raedel R, Hotzinger H (2001) High-energy shock wave treatment of femoral head necrosis in adults. Clin Orthop Relat Res (387):119–126 (Jun) [PubMed]
56. Mont MA, Marulanda GA, Seyler TM, Plate JF, Delanois RE (2007) Core decompression and nonvascularized bone grafting for the treatment of early stage osteonecrosis of the femoral head. Instr Course Lect 56:213–220 [PubMed]
57. Smith KR, Bonfiglio M, Montgomery WJ (1980) Non-traumatic necrosis of the femoral head treated with tibial bone-grafting. A follow-up note. J Bone Jt Surg Am 62(5):845–847 (Jul) [PubMed]
58. Aaron RK, Combor DM, Lord CF (1997) Core decompression augmented with human decalcified bone matrix graft for osteonecrosis of the femoral head. In: Urbaniak JR, Jones JP Jr (eds) Osteonecrosis: etiology, diagnosis and treatment. American Academy of Orthopaedic Surgeons, Rosemont, IL, pp 301–307
59. Mont MA, Carbone JJ, Fairbank AC (1996) Core decompression versus nonoperative management for osteonecrosis of the hip. Clin Orthop Relat Res (324):169–178 (Mar) [PubMed]
60. Radke S, Kirschner S, Seipel V, Rader C, Eulert J (2004) Magnetic resonance imaging criteria of successful core decompression in avascular necrosis of the hip. Skelet Radiol 33(9):519–523 (Sep) [PubMed]
61. rMont MA, Ragland PS, Etienne G (2004) Core decompression of the femoral head for osteonecrosis using percutaneous multiple small-diameter drilling. Clin Orthop Relat Res (429):131–138 (Dec) [PubMed]
62. Lieberman JR, Conduah A, Urist MR (2004) Treatment of osteonecrosis of the femoral head with core decompression and human bone morphogenetic protein. Clin Orthop Relat Res (429):139–145 (Dec) [PubMed]
63. Aigner N, Schneider W, Eberl V, Knahr K (2002) Core decompression in early stages of femoral head osteonecrosis—an MRI-controlled study. Int Orthop 26(1):31–35 [PubMed]
64. Simank HG, Brocai DR, Brill C, Lukoschek M (2001) Comparison of results of core decompression and intertrochanteric osteotomy for nontraumatic osteonecrosis of the femoral head using Cox regression and survivorship analysis. J Arthroplasty 16(6):790–794 (Sep) [PubMed]
65. Yoon TR, Song EK, Rowe SM, Park CH (2001) Failure after core decompression in osteonecrosis of the femoral head. Int Orthop 24(6):316–318 [PubMed]
66. Steinberg ME, Larcom PG, Strafford B, Hosick WB, Corces A, Bands RE et al (2001) Core decompression with bone grafting for osteonecrosis of the femoral head. Clin Orthop Relat Res (386):71–78 (May) [PubMed]
67. Maniwa S, Nishikori T, Furukawa S, Kajitani K, Iwata A, Nishikawa U et al (2000) Evaluation of core decompression for early osteonecrosis of the femoral head. Arch Orthop Trauma Surg 120(5–6):241–244 [PubMed]
68. Chen CH, Chang JK, Huang KY, Hung SH, Lin GT, Lin SY (2000) Core decompression for osteonecrosis of the femoral head at pre-collapse stage. Kaohsiung J Med Sci 16(2):76–82 (Feb) [PubMed]
69. Lavernia CJ, Sierra RJ (2000) Core decompression in atraumatic osteonecrosis of the hip. J Arthroplasty 15(2):171–178 (Feb) [PubMed]
70. Bozic KJ, Zurakowski D, Thornhill TS (1999) Survivorship analysis of hips treated with core decompression for nontraumatic osteonecrosis of the femoral head. J Bone Jt Surg Am 81(2):200–209 (Feb) [PubMed]
71. Simank HG, Brocai DR, Strauch K, Lukoschek M (1999) Core decompression in osteonecrosis of the femoral head: risk-factor-dependent outcome evaluation using survivorship analysis. Int Orthop 23(3):154–159 [PubMed]
