Avascular necrosis

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Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply.<ref name=NIH2015>{{#invoke:citation/CS1|citation |CitationClass=web }}Template:PD-notice</ref> Early on, there may be no symptoms.<ref name=NIH2015/> Gradually joint pain may develop, which may limit the person's ability to move.<ref name=NIH2015/> Complications may include collapse of the bone or nearby joint surface.<ref name=NIH2015/>

Risk factors include bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids.<ref name=NIH2015/> The condition may also occur without any clear reason.<ref name=NIH2015/> The most commonly affected bone is the femur (thigh bone).<ref name=NIH2015/> Other relatively common sites include the upper arm bone, knee, shoulder, and ankle.<ref name=NIH2015/> Diagnosis is typically by medical imaging such as X-ray, CT scan, or MRI.<ref name=NIH2015/> Rarely biopsy may be used.<ref name=NIH2015/>

Treatments may include medication, not walking on the affected leg, stretching, and surgery.<ref name=NIH2015/> Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement.<ref name=NIH2015/>

About 15,000 cases occur per year in the United States.<ref name="Fer2018" /> People 30 to 50 years old are most commonly affected.<ref name="NORD2009">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Males are more commonly affected than females.<ref name="Fer2018">Template:Cite book</ref>

Signs and symptomsEdit

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.<ref name=nih06-4857>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Avascular necrosis most commonly affects the ends of long bones, such as the femur. Other common sites include the humerus (upper arm),<ref name=chapman>Template:Cite journal</ref><ref name=mansat>Template:Cite journal</ref> knees,<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> shoulders,<ref name=chapman/><ref name=mansat/> ankles and the jaw.<ref>Template:Cite journal</ref>

CausesEdit

The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids.<ref name=NIH2015/> Other risk factors include radiation therapy, chemotherapy, and organ transplantation.<ref name=NIH2015/> Osteonecrosis is also associated with cancer, lupus, sickle cell disease,<ref name=":0">Template:Cite journal</ref> HIV infection, Gaucher's disease, and Caisson disease (dysbaric osteonecrosis).<ref name=NIH2015/><ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Bisphosphonates are associated with osteonecrosis of the mandible (jawbone).<ref>Template:Cite journal</ref> The condition may also occur without any clear reason.<ref name=NIH2015/>

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.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

In children, avascular osteonecrosis can have several causes. It can occur in the hip as part of Legg–Calvé–Perthes syndrome,<ref>Template:Cite journal</ref> and it can also occur as a result after malignancy treatment such as acute lymphoblastic leukemia and allotransplantation.<ref>Template:Cite journal</ref>

PathophysiologyEdit

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.<ref name=nawazkhan>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> 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.<ref name=nawazkhan/>

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.<ref name=nawazkhan/> Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts.<ref name=nawazkhan/> Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue.<ref name=nawazkhan/>

DiagnosisEdit

File:OCD Knee WalterReed-1.jpg

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.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

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.<ref name=nawazkhan/> The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts.<ref name=nawazkhan/> 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.Template:Citation needed Template:Anchor

Osteonecrosis humerus 1.jpg

Radiography of total avascular necrosis of right humeral head. Woman of 81 years with diabetes of long evolution.
Osteonecrosis femur 1.jpg

Radiography of avascular necrosis of left femoral head. Man of 45 years with AIDS.
Osteonecrosis femur 2img.jpg

Nuclear magnetic resonance of avascular necrosis of left femoral head. Man of 45 years with AIDS.
Intravertebral vacuum cleft sign.jpg

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.<ref name="FreedmanHeller2009">Template:Cite journal</ref>
Pathology of avascular necrosis.jpg

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.

TypesEdit

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.<ref>Template:Cite journal</ref>

TreatmentEdit

A variety of methods may be used to treat the disease,<ref name=nih06-4857/> 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).<ref name=":1" /> 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.<ref name=":1">Template:Cite journal</ref>

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.<ref name="Hall">Template:Cite book</ref> Bisphosphonates, which reduce the rate of bone breakdown, may prevent collapse (specifically of the hip) due to AVN.<ref>Template:Cite journal</ref>

Core decompressionEdit

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.<ref>Template:Cite journal</ref> 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.<ref name=":0" />

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.<ref name="pmid15743852">Template:Cite journal</ref><ref>Template:Cite journal</ref>

PrognosisEdit

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.<ref name=Hall/> 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.<ref name=Hall/> 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,<ref name=DiGiovanni>Template:Cite journal</ref> and the joint surface breaks down, leading to pain and arthritis.<ref name=NIH2015/>

EpidemiologyEdit

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.Template:Citation needed

Society and cultureEdit

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 a 1991 NFL Playoff game.<ref>Template:Cite news</ref> 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.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> However, Favre would go on to have a long career at the Packers.Template:Citation needed

Another high-profile athlete was American road racing cyclist Floyd Landis,<ref name="New York Times magazine article">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> 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.<ref>Template:Cite news</ref> 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.<ref>Template:Cite news (subscription required)</ref>

Rafael Nadal successfully continued his tennis career after having surgery for Mueller–Weiss syndrome (osteonecrosis of the navicular bone in the foot).<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Youtuber Steve Wallis has revealed that he has the condition in his hip.Template:Where