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Avascular necrosis
Avascular necrosis
Avascular necrosis
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Avascular necrosis
Other namesOsteonecrosis,[1] bone infarction,[2] aseptic necrosis,[1] ischemic bone necrosis[1]
Femoral head showing a flap of cartilage due to avascular necrosis (osteochondritis dissecans). Specimen removed during total hip replacement surgery.
SpecialtyOrthopedics
SymptomsJoint pain, decreased ability to move[1]
ComplicationsOsteoarthritis[1]
Usual onsetGradual[1]
Risk factorsBone fractures, joint dislocations, high dose steroids[1]
Diagnostic methodMedical imaging, biopsy[1]
Differential diagnosisOsteopetrosis, rheumatoid arthritis, Legg–Calvé–Perthes syndrome, sickle cell disease[3]
TreatmentMedication, not walking on the affected leg, stretching, surgery[1]
Frequency~15,000 per year (US)[4]

Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply.[1] Early on, there may be no symptoms.[1] Gradually joint pain may develop, which may limit the person's ability to move.[1] Complications may include collapse of the bone or nearby joint surface.[1]

Risk factors include bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids.[1] The condition may also occur without any clear reason.[1] The most commonly affected bone is the femur (thigh bone).[1] Other relatively common sites include the upper arm bone, knee, shoulder, and ankle.[1] Diagnosis is typically by medical imaging such as X-ray, CT scan, or MRI.[1] Rarely biopsy may be used.[1]

Treatments may include medication, not walking on the affected leg, stretching, and surgery.[1] Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement.[1]

About 15,000 cases occur per year in the United States.[4] People 30 to 50 years old are most commonly affected.[3] Males are more commonly affected than females.[4]

Signs and symptoms

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In many cases, there is pain and discomfort in a joint which increases over time. It can affect any bone, and for in about half of affected people, multiple sites are damaged.[5]

Avascular necrosis most commonly affects the ends of long bones, such as the femur. Other common sites include the humerus (upper arm),[6][7] knees,[8][9] shoulders,[6][7] ankles and the jaw.[10]

Causes

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The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids.[1] Other risk factors include radiation therapy, chemotherapy, and organ transplantation.[1] Osteonecrosis is also associated with cancer, lupus, sickle cell disease,[11] HIV infection, Gaucher's disease, and Caisson disease (dysbaric osteonecrosis).[1][12] Bisphosphonates are associated with osteonecrosis of the mandible (jawbone).[13] The condition may also occur without any clear reason.[1]

Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not well understood.[14][15]

In children, avascular osteonecrosis can have several causes. It can occur in the hip as part of Legg–Calvé–Perthes syndrome,[16] and it can also occur as a result after malignancy treatment such as acute lymphoblastic leukemia and allotransplantation.[17]

Pathophysiology

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The hematopoietic cells are most sensitive to low oxygen and are the first to die after reduction or removal of the blood supply, usually within 12 hours.[2] Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12–48 hours, and that bone marrow fat cells die within 5 days.[2]

Upon reperfusion, repair of bone occurs in two phases. First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris.[2] Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts.[2] Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue.[2]

Diagnosis

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Front X-ray of right knee of an adolescent (epiphyseal plates are open): arrows point to avascular necrosis and developing osteochondritis dissecans in the outer medial condyle of femur

In the early stages, bone scintigraphy and MRI are the preferred diagnostic tools.[18][19]

X-ray images of avascular necrosis in the early stages usually appear normal. In later stages it appears relatively more radio-opaque due to the nearby living bone becoming resorbed secondary to reactive hyperemia.[2] The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts.[2] Late radiographic signs also include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity resulting from saponification and calcification of marrow fat following medullary infarcts.[citation needed]

  • Radiography of total avascular necrosis of right humeral head. Woman of 81 years with diabetes of long evolution.
    Radiography of total avascular necrosis of right humeral head. Woman of 81 years with diabetes of long evolution.
  • Radiography of avascular necrosis of left femoral head. Man of 45 years with AIDS.
    Radiography of avascular necrosis of left femoral head. Man of 45 years with AIDS.
  • Nuclear magnetic resonance of avascular necrosis of left femoral head. Man of 45 years with AIDS.
    Nuclear magnetic resonance of avascular necrosis of left femoral head. Man of 45 years with AIDS.
  • The intravertebral vacuum cleft sign (at white arrow) is a sign of avascular necrosis. Avascular necrosis of a vertebral body after a vertebral compression fracture is called Kümmel's disease.[20]
    The intravertebral vacuum cleft sign (at white arrow) is a sign of avascular necrosis. Avascular necrosis of a vertebral body after a vertebral compression fracture is called Kümmel's disease.[20]
  • Pathology of avascular necrosis, with a photograph of a cross-section of the involved bone at top left. The reactive zone shows irregular trebaculae with empty lacunae, and fibrosis of the marrow space.
    Pathology of avascular necrosis, with a photograph of a cross-section of the involved bone at top left. The reactive zone shows irregular trebaculae with empty lacunae, and fibrosis of the marrow space.