72. Van Laere C, Mulier M, Simon JP, Stuyck J, Fabry G (1998) Core decompression for avascular necrosis of the femoral head. Acta Orthop Belg 64(3):269–272 (Sep) [PubMed]
73. Scully SP, Aaron RK, Urbaniak JR (1998) Survival analysis of hips treated with core decompression or vascularized fibular grafting because of avascular necrosis. J Bone Jt Surg Am 80(9):1270–1275 (Sep) [PubMed]
74. Iorio R, Healy WL, Abramowitz AJ, Pfeifer BA (1998) Clinical outcome and survivorship analysis of core decompression for early osteonecrosis of the femoral head. J Arthroplasty 13(1):34–41 (Jan) [PubMed]
75. Chang MC, Chen TH, Lo WH (1997) Core decompression in treating ischemic necrosis of the femoral head. Zhonghua Yi Xue Za Zhi (Taipei) 60(3):130–136 (Sep) [PubMed]
76. Powell ET, Lanzer WL, Mankey MG (1997) Core decompression for early osteonecrosis of the hip in high risk patients. Clin Orthop Relat Res (335):181–189 (Feb) [PubMed]
77. Mazieres B, Marin F, Chiron P, Moulinier L, Amigues JM, Laroche M et al (1997) Influence of the volume of osteonecrosis on the outcome of core decompression of the femoral head. Ann Rheum Dis 56(12):747–750 (Dec) [PMC free article] [PubMed]
78. Mont MA, Fairbank AC, Petri M, Hungerford DS (1997) Core decompression for osteonecrosis of the femoral head in systemic lupus erythematosus. Clin Orthop Relat Res (334):91–97 (Jan) [PubMed]
79. Styles LA, Vichinsky EP (1996) Core decompression in avascular necrosis of the hip in sickle-cell disease. Am J Hematol 52(2):103–107 (Jun) [PubMed]
80. Markel DC, Miskovsky C, Sculco TP, Pellicci PM, Salvati EA (1996) Core decompression for osteonecrosis of the femoral head. Clin Orthop Relat Res (323):226–233 (Feb) [PubMed]
81. Holman AJ, Gardner GC, Richardson ML, Simkin PA (1995) Quantitative magnetic resonance imaging predicts clinical outcome of core decompression for osteonecrosis of the femoral head. J Rheumatol 22(10):1929–1933 (Oct) [PubMed]
82. Smith SW, Fehring TK, Griffin WL, Beaver WB (1995) Core decompression of the osteonecrotic femoral head. J Bone Jt Surg Am 77(5):674–680 (May) [PubMed]
83. Song WS, Yoo JJ, Kim YM, Kim HJ (2007) Results of multiple drilling compared with those of conventional methods of core decompression. Clin Orthop Relat Res 454:139–146 (Jan) [PubMed]
84. Benke GJ, Baker AS, Dounis E (1982) Total hip replacement after upper femoral osteotomy. A clinical review. J Bone Jt Surg Br 64(5):570–571 [PubMed]
85. Ferguson GM, Cabanela ME, Ilstrup DM (1994) Total hip arthroplasty after failed intertrochanteric osteotomy. J Bone Jt Surg Br 76(2):252–257 (Mar) [PubMed]
86. Dean MT, Cabanela ME (1993) Transtrochanteric anterior rotational osteotomy for avascular necrosis of the femoral head. Long-term results. J Bone Jt Surg Br 75(4):597–601 (Jul) [PubMed]
87. Sugano N, Takaoka K, Ohzono K, Matsui M, Saito M, Saito S (1992) Rotational osteotomy for non-traumatic avascular necrosis of the femoral head. J Bone Jt Surg Br 74(5):734–739 (Sep) [PubMed]
88. Sugioka Y, Hotokebuchi T, Tsutsui H (1992) Transtrochanteric anterior rotational osteotomy for idiopathic and steroid-induced necrosis of the femoral head. Indications and long-term results. Clin Orthop Relat Res (277):111–120 (Apr) [PubMed]
89. Masuda T, Matsuno T, Hasegawa I, Kanno T, Ichioka Y, Kaneda K (1988) Results of transtrochanteric rotational osteotomy for nontraumatic osteonecrosis of the femoral head. Clin Orthop Relat Res (228):69–74 (Mar) [PubMed]
