Avascular necrosis (also osteonecrosisbone infarction[1]aseptic necrosisischemic bone necrosis[2], and AVN) is a disease where there is cellular death (necrosis) of bone components due to interruption of the blood supply.[3] Without blood, the bone tissue dies and the bone collapses.[2] If avascular necrosis involves the bones of a joint, it often leads to destruction of the joint articular surfaces (see Osteochondritis dissecans).




There are many theories about what causes avascular necrosis. Proposed risk factors includealcoholism,[4] excessive steroid use,[5] post trauma,[6][7] caisson disease (decompression sickness),[8][9] vascular compression,[10] hypertensionvasculitisarterial embolism andthrombosis, damage from radiationbisphosphonates (particularly the mandible),[11] sickle cell anaemia,[12] Gaucher's Disease,[13] and deep diving.[14] In some cases it is idiopathic (no cause is found).[15] Rheumatoid arthritis and lupus are also common causes of AVN. 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.

Cell death and repair

The hematopoietic cells are most sensitive to anoxia and are the first to die after reduction or removal of the blood supply, usually within 12 hours.[1] Experimental evidence suggests that bone cells (osteocytesosteoclastsosteoblasts etc.) die within 12-48 hours, and that bone marrow fat cells die within 5 days.[1]

Upon reperfusion, repair of ischemic bone occurs in 2 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.[1] Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts.[1] Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue.[1]


While it can affect any bone, and half of cases show multiple sites of damage, avascular necrosis primarily affects the joints at the shoulder,knee, and hip.

Clinical avascular necrosis most commonly affects the ends (epiphysis) of long bones such as the femur (the bone extending from the knee joint to the hip joint). Other common sites include the humerus (the bone of the upper arm),[16][17] knees,[18][19] shoulders,[16][17] ankles and the jaw.[20] The disease may affect just one bone, more than one bone at the same time, or more than one bone at different times.[21]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. When it occurs in children at the femoral head, it is known as Legg-Calvé-Perthes syndrome.[22]


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

Orthopaedic doctors most often diagnose the disease except when it affects the jaws, when it is usually diagnosed and treated by dental and maxillofacial surgeons.

In the early stages, bone scintigraphy[23] and MRI[24] are the diagnostic modalities of choice.

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.[1] The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts.[1] 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.


Avascular necrosis is especially common in the hip joint. A variety of methods are now used to treat avascular necrosis,[21] the most common being the total hip replacement, or THR. However, THRs have a number of downsides including long recovery times and short life spans. THRs are an effective means of treatment in the geriatric population, however doctors shy away from using them in younger patients due to the reasons above. A new, more promising treatment is hip resurfacingor metal on metal (MOM) resurfacing. It is a form of a THR, however in this procedure, only the head of the femur is removed as opposed to a THR in which the entire neck is removed. MOM resurfacing is still experimental in America but has been endorsed in Great Britain as an excellent alternative to a THR. A MOM Resurfacing may not be suitable in all cases of Avascular Necrosis, its suitability depends on how much damage has occurred to the femoral head of the patient, bone is always undergoing change or remodelling.[25] The bone is broken down by osteoclasts and rebuilt by osteoblasts.[25] Some doctors also prescribe bisphosphonates (e.g. alendronate) which reduces the rate of bone breakdown by osteoclasts, thus preventing collapse (specifically of the hip) due to AVN.[26]

Other treatments include core decompression, where 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.[27]

Progression of the disease could possibly be halted by transplanting nucleated cells from bone marrow into avascular necrosis lesions after core decompression, although much further research is needed to establish this technique.[28]


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.[25]Normally, bone continuously breaks down and rebuilds—old bone is reabsorbed and replaced with new bone. The process keeps the skeleton strong and helps it to maintain a balance of minerals.[25] 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,[2] and the joint surface breaks down,[15] leading to pain and arthritis.[15]

Notable individuals affected

Avascular necrosis cut short the football and baseball careers of star athlete Bo Jackson.[29]

Other sports stars with this condition are former NFL running back Garrison Hearstcyclist Floyd LandisNFL quarterback Brett Favre, professional wrestler "Superstar" Billy Graham, wrestler Joe Heat, Number one draft pick for the Minnesota LynxBen DvorakNBA playerJorge Garbajosa, NHL goaltender Ray Emery and gymnast Jade Barbosa.