Types

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When AVN affects the scaphoid bone, it is known as Preiser disease. Another named form of AVN is Köhler disease, which affects the navicular bone of the foot, primarily in children. Yet another form of AVN is Kienböck's disease, which affects the lunate bone in the wrist.[21]

Treatment

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A variety of methods may be used to treat the disease,[5] with the most common being total hip replacement (THR). However, THRs have a number of downsides, including long recovery times and the lifespans of the hip joints (often around 20 to 30 years).[22] THRs are an effective means of treatment in the older population; however, in younger people, they may wear out before the end of a person's life.[22]

Other techniques, such as metal-on-metal resurfacing, may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head.[23] Bisphosphonates, which reduce the rate of bone breakdown, may prevent collapse (specifically of the hip) due to AVN.[24]

Core decompression

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Other treatments include core decompression, whereby internal bone pressure is relieved by drilling a hole into the bone, and a living bone chip and an electrical device to stimulate new vascular growth are implanted; and the free vascular fibular graft (FVFG), in which a portion of the fibula, along with its blood supply, is removed and transplanted into the femoral head.[25] A 2016 Cochrane review found no clear improvement between people who have had hip core decompression and participate in physical therapy, versus physical therapy alone. There is additionally no strong research on the effectiveness of hip core decompression for people with sickle cell disease.[11]

The disease's progression may be halted by transplanting nucleated cells from the bone marrow into avascular necrosis lesions after core decompression. However, much further research is needed to establish this technique.[26][27]

Prognosis

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The amount of disability that results from avascular necrosis depends on what part of the bone is affected, how large an area is involved, and how effectively the bone rebuilds itself. The process of bone rebuilding takes place after an injury as well as during normal growth.[23] Normally, bone continuously breaks down and rebuilds—old bone is resorbed and replaced with new bone. The process keeps the skeleton strong and helps it to maintain a balance of minerals.[23] In the course of avascular necrosis, however, the healing process is usually ineffective and the bone tissues break down faster than the body can repair them. If left untreated, the disease progresses, the bone collapses,[28] and the joint surface breaks down, leading to pain and arthritis.[1]

Epidemiology

[edit]

Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year.[citation needed]

Society and culture

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Cases of avascular necrosis have been identified in a few high-profile athletes. It abruptly ended the career of American football running-back Bo Jackson in 1991. Doctors discovered Jackson to have lost all of the cartilage supporting his hip while he was undergoing tests following a hip injury he had on the field during an 1991 NFL Playoff game.[29] Avascular necrosis of the hip was also identified in a routine medical check-up on quarterback Brett Favre following his trade to the Green Bay Packers in 1992.[30] However, Favre would go on to have a long career at the Packers.[citation needed]

Another high-profile athlete was American road racing cyclist Floyd Landis,[31] winner of the 2006 Tour de France, the title being subsequently stripped from his record by cycling's governing bodies after his blood samples tested positive for banned substances.[32] During that tour, Landis was allowed cortisone shots to help manage his ailment despite cortisone also being a banned substance in professional cycling at the time.[33]

Rafael Nadal successfully continued his tennis career after having surgery for Mueller–Weiss syndrome (osteonecrosis of the navicular bone in the foot).[34] YouTuber Steve Wallis has revealed that he has the condition in his hip.[where?]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Avascular necrosis

View on Grokipedia
from Grokipedia
Avascular necrosis, also known as osteonecrosis, is the death of tissue due to interrupted blood supply, leading to structural deterioration and potential collapse of the affected . It most commonly affects the of long s in weight-bearing s, with the being the primary site, though it can also involve the , , , or ankle. If untreated, the condition progresses through stages of weakening, microfractures, and eventual destruction, often culminating in secondary . The etiology of avascular necrosis includes both traumatic and non-traumatic factors, with non-traumatic causes accounting for the majority of cases and involving vascular compromise from fat emboli, , or . Common risk factors encompass prolonged use, excessive alcohol consumption, , and underlying conditions such as , systemic lupus erythematosus, , or infection. In the United States, the annual incidence is estimated at 10,000 to 20,000 new cases, representing over 10% of all surgeries, with higher prevalence among adults aged 30 to 50 years and a male predominance (approximately 8:1 ratio). Symptoms typically develop gradually and include persistent pain in the affected that worsens with or movement, accompanied by , limited , and limping in lower extremity involvement. Early diagnosis relies on imaging such as MRI, which detects changes before radiographic evidence appears, while advanced stages show bone collapse on X-rays. Treatment strategies vary by stage: conservative approaches in early phases involve rest, nonsteroidal anti-inflammatory drugs, , and bisphosphonates to alleviate pain and preserve function, whereas advanced disease often requires surgical interventions like core decompression, , , or total replacement. Emerging options, including regenerative therapies such as aspirate concentration and injections, aim to promote and delay progression, particularly in pre-collapse stages.