90. Eyb R, Kotz R (1987) The transtrochanteric anterior rotational osteotomy of Sugioka. Early and late results in idiopathic aseptic femoral head necrosis. Arch Orthop Trauma Surg 106(3):161–167 [PubMed]
91. Tooke SM, Amstutz HC, Hedley AK (1987) Results of transtrochanteric rotational osteotomy for femoral head osteonecrosis. Clin Orthop Relat Res (224):150–157 (Nov) [PubMed]
92. Mont MA, Fairbank AC, Krackow KA, Hungerford DS (1996) Corrective osteotomy for osteonecrosis of the femoral head. J Bone Jt Surg Am 78(7):1032–1038 (Jul) [PubMed]
93. Scher MA, Jakim I (1993) Intertrochanteric osteotomy and autogenous bone-grafting for avascular necrosis of the femoral head. J Bone Jt Surg Am 75(8):1119–1133 (Aug) [PubMed]
94. Jacobs MA, Hungerford DS, Krackow KA (1989) Intertrochanteric osteotomy for avascular necrosis of the femoral head. J Bone Jt Surg Br 71(2):200–204 (Mar) [PubMed]
95. Gottschalk F (1989) Indications and results of intertrochanteric osteotomy in osteonecrosis of the femoral head. Clin Orthop Relat Res (249):219–222 (Dec) [PubMed]
96. Maistrelli G, Fusco U, Avai A, Bombelli R (1988) Osteonecrosis of the hip treated by intertrochanteric osteotomy. A four- to 15-year follow-up. J Bone Jt Surg Br 70(5):761–766 (Nov) [PubMed]
97. Merle D’Aubigne R, Postel M, Mazabraud A, Massias P, Gueguen J, France P (1965) Idiopathic necrosis of the femoral head in adults. J Bone Jt Surg Br 47(4):612–633 (Nov) [PubMed]
98. Ganz R, Buchler U (1983) Overview of attempts to revitalize the dead head in aseptic necrosis of the femoral head—osteotomy and revascularization. Hip 1983:296–305 [PubMed]
99. Meyers MH, Jones RE, Bucholz RW, Wenger DR (1983) Fresh autogenous grafts and osteochondral allografts for the treatment of segmental collapse in osteonecrosis of the hip. Clin Orthop Relat Res (174):107–112 (Apr) [PubMed]
100. Rosenwasser MP, Garino JP, Kiernan HA, Michelsen CB (1994) Long term follow-up of thorough debridement and cancellous bone grafting of the femoral head for avascular necrosis. Clin Orthop Relat Res (306):17–27 (Sep) [PubMed]
101. Saito S, Ohzono K, Ono K (1988) Joint-preserving operations for idiopathic avascular necrosis of the femoral head. Results of core decompression, grafting and osteotomy. J Bone Jt Surg Br 70(1):78–84 (Jan) [PubMed]
102. Mont MA, Einhorn TA, Sponseller PD, Hungerford DS (1998) The trapdoor procedure using autogenous cortical and cancellous bone grafts for osteonecrosis of the femoral head. J Bone Jt Surg Br 80(1):56–62 (Jan) [PubMed]
103. Ko JY, Meyers MH, Wenger DR (1995) “Trapdoor” procedure for osteonecrosis with segmental collapse of the femoral head in teenagers. J Pediatr Orthop 15(1):7–15 (Jan–Feb) [PubMed]
104. Rijnen WH, Gardeniers JW, Buma P, Yamano K, Slooff TJ, Schreurs BW (2003) Treatment of femoral head osteonecrosis using bone impaction grafting. Clin Orthop Relat Res (417):74–83 (Dec) [PubMed]
105. Plakseychuk AY, Kim SY, Park BC, Varitimidis SE, Rubash HE, Sotereanos DG (2003) Vascularized compared with nonvascularized fibular grafting for the treatment of osteonecrosis of the femoral head. J Bone Jt Surg Am 85-A(4):589–596 (Apr) [PubMed]
106. Mont MA, Etienne G, Ragland PS (2003) Outcome of nonvascularized bone grafting for osteonecrosis of the femoral head. Clin Orthop Relat Res (417):84–92 (Dec) [PubMed]
107. Urbaniak JR, Coogan PG, Gunneson EB, Nunley JA (1995) Treatment of osteonecrosis of the femoral head with free vascularized fibular grafting. A long-term follow-up study of one hundred and three hips. J Bone Jt Surg Am 77(5):681–694 (May) [PubMed]
