Avascular necrosis
Other names	Osteonecrosis,[1] bone infarction,[2] aseptic necrosis,[1] ischemic bone necrosis[1]
Femoral head showing a flap ofcartilage due to avascular necrosis (osteochondritis dissecans). Specimen removed duringtotal hip replacement surgery.
Specialty	Orthopedics
Symptoms	Joint pain, decreased ability to move[1]
Complications	Osteoarthritis[1]
Usual onset	Gradual[1]
Risk factors	Bone fractures,joint dislocations, high dosesteroids[1]
Diagnostic method	Medical imaging,biopsy[1]
Differential diagnosis	Osteopetrosis,rheumatoid arthritis,Legg–Calvé–Perthes syndrome,sickle cell disease[3]
Treatment	Medication, not walking on the affected leg, stretching, surgery[1]
Frequency	~15,000 per year (US)[4]

Avascular necrosis (AVN), also calledosteonecrosis orbone infarction, isdeath of bone tissue due to interruption of theblood supply.^[1] Early on, there may be no symptoms.^[1] Graduallyjoint pain may develop, which may limit the person's ability to move.^[1] Complications may include collapse of the bone or nearbyjoint surface.^[1]

Risk factors includebone fractures,joint dislocations,alcoholism, and theuse of high-dose steroids.^[1] The condition may also occur without any clear reason.^[1] The most commonly affected bone is thefemur (thigh bone).^[1] Other relatively common sites include the upper arm bone, knee, shoulder, and ankle.^[1] Diagnosis is typically bymedical imaging such asX-ray,CT scan, orMRI.^[1] Rarelybiopsy 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 includecore decompression,osteotomy,bone grafts, orjoint 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]

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 affectsthe ends oflong bones, such as thefemur. Other common sites include thehumerus (upper arm),^[6][7] knees,^[8][9] shoulders,^[6][7] ankles and thejaw.^[10]

The main risk factors arebone fractures,joint dislocations,alcoholism, and the use of high-dosesteroids.^[1] Other risk factors includeradiation therapy,chemotherapy, andorgan transplantation.^[1] Osteonecrosis is also associated with cancer,lupus,sickle cell disease,^[11]HIV infection,Gaucher's disease, andCaisson disease (dysbaric osteonecrosis).^[1][12]Bisphosphonates are associated withosteonecrosis 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 militarydivers) 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 ofLegg–Calvé–Perthes syndrome,^[16] and it can also occur as a result after malignancy treatment such asacute lymphoblastic leukemia andallotransplantation.^[17]

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

Uponreperfusion, repair of bone occurs in two phases. First, there isangiogenesis and movement of undifferentiatedmesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry ofmacrophages that degrade dead cellular and fat debris.^[2] Second, there iscellular differentiation of mesenchymal cells intoosteoblasts orfibroblasts.^[2] Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue.^[2]

In the early stages,bone scintigraphy andMRI 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 becomingresorbed secondary to reactivehyperemia.^[2] The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by livingosteoclasts.^[2] Late radiographic signs also include a radiolucency area following the collapse ofsubchondral bone (crescent sign) and ringed regions of radiodensity resulting fromsaponification 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 avascular necrosis of left femoral head. Man of 45 years withAIDS.
• 
  Nuclear magnetic resonance of avascular necrosis of left femoral head. Man of 45 years with AIDS.
• 
  Theintravertebral vacuum cleft sign (at white arrow) is a sign of avascular necrosis. Avascular necrosis of a vertebral body after avertebral compression fracture is calledKümmel'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.

When AVN affects the scaphoid bone, it is known asPreiser disease. Another named form of AVN isKöhler disease, which affects thenavicular bone of the foot, primarily in children. Yet another form of AVN isKienböck's disease, which affects the lunate bone in the wrist.^[21]

A variety of methods may be used to treat the disease,^[5] with the most common beingtotal 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]

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 2016Cochrane review found no clear improvement between people who have had hip core decompression and participate inphysical 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 transplantingnucleated cells from the bone marrow into avascular necrosis lesions after core decompression. However, much further research is needed to establish this technique.^[26][27]

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]

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]}

Cases of avascular necrosis have been identified in a few high-profile athletes. It abruptly ended the career ofAmerican footballrunning-backBo 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 a1991 NFL Playoff game.^[29] Avascular necrosis of the hip was also identified in a routine medical check-up onquarterbackBrett Favre following his trade to theGreen 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 Americanroad racing cyclistFloyd Landis,^[31] winner of the2006 Tour de France, the title being subsequently stripped from his record bycycling's governing bodies after his blood samples tested positive for banned substances.^[32] During that tour, Landis was allowedcortisone 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 forMueller–Weiss syndrome (osteonecrosis of thenavicular bone in the foot).^[34]YouTuberSteve Wallis has revealed that he has the condition in his hip.^[where?]

• Sperm whale skeletons can show damage from avascular necrosis caused by decompression.^[35]

Steve Wallis Step 2 livestream 19 December 2020https://www.youtube.com/live/5cOJC4ZE-Mo?si=BSgkpYNOTxM4QgGD

• Osteonecrosis / Avascular Necrosis at theNational Institute of Health
• Osteonecrosis / Avascular necrosis atMerck Manual for patients
• Osteonecrosis / Avascular necrosis atMerck Manual for medical professionals

• Osteopathies
• Underwater diving medicine
• Osteonecrosis

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