Overview

Definition and Classification

Avascular (AVN), also known as osteonecrosis or aseptic , is defined as the cellular death of bone components resulting from the interruption of blood supply to the subchondral bone. This condition leads to bone and structural compromise, most frequently affecting the , though it can involve other sites such as the humeral head, knees, shoulders, and ankles. The process typically progresses through stages of ischemia, , repair, and potential collapse, ultimately risking joint degeneration if untreated. AVN is broadly classified by into traumatic and atraumatic categories. Traumatic AVN arises from direct vascular disruption due to fractures, dislocations, or , often unilateral and linked to mechanical injury. Atraumatic AVN, comprising the majority of cases, is multifactorial and frequently bilateral (up to 70% in some series), associated with conditions like use, alcohol abuse, , systemic lupus erythematosus, or idiopathic origins. This etiological distinction guides prognosis and management, with atraumatic forms often progressing more insidiously. Staging systems for AVN, particularly of the , standardize assessment using clinical, radiographic, MRI, and sometimes scintigraphic findings to predict progression and inform treatment. The seminal Ficat and Arlet classification, originally proposed in 1964 and modified in 1985, delineates four stages: Stage 0 (preclinical, normal imaging but abnormal marrow biopsy); Stage I (normal radiographs, but MRI shows low-signal zones indicating or ); Stage II (radiographic sclerosis or cysts without ); Stage III (subchondral lucency or signifying fracture); and Stage IV ( flattening with secondary ). This system emphasizes early detection via advanced imaging for intervention before . The (Association Research Circulation Osseous) classification, first established in 1993 and revised in 2019, provides an international framework integrating multiple modalities for greater reproducibility. It includes five stages: Stage 0 (normal all imaging); Stage I (normal s, but MRI reveals delineated by low-signal bands); Stage II ( shows focal sclerosis, cysts, or osteophytes without , subdivided by : A <15%, B 15-30%, C >30% of head surface); Stage III (subchondral line on or CT, with subtypes); and Stage IV (collapse >2 mm or head depression >3 mm, plus ). The subtyping in ARCO enhances prognostic value, as larger lesions correlate with higher collapse risk. Other systems, like (), mirror Ficat but quantify extent more precisely, though ARCO is increasingly favored for its multimodal approach and interobserver reliability.

Epidemiology

Avascular necrosis (AVN), also known as osteonecrosis, is a relatively uncommon condition in the general population, with an estimated annual incidence ranging from 1.4 to 3.0 cases per 100,000 individuals in regions such as the United Kingdom. In the United States, approximately 10,000 to 20,000 new cases are diagnosed each year, predominantly involving the femoral head. Incidence rates vary geographically; for example, reports from Korea indicate 28.9 cases per 100,000 population, while Japan reports a lower rate of 1.9 per 100,000. These differences may reflect variations in diagnostic practices, risk factor exposure, or population genetics. The femoral head is the most frequently affected site, accounting for about 80% of cases, followed by the humeral head, knee, and talus. Demographically, AVN predominantly affects adults in their third to fifth decades of life, with a peak incidence between ages 30 and 50 years. The condition is more common in males, with a male-to-female ratio of approximately 2:1 to 3:1, though this disparity may be influenced by higher rates of risk factors like alcohol consumption in men. There is no strong racial predilection in the general population, but AVN associated with shows increased prevalence among individuals of African descent due to the higher incidence of hemoglobinopathies. In older adults, such as those over 60 in , the 10-year risk of osteonecrosis is about 0.40%, rising slightly in women to 0.49%. Prevalence is challenging to estimate due to asymptomatic cases detected incidentally on imaging, but studies suggest an overall prevalence of nontraumatic femoral head AVN around 0.7% in selected populations. In high-risk groups, such as patients with systemic lupus erythematosus (SLE), prevalence can reach 31.5 to 34.2 per 1,000, with an incidence of 8.4 to 9.8 per 1,000 person-years. Similarly, in inflammatory bowel disease cohorts, the risk of AVN is elevated compared to the general population (adjusted hazard ratio 1.42). These elevated rates underscore the role of underlying conditions and treatments, such as corticosteroid use, in driving AVN epidemiology beyond the baseline population risk.