108. Kane SM, Ward WA, Jordan LC, Guilford WB, Hanley EN Jr (1996) Vascularized fibular grafting compared with core decompression in the treatment of femoral head osteonecrosis. Orthopedics 19(10):869–872 (Oct) [PubMed]
109. Vail TP, Urbaniak JR (1996) Donor-site morbidity with use of vascularized autogenous fibular grafts. J Bone Jt Surg Am 78(2):204–211 (Feb) [PubMed]
110. Aluisio FV, Urbaniak JR (1998) Proximal femur fractures after free vascularized fibular grafting to the hip. Clin Orthop Relat Res (356):192–201 (Nov) [PubMed]
111. Mont MA, Rajadhyaksha AD, Hungerford DS (2001) Outcomes of limited femoral resurfacing arthroplasty compared with total hip arthroplasty for osteonecrosis of the femoral head. J Arthroplasty 16(8 Suppl 1):134–139 (Dec) [PubMed]
112. Mont MA, Ragland PS, Parvizi J (2006) Surgical treatment of osteonecrosis of the hip. Instr Course Lect 55:167–172 [PubMed]
113. Seyler TM, Cui Q, Mihalko WM, Mont MA, Saleh KJ (2007) Advances in hip arthroplasty in the treatment of osteonecrosis. Instr Course Lect 56:221–233 [PubMed]
114. Cuckler JM, Moore KD, Estrada L (2004) Outcome of hemiresurfacing in osteonecrosis of the femoral head. Clin Orthop Relat Res (429):146–150 (Dec) [PubMed]
115. Beaule PE, Amstutz HC, Le Duff M, Dorey F (2004) Surface arthroplasty for osteonecrosis of the hip: hemiresurfacing versus metal-on-metal hybrid resurfacing. J Arthroplasty 19(8 Suppl 3):54–58 (Dec) [PubMed]
116. Adili A, Trousdale RT (2003) Femoral head resurfacing for the treatment of osteonecrosis in the young patient. Clin Orthop Relat Res (417):93–101 (Dec) [PubMed]
117. Beaule PE, Schmalzried TP, Campbell P, Dorey F, Amstutz HC (2001) Duration of symptoms and outcome of hemiresurfacing for hip osteonecrosis. Clin Orthop Relat Res (385):104–117 (Apr) [PubMed]
118. Siguier T, Siguier M, Judet T, Charnley G, Brumpt B (2001) Partial resurfacing arthroplasty of the femoral head in avascular necrosis. Methods, indications, and results. Clin Orthop Relat Res (386):85–92 (May) [PubMed]
119. Nelson CL, Walz BH, Gruenwald JM (1997) Resurfacing of only the femoral head for osteonecrosis. Long-term follow-up study. J Arthroplasty 12(7):736–740 (Oct) [PubMed]
120. Grecula MJ, Grigoris P, Schmalzried TP, Dorey F, Campbell PA, Amstutz HC (1995) Endoprostheses for osteonecrosis of the femoral head. A comparison of four models in young patients. Int Orthop 19(3):137–143 [PubMed]
121. Tooke SM, Amstutz HC, Delaunay C (1987) Hemiresurfacing for femoral head osteonecrosis. J Arthroplasty 2(2):125–133 [PubMed]
122. Langlais F, Barthas J, Postel M (1979) Adjusted cups for idiopathic necrosis. Radiological results. Rev Chir Orthop Repar Appar Mot 65(3):151–155 (Apr–May) [PubMed]
123. Daniel J, Pynsent PB, McMinn DJ (2004) Metal-on-metal resurfacing of the hip in patients under the age of 55 years with osteoarthritis. J Bone Jt Surg Br 86(2):177–184 (Mar) [PubMed]
124. Mont MA, Seyler TM, Ragland PS, Starr R, Erhart J, Bhave A (2007) Gait analysis of patients with resurfacing hip arthroplasty compared with hip osteoarthritis and standard total hip arthroplasty. J Arthroplasty 22(1):100–108 (Jan) [PubMed]
125. Ragland PS, Mont MA, Marulanda GA, Delanois R, Seyler T (2006) Use of metal-on-metal resurfacing arthroplasty for avascular necrosis of the hip. Journal of Bone and Joint Surgery – British Volume 88-B (Supplement 2):310
126. Amstutz HC, Beaule PE, Dorey FJ, Le Duff MJ, Campbell PA, Gruen TA (2004) Metal-on-metal hybrid surface arthroplasty: two to six-year follow-up study. J Bone Jt Surg Am 86-A(1):28–39 (Jan) [PubMed]
