ORTHOPAEDICS Osteonecrosis of the femoral head

Osteonecrosis of the femoral head Diagnosing and treating a rare condition

BY PAUL HOOGERVORST, MD, AND EDWARD CHENG, MD

Osteonecrosis (also known as avascular necrosis, aseptic necrosis, ischemic necrosis, and atraumatic/non-traumatic necrosis) is characterized as a bone infarct with dead osteocytes due to numerous possible etiologies. While the exact pathophysiology is unknown, etiologic risk factors most often are corticosteroids, ethanol, trauma, and diseases such as lupus erythematosus (SLE) and sickle cell disease. The final common pathway most likely involves a compromised blood supply to the osteocyte with loss of normal bone remodeling. This often occurs adjacent to a joint surface, resulting in subchondral fracture with bony collapse and cartilage delamination leading to disabling osteoarthritis. Although any bone can be affected, the most frequently affected sites are the femoral head, proximal humerus, distal femur, proximal tibia, ankle, elbow, lunate (Kienbock’s disease), navicular (Köhler’s disease or Mueller Weiss syndrome) and metatarsals (Freiberg’s disease).

Epidemiology

Osteonecrosis of the femoral head (ONFH) has an incidence of 10,000 to 30,000 new cases annually in the US. It is estimated that 5%–12% of all total

hip arthroplasties (THA) are performed because of ONFH. Although most hip arthroplasties are performed for degenerative joint disease in older individuals, osteonecrosis often affects younger adults, which is especially problematic as joint replacements at this age are not durable enough to last a lifetime.

Pathophysiology

Traumatic ONFH can be a sequela of childhood disorders such as slipped capital femoral epiphysis, or secondary to events such as hip dislocation or displaced femoral neck fractures. Disruption of the arterial vasculature supplying the femoral head causes ischemia. Non-traumatic ONFH, however, is not secondary to a mechanical injury but instead related to various biologic insults that are not completely understood. Proposed explanations include intraosseous adipocyte hypertrophy compressing marrow microcirculation (steroids, ethanol), direct cellular toxicity (chemotherapy, radiation therapy, smoking), and coagulopathic states (pregnancy, sickle cell crises, thrombophilia, and hypofibrinolysis). Studies have clearly shown presence of an elevated intraosseous pressure, perhaps due to marrow fat hypertrophy or inflammatory response.

Of the known factors associated with ONFH, glucocorticoids and alcohol exposure are the most common. Although several studies have shown a dose-dependent relationship between glucocorticoid exposure and osteonecrosis, a threshold dose for developing osteonecrosis is unknown. However, the relative risk for developing osteonecrosis is 4.5 times greater for every 10 mg increase in oral steroids for renal transplant patients and 1.3 times greater for every 20 mg increase in the non-transplant population. There is some evidence to show that even a short oral course of steroids for less than one week (methylprednisolone dose >300 mg) subjects individuals to a tenfold higher risk for having osteonecrosis. It is important to discuss this side effect with patients when prescribing these types of medications.

Other risk factors for ONFH are sickle cell disease, SLE, acute lymphoblastic leukemia, Caisson disease, Gaucher’s disease, and HIV. However, in some patients it is idiopathic as a clearly identifiable risk factor is absent.

Symptoms

Treatment outcomes are better when performed in the early stage of disease, yet this is difficult as most patients are asymptomatic at this time. Therefore, it is imperative to maintain a high level of suspicion in high-risk groups. Treatment is directed at preventing femoral head subchondral fracture and collapse, thereby preserving the native joint. Once subchondral fracture occurs, disabling osteoarthritis almost always ensues.

Pain, of varying intensity, is the most common presenting symptom in ONFH. It is experienced in the groin, thigh, or buttock and may be related to weight bearing or activity. Approximately two-thirds of patients endorse pain at rest and one-third acknowledge night pain.

Findings during physical examination are largely nonspecific. In later stages of disease, once a subchondral fracture develops, a limp may be present and exam findings are similar to any patient with end-stage arthritis. These commonly are a limited, painful range of motion, particularly during internal rotation and abduction.

Imaging

As history and physical examination are not diagnostic, imaging studies are essential. Magnetic resonance imaging (MRI) is the best study to detect or rule out osteonecrosis. Plain radiographs (XR) may demonstrate sclerotic and cystic areas within the femoral head with subchondral fracture, but often are normal.

Once a subchondral fracture occurs, a thin lucency beneath the joint surface is evident and this heralds the onset of later stages of disease. This so-called “crescent sign” is best visualized on the lateral frog leg hip view as the bony infarct is usually in the anterior and superior segment of the femoral head. A single anterior-posterior (AP) hip view is insufficient.

Detecting a subchondral fracture is important for assessing disease stage and determining treatment and best imaged using computed tomography (CT). In symptomatic patients with known ONFH, if XR’s do not show the subchondral fracture, CT should be obtained. Once collapse ensues, i.e., compaction of the necrotic bone, the femoral head loses its spherical contour and does not rotate freely in the acetabular socket, causing irreversible osteoarthritic changes. ONFH is bilateral in approximately 70% of patients, so imaging of the contralateral side should be obtained. CD is two-fold. First, it is thought to reduce the intraosseous pressure in the femoral head, thereby providing analgesia. Second, by opening up the osteonecrotic lesion, the healing response may stimulate local vascularity, thereby facilitating osteoprogenitor cell ingrowth. Despite this theoretical benefit, many patients will progress to develop a subchondral fracture. Therefore, many biological and mechanical adjuncts to CD have been proposed and investigated. These range from vascularized and non-vascularized bone allografts and autografts, growth factors with bone morphogenic protein (BMP), and stem cell grafting harvested from either bone marrow aspiration or other sites. To achieve immediate structural support, porous tantalum rods and polymethylmethacrylate cement (PMMA) augmentation have been trialed with meager success. CD with or without augmentation by one of the aforementioned options (except the vascularized bone allograft) is a relatively safe and simple procedure and does not negatively influence the technical aspect of performing a future total hip arthroplasty.

Any lesion with subchondral collapse or arthritis. Once collapse of the femoral head has occurred, the potential benefit from CD is minimal and attempts at restoration of the native joint surface have not been successful. The exact pathophysiology is unknown.

Besides detection, MR imaging provides additional information for staging and prognosis such as quantifying the extent of the osteonecrotic lesion and evaluating treatment efficacy.

Osteonecrosis of the femoral head to page 344

Classifications

There have been many classification systems for osteonecrosis, however, the most important prognostic variables predicting a poorer outcome are the presence of a subchondral fracture, a larger size (extent of disease), and the location of the necrotic bone in the weight bearing, lateral portion of the femoral head where the mechanical compressive forces are highest. The most widely used classification systems, such as the Association Research Circulation Osseous (ARCO) system, include these variables.

Treatment strategies

There is no known treatment that is universally effective in either controlling or curing this disease. Larger lesions tend to have poorer prognosis and warrant treatment.

Small osteonecrotic lesions. In symptomatic patients with small osteonecrotic lesions, the large majority will remain pain free for many years and intervention may be deferred. If patients with small lesions have pain, alternative pathologies should be considered. Non-operative management, such as pain control and adaptations in weightbearing, are ineffective.

Larger osteonecrotic lesions without subchondral fracture. The goal of surgical treatment in the early stages of ONFH is the prevention of subchondral fracture and subsequent collapse. This is attempted by pursuing biological pathways that reconstitute the bone architecture in the lesion or by offering immediate structural support.

The most commonly employed treatment for pre-collapse disease is core decompression (CD). The evidence for pain reduction is stronger than for preventing a subchondral fracture. The theoretical benefit of

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