Clinical Presentation

Signs and Symptoms

Avascular necrosis (AVN), also known as osteonecrosis, frequently manifests with in the affected , which is often the initial and most prominent symptom. This typically begins insidiously during activities or movements that stress the , such as walking or stairs, and may radiate to adjacent areas depending on the site of involvement. For instance, when the is affected—the most common location— is commonly felt in the , , or buttock. In the early stages of AVN, many individuals experience no symptoms, allowing the condition to progress undetected until damage becomes more extensive. As the disease advances, intensifies and becomes more persistent, often occurring even at rest or during non-weight-bearing activities like lying down. Additional signs include stiffness, limited due to and mechanical dysfunction, and a noticeable or alteration in to avoid stressing the affected area. These symptoms can vary in severity and may mimic other musculoskeletal disorders, such as or fractures, necessitating thorough clinical evaluation. While the is the primary site, AVN can affect other weight-bearing joints like the , , or ankle, leading to localized and functional limitations in those regions. In bilateral cases, which occur in 50% to 80% of patients (particularly in atraumatic etiologies), symptoms may appear symmetrically on both sides. The progression from onset to significant can span months to over a year, with severity correlating to the extent of . Early recognition of these signs is crucial, as timely intervention can potentially halt progression.

Etiology

Causes

Avascular necrosis (AVN), also known as osteonecrosis, results from the interruption or reduction of blood supply to the , leading to . This vascular compromise can occur through direct or indirect mechanisms that damage blood vessels or increase intraosseous pressure. Traumatic causes are among the most straightforward etiologies, where physical damage directly disrupts blood flow. For instance, fractures or dislocations of the , particularly femoral neck fractures, can compress or sever the supplying arteries, with AVN occurring in up to 30% of displaced femoral neck fractures in some studies. Joint trauma from high-impact injuries, such as those in athletes or accident victims, similarly impairs vascular integrity. for cancers near sites can also induce vascular damage as a traumatic-like effect, leading to secondary AVN. Non-traumatic causes often involve systemic factors that indirectly compromise bone perfusion. Prolonged high-dose use, common in treatments for autoimmune diseases or organ transplants, is a leading culprit; it promotes fat emboli, lipid deposition in vessels, and , with AVN risk rising after cumulative doses exceeding 2,000 mg of . Excessive alcohol consumption contributes via , fatty liver, and increased marrow fat that elevates intraosseous pressure and obstructs sinusoidal vessels. Certain medical conditions heighten susceptibility through hypercoagulability or vaso-occlusive effects. causes AVN in 10-20% of patients due to sickled red blood cells blocking small vessels, particularly in the . Systemic lupus erythematosus (SLE), often treated with steroids, independently raises risk via antiphospholipid antibodies that promote thrombosis. Other associations include , where lipid accumulation in marrow impairs circulation, with , infection potentially through immune dysregulation or antiretroviral drugs, and in divers from nitrogen bubble embolization. has also been implicated in rare cases via vascular toxicity. In approximately 20-30% of cases, no identifiable cause is found, termed idiopathic AVN, though genetic predispositions like in thrombophilic genes may play a role in these instances. Overall, the multifactorial nature underscores the importance of addressing modifiable risks to prevent progression.

Risk Factors

Avascular necrosis (AVN), also known as osteonecrosis, is associated with several risk factors that can disrupt blood supply to the , leading to . These factors are broadly categorized into traumatic and nontraumatic causes, though many cases are multifactorial. Long-term use of corticosteroids is one of the most significant risk factors, implicated in 10-30% of cases in retrospective studies, as they can induce fat emboli, hyperlipidemia, and apoptosis of osteocytes, thereby compromising vascular integrity. Excessive alcohol consumption ranks as a top modifiable risk factor, promoting fatty infiltration of the bone marrow and increasing intraosseous pressure, which hinders perfusion; heavy drinkers are particularly susceptible. Smoking is also a key modifiable risk factor, as it narrows blood vessels and reduces blood flow to the bone. Trauma, such as fractures or dislocations of the , accounts for a substantial portion of cases by directly damaging blood vessels supplying the . Certain medical conditions elevate risk through mechanisms like vaso-occlusion or chronic inflammation; for instance, causes red blood cell sickling that blocks small vessels, while systemic often co-occurs with steroid therapy. Other hematologic disorders, including and , contribute via lipid accumulation or affecting bone vasculature. Hyperlipidemia, whether primary or induced by steroids or alcohol, leads to fat emboli obstructing nutrient arteries in the . Infections like increase susceptibility, potentially through associated immune dysregulation or antiretroviral therapies that mimic steroid effects. , , and (as in divers) are additional risks, often linked to hypercoagulability or fat globule formation. and for malignancies can also precipitate AVN by damaging endothelial cells and promoting . Idiopathic cases, lacking identifiable risks, comprise up to 20-30% of osteonecrosis occurrences, highlighting gaps in understanding.