127. Mohamad JA, Kwan MK, Merican AM, Abbas AA, Kamari ZH, Hisa MK et al (2004) Early results of metal on metal articulation total hip arthroplasty in young patients. Med J Malaysia 59(Suppl F):3–7 (Dec) [PubMed]
128. Yoo MC, Cho YJ, Kim KI, Chun YS, Ha JH, Park JY (2004) Resurfacing arthroplasty in patients with osteonecrosis of the femoral head. Journal of Bone and Joint Surgery – British Volume 86-B (Supplement 2):151
129. Dutton RO, Amstutz HC, Thomas BJ, Hedley AK (1982) Tharies surface replacement for osteonecrosis of the femoral head. J Bone Jt Surg Am 64(8):1225–1237 (Oct) [PubMed]
130. Cabanela ME (1990) Bipolar versus total hip arthroplasty for avascular necrosis of the femoral head. A comparison. Clin Orthop Relat Res (261):59–62 (Dec) [PubMed]
131. Lachiewicz PF, Desman SM (1988) The bipolar endoprosthesis in avascular necrosis of the femoral head. J Arthroplasty 3(2):131–138 [PubMed]
132. Takaoka K, Nishina T, Ohzono K, Saito M, Matsui M, Sugano N et al (1992) Bipolar prosthetic replacement for the treatment of avascular necrosis of the femoral head. Clin Orthop Relat Res (277):121–127 (Apr) [PubMed]
133. Tsumura H, Torisu T, Kaku N, Higashi T (2005) Five- to fifteen-year clinical results and the radiographic evaluation of acetabular changes after bipolar hip arthroplasty for femoral head osteonecrosis. J Arthroplasty 20(7):892–897 (Oct) [PubMed]
134. Yamano K, Atsumi T, Kajiwara T, Hiranuma Y, Tamaoki S, Asakura Y (2004) Bipolar endoprosthesis for osteonecrosis of the femoral head: A 12-year follow-up of 29 hip. Journal of Bone and Joint Surgery – British Volume 86-B (Supplement 2):150–151
135. Lee SB, Sugano N, Nakata K, Matsui M, Ohzono K (2004) Comparison between bipolar hemiarthroplasty and THA for osteonecrosis of the femoral head. Clin Orthop Relat Res (424):161–165 (Jul) [PubMed]
136. Nagai I, Takatori Y, Kuruta Y, Moro T, Karita T, Mabuchi A et al (2002) Nonself-centering Bateman bipolar endoprosthesis for nontraumatic osteonecrosis of the femoral head: a 12- to 18-year follow-up study. J Orthop Sci 7(1):74–78 [PubMed]
137. Ito H, Matsuno T, Kaneda K (2000) Bipolar hemiarthroplasty for osteonecrosis of the femoral head. A 7- to 18-year follow-up. Clin Orthop Relat Res (374):201–211 (May) [PubMed]
138. Chan YS, Shih CH (2000) Bipolar versus total hip arthroplasty for hip osteonecrosis in the same patient. Clin Orthop Relat Res (379):169–177 (Oct) [PubMed]
139. Sanjay BK, Moreau PG (1996) Bipolar hip replacement in sickle cell disease. Int Orthop 20(4):222–226 [PubMed]
140. Murzic WJ, McCollum DE (1994) Hip arthroplasty for osteonecrosis after renal transplantation. Clin Orthop Relat Res (299):212–219 (Feb) [PubMed]
141. Learmonth ID, Opitz M (1993) Treatment of grade III osteonecrosis of the femoral head with a Charnley/Bicentric hemiarthroplasty. J R Coll Surg Edinb 38(5):311–314 (Oct) [PubMed]
142. Chiu KH, Shen WY, Ko CK, Chan KM (1997) Osteonecrosis of the femoral head treated with cementless total hip arthroplasty. A comparison with other diagnoses. J Arthroplasty 12(6):683–688 (Sep) [PubMed]
143. Brinker MR, Rosenberg AG, Kull L, Galante JO (1994) Primary total hip arthroplasty using noncemented porous-coated femoral components in patients with osteonecrosis of the femoral head. J Arthroplasty 9(5):457–468 (Oct) [PubMed]
