Avascular necrosis

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Avascular necrosis_table_infobox_0

Avascular necrosisAvascular necrosis_header_cell_0_0_0
Other namesAvascular necrosis_header_cell_0_1_0 Osteonecrosis, bone infarction, aseptic necrosis, ischemic bone necrosisAvascular necrosis_cell_0_1_1
SpecialtyAvascular necrosis_header_cell_0_2_0 OrthopedicsAvascular necrosis_cell_0_2_1
SymptomsAvascular necrosis_header_cell_0_3_0 Joint pain, decreased ability to moveAvascular necrosis_cell_0_3_1
ComplicationsAvascular necrosis_header_cell_0_4_0 OsteoarthritisAvascular necrosis_cell_0_4_1
Usual onsetAvascular necrosis_header_cell_0_5_0 GradualAvascular necrosis_cell_0_5_1
Risk factorsAvascular necrosis_header_cell_0_6_0 Bone fractures, joint dislocations, alcoholism, high dose steroidsAvascular necrosis_cell_0_6_1
Diagnostic methodAvascular necrosis_header_cell_0_7_0 Medical imaging, biopsyAvascular necrosis_cell_0_7_1
Differential diagnosisAvascular necrosis_header_cell_0_8_0 Osteopetrosis, rheumatoid arthritis, Legg–Calvé–Perthes syndrome, sickle cell diseaseAvascular necrosis_cell_0_8_1
TreatmentAvascular necrosis_header_cell_0_9_0 Medication, not walking on the affected leg, stretching, surgeryAvascular necrosis_cell_0_9_1
FrequencyAvascular necrosis_header_cell_0_10_0 ~15,000 per year (US)Avascular necrosis_cell_0_10_1

Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply. Avascular necrosis_sentence_0

Early on, there may be no symptoms. Avascular necrosis_sentence_1

Gradually joint pain may develop which may limit the ability to move. Avascular necrosis_sentence_2

Complications may include collapse of the bone or nearby joint surface. Avascular necrosis_sentence_3

Risk factors include bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. Avascular necrosis_sentence_4

The condition may also occur without any clear reason. Avascular necrosis_sentence_5

The most commonly affected bone is the femur. Avascular necrosis_sentence_6

Other relatively common sites include the upper arm bone, knee, shoulder, and ankle. Avascular necrosis_sentence_7

Diagnosis is typically by medical imaging such as X-ray, CT scan, or MRI. Avascular necrosis_sentence_8

Rarely biopsy may be used. Avascular necrosis_sentence_9

Treatments may include medication, not walking on the affected leg, stretching, and surgery. Avascular necrosis_sentence_10

Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement. Avascular necrosis_sentence_11

About 15,000 cases occur per year in the United States. Avascular necrosis_sentence_12

People 30 to 50 years old are most commonly affected. Avascular necrosis_sentence_13

Males are more commonly affected than females. Avascular necrosis_sentence_14

Signs and symptoms Avascular necrosis_section_0

In many cases, there is pain and discomfort in a joint which increases over time. Avascular necrosis_sentence_15

While it can affect any bone, about half of cases show multiple sites of damage. Avascular necrosis_sentence_16

Avascular necrosis most commonly affects the ends of long bones such as the femur. Avascular necrosis_sentence_17

Other common sites include the humerus, knees, shoulders, ankles and the jaw. Avascular necrosis_sentence_18

Causes Avascular necrosis_section_1

The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. Avascular necrosis_sentence_19

Other risk factors include radiation therapy, chemotherapy, and organ transplantation. Avascular necrosis_sentence_20

Osteonecrosis is also associated with cancer, lupus, sickle cell disease, HIV infection, Gaucher's disease, and Caisson disease. Avascular necrosis_sentence_21

The condition may also occur without any clear reason. Avascular necrosis_sentence_22

Bisphosphonates are associated with osteonecrosis of the mandible. Avascular necrosis_sentence_23

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. Avascular necrosis_sentence_24

Pathophysiology Avascular necrosis_section_2

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. Avascular necrosis_sentence_25

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. Avascular necrosis_sentence_26

Upon reperfusion, repair of bone occurs in 2 phases. Avascular necrosis_sentence_27

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. Avascular necrosis_sentence_28

Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts. Avascular necrosis_sentence_29

Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue. Avascular necrosis_sentence_30

Diagnosis Avascular necrosis_section_3

In the early stages, bone scintigraphy and MRI are the preferred diagnostic tools. Avascular necrosis_sentence_31

X-ray images of avascular necrosis in the early stages usually appear normal. Avascular necrosis_sentence_32

In later stages it appears relatively more radio-opaque due to the nearby living bone becoming resorbed secondary to reactive hyperemia. Avascular necrosis_sentence_33

The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts. Avascular necrosis_sentence_34

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_sentence_35

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Types Avascular necrosis_section_4

When AVN affects the scaphoid bone, it is known as Preiser disease. Avascular necrosis_sentence_36

Another named form of AVN is Köhler disease, which affects the navicular bone of the foot, primarily in children. Avascular necrosis_sentence_37

Yet another form of AVN is Kienböck's disease, which affects the lunate bone in the wrist. Avascular necrosis_sentence_38

Treatment Avascular necrosis_section_5

A variety of methods may be used to treat the most common being the total hip replacement (THR). Avascular necrosis_sentence_39

However, THRs have a number of downsides including long recovery times and short life spans (of the hip joints). Avascular necrosis_sentence_40

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. Avascular necrosis_sentence_41

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. Avascular necrosis_sentence_42

Bisphosphonates which reduce the rate of bone breakdown may prevent collapse (specifically of the hip) due to AVN. Avascular necrosis_sentence_43

Core decompression Avascular necrosis_section_6

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. Avascular necrosis_sentence_44

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. Avascular necrosis_sentence_45

There is additionally no strong research on the effectiveness of hip core decompression for people with sickle cell disease. Avascular necrosis_sentence_46

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. Avascular necrosis_sentence_47

Prognosis Avascular necrosis_section_7

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. Avascular necrosis_sentence_48

The process of bone rebuilding takes place after an injury as well as during normal growth. Avascular necrosis_sentence_49

Normally, bone continuously breaks down and rebuilds—old bone is resorbed and replaced with new bone. Avascular necrosis_sentence_50

The process keeps the skeleton strong and helps it to maintain a balance of minerals. Avascular necrosis_sentence_51

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. Avascular necrosis_sentence_52

If left untreated, the disease progresses, the bone collapses, and the joint surface breaks down, leading to pain and arthritis. Avascular necrosis_sentence_53

Epidemiology Avascular necrosis_section_8

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. Avascular necrosis_sentence_54

When it occurs in children at the femoral head, it is known as Legg–Calvé–Perthes syndrome. Avascular necrosis_sentence_55

Society and culture Avascular necrosis_section_9

Cases of avascular necrosis have been identified in a few high-profile athletes. Avascular necrosis_sentence_56

It abruptly ended the career of American football running-back Bo Jackson in 1991. Avascular necrosis_sentence_57

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 a 1991 NFL Playoff game. Avascular necrosis_sentence_58

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 1991. Avascular necrosis_sentence_59

However, Favre would go on to have a long career at the Packers. Avascular necrosis_sentence_60

Another high-profile athlete was American road racing cyclist Floyd Landis, 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. Avascular necrosis_sentence_61

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. Avascular necrosis_sentence_62

Credits to the contents of this page go to the authors of the corresponding Wikipedia page: en.wikipedia.org/wiki/Avascular necrosis.