Pathophysiology

Avascular necrosis (AVN), also known as osteonecrosis, results from the interruption of blood supply to the bone, leading to ischemia and death of osteocytes and surrounding tissues. The condition primarily affects bones with limited vascular redundancy, such as the , which relies on a single retinacular arterial supply, making it susceptible to even minor disruptions. The underlying mechanisms can be categorized into three main pathways: direct vascular injury, intravascular occlusion, and extravascular compression. Direct injury occurs from trauma or fractures that damage vessels. Intravascular occlusion involves blockage by thrombi, emboli (often associated with use or lipid disorders), or sickled red cells in conditions like . Extravascular compression arises from increased intraosseous pressure due to adipocyte hypertrophy from or steroids, or from edema. The ischemic process begins with hypoxia, causing within 2 to 3 hours of anoxia. This is followed by death of hematopoietic cells and adipocytes, leading to marrow and an inflammatory response with infiltration of neutrophils and macrophages. As the bone attempts repair, forms, but the necrotic subchondral bone weakens, resulting in microfractures, sclerosis, and eventual collapse under mechanical stress. This structural failure deforms the surface, accelerating degeneration and secondary . Without intervention, the disease progresses over months to years, with early histologic changes visible 24 to 72 hours after ischemia onset.

Diagnosis

Clinical Evaluation

Clinical evaluation of avascular necrosis (AVN), also known as osteonecrosis, begins with a thorough to identify symptoms and potential risk factors. Patients often report insidious onset of joint pain, typically in weight-bearing areas such as the , where discomfort may localize to the , thigh, or buttock; pain is initially activity-related but can become constant and severe as the disease progresses. Early stages may be , with symptoms emerging only after collapse occurs. History taking emphasizes risk factors, including long-term use, excessive alcohol consumption, trauma, tobacco use, and underlying conditions like , systemic lupus erythematosus, or , which disrupt blood supply to the . A family history of similar issues or prior decompression procedures may also be noted, as AVN can be bilateral in up to 50% of cases. Non-traumatic presentations often involve mechanical pain of variable severity that is difficult to localize precisely. Physical examination focuses on the affected , starting with observation of , which may show an antalgic limp due to pain avoidance. Palpation can reveal tenderness over the , while testing demonstrates stiffness and pain, particularly with internal rotation, abduction, and extension in hip AVN; forced internal rotation is especially provocative. Limited joint mobility and secondary to disuse are common, with no systemic signs like fever unless an underlying condition is present. Special maneuvers, such as the log roll test for the , may elicit pain by stressing the . These clinical findings raise suspicion for AVN, particularly when corroborated by risk factors, prompting further diagnostic imaging to confirm the diagnosis and stage the disease; laboratory tests are generally nonspecific but may evaluate for associated conditions like hyperlipidemia or coagulopathies. Differential considerations include osteoarthritis, stress fractures, or transient osteoporosis, underscoring the need for integrated history and exam assessment.

Imaging and Staging

Imaging for avascular necrosis (AVN), also known as osteonecrosis, of the relies on multiple modalities to detect disease presence, extent, and progression, with (MRI) serving as the gold standard due to its high exceeding 90-99% for early detection. Plain is typically the initial imaging tool, offering low cost and accessibility, but it lacks sensitivity for preclinical stages, often appearing normal until subchondral occurs in later disease. Characteristic radiographic findings in advanced AVN include femoral head sclerosis, cystic changes, the indicating subchondral fracture, and eventual flattening or . Computed tomography (CT) provides superior bone detail compared to radiography, aiding in the assessment of subchondral fractures and , though its sensitivity for early marrow changes is lower than MRI, around 55-92% in reported studies. , using , detects increased uptake from repair processes with high sensitivity (up to 97%) but lower specificity due to overlap with other conditions like fractures or tumors. has limited utility in adults for AVN evaluation, primarily used in pediatric cases to assess . MRI excels in delineating early ischemic changes, such as , geographic patterns, and the double-line sign representing necrotic bone margins, with reported sensitivity of 88-100% and specificity near 100%. It also quantifies size and location, crucial for and treatment planning, and is recommended as the first-line advanced imaging by the American College of Radiology for suspected osteonecrosis. Advanced MRI sequences, like contrast-enhanced or diffusion-weighted imaging, further improve characterization but are not routinely required. Staging systems for AVN standardize disease progression to guide management, with the Ficat and Arlet classification being one of the earliest and most widely adopted, originally described in and modified in 1985. This system integrates clinical, radiographic, scintigraphic, and MRI findings into five stages:
StageDescriptionKey Imaging Features
0Preclinical; normal clinically and radiographicallyNormal ; abnormal only
IEarly; possible pain, normal Normal ; abnormal MRI (marrow edema) or (cold spot)
IIRadiographic abnormalities without collapseSclerosis, cysts, or osteophytes on ; MRI shows demarcation
IIISubchondral collapse or subchondral fracture on /MRI
IVAdvanced; secondary flattening, joint space narrowing on
The Steinberg classification, developed in the 1990s, expands on Ficat by incorporating lesion size (A: <15%, B: 15-30%, C: >30% of ) and uses a six-stage system based on and MRI to better predict risk.
StageDescriptionKey Features
INormal Abnormal MRI or
IINo Cystic/sclerotic changes on /MRI
IIIEarly Subchondral <15% (A), 15-30% (B), >30% (C)
IVAdvanced Flattening >15% (A), etc.
V space narrowingSecondary OA changes
VITotal destructionSevere OA
The revised Association Research Circulation Osseous (ARCO) system from 2019 provides a modern framework for non-traumatic osteonecrosis of the femoral head, focusing on imaging findings across four stages to improve interobserver reliability. It is MRI-centric for early stages. Stage 1: normal X-ray but positive MRI (e.g., low-signal band); Stage 2: abnormal X-ray (e.g., osteosclerosis or cystic changes) without subchondral fracture or collapse; Stage 3: subchondral fracture with femoral head depression ≤2 mm (3A) or >2 mm (3B); Stage 4: osteoarthritis with joint space narrowing or acetabular changes. Lesion size (small <15%, moderate 15-30%, large >30%) and location (medial, central, lateral), which influence prognosis, are classified separately using the 2021 ARCO system for pre-collapse osteonecrosis, as they predict progression risk.