144. Chandler HP, Reineck FT, Wixson RL, McCarthy JC (1981) Total hip replacement in patients younger than thirty years old. A five-year follow-up study. J Bone Jt Surg Am 63(9):1426–1434 (Dec) [PubMed]
145. Saito S, Saito M, Nishina T, Ohzono K, Ono K (1989) Long-term results of total hip arthroplasty for osteonecrosis of the femoral head. A comparison with osteoarthritis. Clin Orthop Relat Res (244):198–207 (Jul) [PubMed]
146. Kim YH, Oh SH, Kim JS, Koo KH (2003) Contemporary total hip arthroplasty with and without cement in patients with osteonecrosis of the femoral head. J Bone Jt Surg Am 85-A(4):675–681 (Apr) [PubMed]
147. Fyda TM, Callaghan JJ, Olejniczak J, Johnston RC (2002) Minimum ten-year follow-up of cemented total hip replacement in patients with osteonecrosis of the femoral head. Iowa Orthop J 22:8–19 [PMC free article] [PubMed]
148. Ortiguera CJ, Pulliam IT, Cabanela ME (1999) Total hip arthroplasty for osteonecrosis: matched-pair analysis of 188 hips with long-term follow-up. J Arthroplasty 14(1):21–28 (Jan) [PubMed]
149. Garino JP, Steinberg ME (1997) Total hip arthroplasty in patients with avascular necrosis of the femoral head: a 2- to 10-year follow-up. Clin Orthop Relat Res (334):108–115 (Jan) [PubMed]
150. Kantor SG, Huo MH, Huk OL, Salvati EA (1996) Cemented total hip arthroplasty in patients with osteonecrosis. A 6-year minimum follow-up study of second-generation cement techniques. J Arthroplasty 11(3):267–271 (Apr) [PubMed]
151. Katz RL, Bourne RB, Rorabeck CH, McGee H (1992) Total hip arthroplasty in patients with avascular necrosis of the hip. Follow-up observations on cementless and cemented operations. Clin Orthop Relat Res (281):145–151 (Aug) [PubMed]
152. Schneider W, Knahr K (2004) Total hip replacement in younger patients: survival rate after avascular necrosis of the femoral head. Acta Orthop Scand 75(2):142–146 (Apr) [PubMed]
153. Taylor AH, Shannon M, Whitehouse SL, Lee MB, Learmonth ID (2001) Harris Galante cementless acetabular replacement in avascular necrosis. J Bone Jt Surg Br 83(2):177–182 (Mar) [PubMed]
154. Xenakis TA, Beris AE, Malizos KK, Koukoubis T, Gelalis J, Soucacos PN (1997) Total hip arthroplasty for avascular necrosis and degenerative osteoarthritis of the hip. Clin Orthop Relat Res (341):62–68 (Aug) [PubMed]
155. Delank KS, Drees P, Eckardt A, Heine J (2001) Results of the uncemented total hip arthroplasty in avascular necrosis of the femoral head. Z Orthop Ihre Grenzgeb 139(6):525–530 (Nov–Dec) [PubMed]
156. Xenakis TA, Gelalis J, Koukoubis TA, Zaharis KC, Soucacos PN (2001) Cementless hip arthroplasty in the treatment of patients with femoral head necrosis. Clin Orthop Relat Res (386):93–99 (May) [PubMed]
157. Hartley WT, McAuley JP, Culpepper WJ, Engh CA Jr, Engh CAS (2000) Osteonecrosis of the femoral head treated with cementless total hip arthroplasty. J Bone Jt Surg Am 82-A(10):1408–1413 (Oct) [PubMed]
158. Fye MA, Huo MH, Zatorski LE, Keggi KJ (1998) Total hip arthroplasty performed without cement in patients with femoral head osteonecrosis who are less than 50 years old. J Arthroplasty 13(8):876–881 (Dec) [PubMed]
159. D’Antonio JA, Capello WN, Manley MT, Feinberg J (1997) Hydroxyapatite coated implants. Total hip arthroplasty in the young patient and patients with avascular necrosis. Clin Orthop Relat Res (344):124–138 (Nov) [PubMed]
160. Gonzalez MH, Ortinau ET, Buonanno W, Prieto J (1997) Cementless total hip arthroplasty in patients with advanced avascular necrosis. J South Orthop Assoc 6(3):162–168 (Fall) [PubMed]