In addition to the athletes listed, AVN has affected Edward Van Halen, lead guitarist for the rock band Van HalenEd Graham, drummer of the bands The Darkness and Stone Gods, and Micky Dolenz, the drummer/singer of the band The Monkees.

Recent research into the cause of death of Tutankhamun suggests that it may have been a factor in the pharaoh's death.

Bill Shannon, despite being born with degenerative hip condition, developed a way to express himself through dance and skateboarding on crutches, and became prominent in Disabled dance.

The Staging of Avascular Necrosis



Surgical potential

Stage 0Theoretical stage: 
All diagnostic tests are normal. 
Biopsy from histology - is the only 
Nil Required : 
Theoretical stage only
Not a clinical problem.
Stage 1X-Rays and CT-scan are normal 
MRI and Tc99 and histology are abnormal. 
Symptoms may or may not be present.
Surgery is possible / desirable.
Core - decompression possible.
Stage 2X-Rays are abnormal - 
With linear sclerosis or cysts. 
There is no Subchondral lucency 
Head of the femur is still spherical.
Surgery is possible / desirable.
Core - decompression possible.
Stage 3The femoral head starts to fail 
mechanically - 
With Trabecular collapse. 
The radioluscent crescent sign is visible 
at the Subchondral endplate. 
The femoral head itself is still spherical
Surgery is possible 
Core - decompression possible.
Success depends on degree of changes.
Stage 3a.Crescent < 15%Surgery still possible.
Stage 3bCrescent 15-30%Increasing risk of failure of preventative surgery.
Stage 3cCrescent>30%Increasing risk of failure of preventative surgery.
Stage 4Flattening of the femoral head is now seenPreventative surgery NO HELP
Medical Management.
Total Hip Replacement Required.
Stage 4a<15% of the surface is collapsed 
Depression <4mm
Preventative surgery NO HELP
Medical Management.
Total Hip Replacement Required.
Stage 4b15-30% collapse or 2-4mm depressionPreventative surgery NO HELP
Medical Management.
Total Hip Replacement Required.
Stage 4c>30% Collapse or >4mm depression.Preventative surgery NO HELP
Medical Management.
Total Hip Replacement Required.
Stage 5Any or all Xray features may be present 
There is a decrease in joint space. 
Secondary Osteoarthritis is present with: 
Sclerosis / Cysts / Osteophytes
Preventative surgery NO HELP
Medical Management.
Hip Replacement Required.
Stage 6Extensive destructionTotal Hip Replacement - 
Where available / Possible.

FOR AVN of Knee joint region, with resultant Osteochondritis dessicans, the following treatment may be useful



Hyaline articular cartilage

Hyaline articular cartilage is a firm and durable tissue.  Cartilage covers the ends of bones in joints and enables the bones to move smoothly over one another. Therefore, healthy cartilage is crucial to the smooth and painless mobility of most joints, including the knee.

Cartilage damage can be caused by athletic activity, traumatic injury, and even daily wear and tear. Injuries to the articular cartilage of the knee can take the form of lesions, which are like potholes in the cartilage. Symptoms of an injury can include aching, pain, swelling, locking, catching and giving way.

Damaged cartilage has limited capacity to repair or restore itself. If untreated, the damage may progressively worsen and may lead to chronic conditions such as osteoarthritis.

Current treatment options

cartilage injuryCurrent treatment options are limited and vary depending on individual patient factors and surgeon preference.

Despite the availability of a range of procedures and treatments, patients are often left searching for new options due to incomplete recovery or limited duration of effect. Microfracture is commonly performed and is considered the current standard of care for most cases of severe cartilage injury in the knee.  Microfracture works by creating tiny holes, or “fractures,” in the bone underneath the injured cartilage, leading to formation of a blood clot in the affected area.  The blood and bone marrow that seep out to form the clot contain stem cells, which are thought to grow into cartilage-building cells.  Although symptoms may improve for a period of time after the surgery, microfracture has been unsuccessful in reliably solving the underlying problem of the injured cartilage. In most cases, the repair tissue formed by the procedure is not the same healthy joint cartilage that joints require to withstand the normal forces of movement and weightbearing.

Made from a patient’s own cells, NeoCart® is an investigational cartilage tissue implant to treat knee cartilage injuries. Learn more about NeoCart and its potential benefits to people suffering from cartilage injury in the knee.


See also

Dysbaric osteonecrosis


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