Management

Nonsurgical Treatments

Nonsurgical treatments for avascular necrosis (AVN), also known as osteonecrosis, focus on symptom relief, preservation of function, and delaying disease progression, particularly in early stages (pre-collapse) of the , the most common site affected. follows staging systems like Ficat or , with guidelines recommending conservative measures for early stages. These approaches are often recommended for patients with small necrotic lesions or those unsuitable for surgery, though evidence for long-term efficacy remains limited and variable across studies. Specifically for symptomatic stage 1 femoral head necrosis, options like medications, physical therapy, and extracorporeal shock wave therapy exist but have weaker evidence for effectiveness in preventing progression compared to decompression surgery; meta-analyses report success rates of 40–61% for conservative treatments versus 66–84% for core decompression. Primary strategies include conservative measures, pharmacological interventions, and biophysical modalities, with outcomes generally better when initiated early. Conservative management emphasizes protective weight-bearing to minimize mechanical loading on the affected , typically through the use of crutches, walkers, or canes for 6–12 months or longer, combined with activity modification to avoid high-impact exercises. This approach reduces intraosseous pressure and may help maintain structural integrity in Ficat stage I or II AVN, though it does not reverse necrosis and is most effective as an adjunct to other therapies. plays a supportive role by incorporating low-impact exercises, such as or stationary , to improve , strengthen hip stabilizers, and prevent without exacerbating symptoms. Studies indicate that such non-pharmacological measures can alleviate and improve function in up to 50% of early-stage cases, but progression to collapse occurs in 70–80% without additional intervention. Pharmacological treatments target pain control and bone remodeling. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or celecoxib, are commonly prescribed to manage and inflammation, providing symptomatic relief but no disease-modifying effects. Bisphosphonates, like alendronate or , inhibit activity to reduce and have shown promise in early AVN; a randomized trial demonstrated that alendronate (70 mg weekly for one year) delayed femoral head collapse and reduced the need for total hip arthroplasty in 60% of stage II patients at 5-year follow-up compared to controls. Other agents, including statins (e.g., ) for lipid-related cases or vasodilators like , aim to improve vascular supply, with meta-analyses reporting improved Harris Hip Scores and reduced progression rates in select cohorts. However, side effects such as gastrointestinal issues or limit widespread use, and long-term data are inconsistent. Biophysical therapies offer non-invasive options to enhance and repair. Extracorporeal shock wave (ESWT) delivers high-energy acoustic waves to stimulate and bone regeneration; clinical trials report pain reduction and improved function in 70–90% of early-stage AVN patients, with studies showing delayed collapse in treated hips compared to controls after 2 years. Pulsed electromagnetic field (PEMF) modulates cellular repair via electromagnetic stimulation, yielding similar benefits in small series, including decreased size on MRI in stage I . (HBOT), involving 100% oxygen at 2.5 atmospheres for 20–30 sessions, promotes neovascularization and has been associated with clinical improvement and radiographic stability in pre-collapse AVN, with a indicating success rates of 80–90% in avoiding surgery at 5 years. Emerging biologics, such as (PRP) injections, concentrate growth factors to support tissue repair; case series describe pain relief and functional gains in advanced stages, though randomized evidence is preliminary and shows variable outcomes. These modalities are generally safe but require specialized equipment, and their efficacy is best in combination with conservative care.