161. Stulberg BN, Singer R, Goldner J, Stulberg J (1997) Uncemented total hip arthroplasty in osteonecrosis: a 2- to 10-year evaluation. Clin Orthop Relat Res (334):116–123 (Jan) [PubMed]
162. Kim YH, Oh JH, Oh SH (1995) Cementless total hip arthroplasty in patients with osteonecrosis of the femoral head. Clin Orthop Relat Res (320):73–84 (Nov) [PubMed]
163. Phillips FM, Pottenger LA, Finn HA, Vandermolen J (1994) Cementless total hip arthroplasty in patients with steroid-induced avascular necrosis of the hip. A 62-month follow-up study. Clin Orthop Relat Res (303):147–154 (Jun) [PubMed]
164. Piston RW, Engh CA, De Carvalho PI, Suthers K (1994) Osteonecrosis of the femoral head treated with total hip arthroplasty without cement. J Bone Jt Surg Am 76(2):202–214 (Feb) [PubMed]
165. Lins RE, Barnes BC, Callaghan JJ, Mair SD, McCollum DE (1993) Evaluation of uncemented total hip arthroplasty in patients with avascular necrosis of the femoral head. Clin Orthop Relat Res (297):168–173 (Dec) [PubMed]
166. Acurio MT, Friedman RJ (1992) Hip arthroplasty in patients with sickle-cell haemoglobinopathy. J Bone Jt Surg Br 74(3):367–371 (May) [PubMed]
167. Zangger P, Gladman DD, Urowitz MB, Bogoch ER (2000) Outcome of total hip replacement for avascular necrosis in systemic lupus erythematosus. J Rheumatol 27(4):919–923 (Apr) [PubMed]
168. Chen YW, Chang JK, Huang KY, Lin GT, Lin SY, Huang CY (1999) Hip arthroplasty for osteonecrosis in patients with systemic lupus erythematosus. Kaohsiung J Med Sci 15(12):697–703 (Dec) [PubMed]
169. Al-Mousawi F, Malki A, Al-Aradi A, Al-Bagali M, Al-Sadadi A, Booz MM (2002) Total hip replacement in sickle cell disease. Int Orthop 26(3):157–161 [PubMed]
170. Hickman JM, Lachiewicz PF (1997) Results and complications of total hip arthroplasties in patients with sickle-cell hemoglobinopathies. Role of cementless components. J Arthroplasty 12(4):420–425 (Jun) [PubMed]
171. Moran MC, Huo MH, Garvin KL, Pellicci PM, Salvati EA (1993) Total hip arthroplasty in sickle cell hemoglobinopathy. Clin Orthop Relat Res (294):140–148 (Sep) [PubMed]
172. Clarke HJ, Jinnah RH, Brooker AF, Michaelson JD (1989) Total replacement of the hip for avascular necrosis in sickle cell disease. J Bone Jt Surg Br 71(3):465–470 (May) [PubMed]
173. Hanker GJ, Amstutz HC (1988) Osteonecrosis of the hip in the sickle-cell diseases. Treatment and complications. J Bone Jt Surg Am 70(4):499–506 (Apr) [PubMed]
174. Lieberman JR, Fuchs MD, Haas SB, Garvin KL, Goldstock L, Gupta R et al (1995) Hip arthroplasty in patients with chronic renal failure. J Arthroplasty 10(2):191–195 (Apr) [PubMed]
175. Berend KR, Gunneson E, Urbaniak JR, Vail TP (2003) Hip arthroplasty after failed free vascularized fibular grafting for osteonecrosis in young patients. J Arthroplasty 18(4):411–419 (Jun) [PubMed]
176. Nam KW, Kim YL, Yoo JJ, Koo KH, Yoon KS, Kim HJ (2008) Fate of untreated asymptomatic osteonecrosis of the femoral head. J Bone Jt Surg Am 90(3):477–484 (Mar) [PubMed]
177. Steinberg ME, Bands RE, Parry S, Hoffman E, Chan T, Hartman KM (1999) Does lesion size affect the outcome in avascular necrosis? Clin Orthop Relat Res (367):262–271 (Oct) [PubMed]
178. Scribner AN, Troia-Cancio PV et al (2000) Osteonecrosis in HIV: a case control study. JAIDS 25(1):19–25 (Sept) [PubMed]
179. Gutierrez F, Padilla S et al (2002) Avascular necrosis of the bone in HIV infected patients. AID 16(3):481–483 (Feb) [PubMed]

Articles from HSS Journal are provided here courtesy of Springer-Verlag