Surgical Interventions

Surgical interventions for avascular necrosis (AVN) of the are primarily indicated when conservative treatments fail or in cases of progression, aiming to preserve function in early stages or restore mobility in advanced stages. These procedures are tailored to the stage, with joint-preserving techniques preferred for pre-collapse lesions (Ficat stages I-II) to alleviate intraosseous pressure, promote , and prevent femoral head collapse, while total replacement is reserved for collapsed or end-stage (stages III-IV). Outcomes vary by stage and technique, with success rates for preservation ranging from 60-80% in early AVN, though conversion to occurs in 20-40% of cases over 5-10 years. Core decompression is the most common joint-preserving surgery for early-stage AVN and demonstrates stronger evidence of effectiveness compared to conservative treatments, such as medications, physical therapy, and extracorporeal shock wave therapy, particularly for symptomatic stage 1 femoral head necrosis in preventing disease progression. It involves drilling into the to reduce elevated intramedullary pressure and facilitate flow restoration. It is typically performed via a single or multiple small-diameter tunnels (3-8 mm) using fluoroscopic guidance, often in stages I-II where the remains intact. When combined with autologous or cancellous , success rates improve to approximately 70-85% in delaying collapse, with pain relief achieved in over 80% of patients at 2-year follow-up. However, without adjuncts, about 38% of patients may progress to total arthroplasty within 2-3 years. Bone grafting techniques, either non-vascularized or vascularized, augment core decompression by providing structural support and osteogenic cells to the necrotic area. Non-vascularized grafts, such as autologous bone or allografts packed into the decompression tract, are used in pre-collapse AVN to fill defects and promote , yielding survival rates of 70-90% at 5 years in small lesions (<30% head involvement). Vascularized free fibular grafting, involving transfer of a vascularized bone segment (e.g., fibula) with microvascular anastomosis, is more complex but restores blood supply effectively in larger lesions, with 70-80% joint survival at 10 years and reduced collapse rates compared to non-vascularized methods. These procedures are contraindicated in advanced collapse due to poor graft integration. Proximal femoral osteotomy, including rotational (e.g., transtrochanteric anterior or posterior) or varus types, realigns the femoral head to shift the necrotic segment away from weight-bearing zones, preserving the joint in young, active patients with early-to-moderate AVN. Indications include stages II-III with viable bone stock and lesion size allowing rotation (typically <30% head involvement), performed via curved or spherical cuts fixed with plates. Long-term outcomes show 70-85% survival free of arthroplasty at 10 years, with improved Harris Hip Scores (average 85-90 points) and low complication rates (e.g., 5-10% nonunion), though technical demands limit its widespread use. Arthroscopy-assisted core decompression represents a minimally invasive evolution, combining hip arthroscopy to address intra-articular pathology (e.g., labral tears, synovitis) with percutaneous drilling and grafting. Indicated for early AVN with concomitant soft-tissue issues, it allows direct visualization, reducing iatrogenic damage and enabling staged treatment. Studies report excellent patient-reported outcomes, with low collapse rates (10-20%) and high satisfaction (over 90%) at 2-5 years, particularly when bone marrow concentrate is injected. This approach is not suitable for advanced collapse. For advanced AVN with subchondral collapse, femoral head deformity, or secondary , total hip arthroplasty (THA) provides reliable pain relief and functional restoration using uncemented or cemented implants. It is the standard for stages III-IV, especially in older patients or those with extensive necrosis (>50% head involvement), with 10-year implant survival rates of 90-95% for aseptic loosening and overall function (Harris Hip Score >90). Compared to cases, THA in AVN shows similar functional gains but slightly higher revision risks (e.g., 5-10% at 10 years due to periprosthetic issues), particularly in younger patients (<50 years). Complications include (1-2%) and (3-5%), mitigated by modern designs.

Emerging Therapies

Emerging therapies for avascular necrosis (AVN) primarily focus on regenerative strategies to restore blood supply, promote bone repair, and delay disease progression, particularly in early stages. These approaches leverage advances in biology, biophysical interventions, and to address the limitations of traditional core decompression and joint replacement. Recent clinical evidence indicates that combining these therapies with established techniques yields superior outcomes in pain relief, functional improvement, and joint preservation compared to alone. Stem cell therapies, especially those using bone marrow-derived mesenchymal s (BM-MSCs), represent a cornerstone of emerging treatments. Autologous BM-MSCs are harvested, concentrated, and injected into the necrotic , often alongside core decompression to enhance and osteogenesis. A 2025 of randomized controlled trials demonstrated that BM-MSC combined with core decompression significantly improved Harris Hip Scores by an average of 15-20 points at 12-24 months follow-up, with a treatment below 20% in Ficat stages I-II, outperforming core decompression alone. These cells differentiate into osteoblasts and secrete growth factors like (VEGF), fostering . However, alone shows limited efficacy without mechanical support, as evidenced by a 2025 reporting higher progression rates in isolated injections. Ongoing trials explore induced pluripotent stem cells (iPSCs) for scalable, patient-specific regeneration, though clinical translation remains preclinical. Biophysical modalities such as extracorporeal shock wave therapy (ESWT) have gained traction for their non-invasive promotion of neovascularization and modulation. High-energy ESWT stimulates mechanotransduction pathways, upregulating VEGF and bone morphogenetic proteins (BMPs) to repair necrotic tissue. A 2023 dose-response study in early-stage AVN patients ( I-II) found that 2000-3000 shocks per session, administered weekly for 3-5 weeks, reduced scores by 40-60% and improved hip function at 12 months, with radiographic of regression in 70% of cases. When combined with stem cells, ESWT enhances cell proliferation and migration, as shown in a 2024 analysis where it boosted MSC osteogenic differentiation by 2-3 fold via core-binding factor alpha-1 upregulation. ESWT is particularly promising for patients unsuitable for , with low complication rates under 5%. Precision surgical innovations, including 3D-navigated core decompression, optimize targeting of necrotic areas while minimizing bone loss. Utilizing preoperative CT-based and intraoperative computer navigation, this technique allows for accurate drilling paths, reducing operative time by up to 30% and exposure. A 2024 Yale study reported successful delivery of BM-MSC injections to the necrotic region in 30 of 31 early AVN cases using 3D-guided decompression, allowing immediate post-surgery. Long-term data from a 2025 follow-up of 3D-printed guide-assisted procedures confirmed sustained survival rates above 80% at 10 years in pre-collapse stages. Pharmacological adjuncts are emerging to enhance homing and efficacy. Simvastatin, a , activates the Rho/ROCK pathway to mobilize MSCs toward hypoxic lesions, increasing local concentrations by 2-4 fold in animal models of necrosis. This approach, tested in 2025 preclinical studies, delayed AVN progression without systemic side effects when delivered locally. Exosome-based therapies offer a cell-free alternative by harnessing extracellular vesicles from s or immune cells to modulate the microenvironment. M2 macrophage-derived exosomes inhibit and , promoting osteogenesis in ONFH models; a 2025 study showed they restored by 50% in rat s via anti-inflammatory signaling. Similarly, magnesium-preconditioned BMSC exosomes enhanced and repair in 2025 experiments, with VEGF expression upregulated 3-fold. These acellular agents avoid immunogenicity risks of live cells and are entering phase I trials for targeted delivery in early AVN.

Outcomes

Prognosis

The prognosis of avascular necrosis (AVN) is generally poor if left untreated, with the majority of cases progressing to bone collapse, persistent pain, debilitation, and secondary , often necessitating joint replacement surgery. In lesions, approximately 59% progress to symptomatic disease or collapse over time. Untreated AVN leads to irreversible bone destruction due to disrupted blood supply, resulting in joint deformity and severe , particularly in weight-bearing sites like the . Factors such as lesion size, location, and patient age significantly influence outcomes, with smaller lesions (<25% of the surface) in younger patients showing better preservation potential. Early diagnosis and intervention markedly improve prognosis, especially in pre-collapse stages (e.g., Ficat stages I-II or stages I-III). Joint-preserving procedures like core decompression can halt progression in 60-80% of early cases, delaying the need for total hip (THA) by several years. However, in advanced stages (III-IV), occurs in over 90% of cases, leading to rapid functional decline and high rates of surgical intervention. Long-term outcomes post-treatment are favorable with THA, which is the definitive option for collapsed AVN, achieving 10-year implant survival rates of 93.9-98.9% for aseptic loosening and major revisions. For specific procedures like transtrochanteric rotational in early-to-moderate AVN, 5- and 10-year hip survival rates reach 89-90%, though results are slightly lower in non-Asian populations due to demographic differences in bone quality and etiology. Complications such as recurrent , , or prosthesis failure occur in 5-10% of THA cases for AVN, higher than in alone, underscoring the need for vigilant follow-up. Overall, while early management preserves native joints in select patients, advanced AVN often results in lifelong without .

Complications

Avascular necrosis (AVN) can lead to progressive deterioration if left untreated, ultimately resulting in structural collapse of the affected , most commonly the . This collapse occurs as necrotic tissue weakens the 's integrity, leading to and in the . A primary long-term complication is the development of secondary , where the loss of smooth and subchondral deformation causes chronic pain, stiffness, and reduced mobility. In the hip, this often progresses to severe degenerative changes requiring total replacement to restore function. Fragmentation of necrotic bone can also occur, releasing debris into the space and exacerbating , , and further cartilage damage. Patients may experience worsening symptoms such as limping, restricted , and significant , particularly in weight-bearing joints like the or . Treatment-related complications, especially following surgical interventions like core decompression or , include infection at the surgical site, implant loosening or malfunction, and neurovascular injury. These risks are heightened in AVN patients compared to those undergoing primary procedures, potentially necessitating revision surgeries.

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