Avascular necrosis ( AVN ), also called osteonecrosis or bone infarction , is bone tissue death due to impairment from the blood supply. At the beginning there may be no symptoms. Gradually joint pain can develop that can limit the ability to move. Complications may include collapse of bone or joint surface nearby.
Risk factors include fractures, joint dislocation, alcoholism, and high-dose steroid use. This condition can also occur for no apparent reason. The most commonly affected bone is the femur. Other relatively common sites include the upper arm bone, knees, shoulders, and ankles. Diagnosis is usually done with medical imaging such as X-ray, CT scan, or MRI. Biopsy rarely can be used.
Treatment may include medication, not walking on affected legs, stretching, and surgery. Most of the time the surgery is finally needed and may include decompression of the core, osteotomy, bone graft, or joint replacement. Approximately 15,000 cases occur annually in the United States. People aged 30 to 50 are most often affected. Men are more affected than women.
Video Avascular necrosis
Signs and symptoms
In many cases there is increased pain and discomfort in the joints over time. Although it can affect bone, about half of the cases show some site damage. Avascular necrosis mainly affects joints in the shoulders, knees, and hips. The classic sites are: head of femur, talus neck and scaphoid waist.
Avascular necrosis most commonly affects the ends of long bones such as the femur (the bone extends from the knee joint to the hip joint). Other common sites include the humerus (upper arm bone), knees, shoulders, ankles and jaws.
Maps Avascular necrosis
Cause
The major risk factors are fracture, joint dislocation, alcoholism, and high-dose steroid use. Other risk factors include radiation therapy, chemotherapy, and organ transplantation. Osteonecrosis is also associated with cancer, lupus, sickle cell disease, HIV infection, Gaucher's disease, and Caisson disease. This condition can also occur for no apparent reason.
Bisphosphonates are associated with mandibular osteonecrosis. Repeated prolonged exposure to high pressure (as experienced by commercial and military divers) has been attributed to AVN, although the relationship is not well understood.
Pathophysiology
The hematopoietic cells are most sensitive to low oxygen and are the first to die after the reduction or discharge of the blood supply, usually within 12 hours. Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts, etc.) die within 12-48 hours, and bone marrow fat cells die within 5 days.
After reperfusion, bone repair occurs in 2 phases. First, there is an angiogenesis and the undifferentiated mesenchyme cell movement of adjacent living bone tissue growing into the dead marrow space, as well as the entry of macrophages that degrade dead cells and fats. Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts. Under favorable conditions, the volume of inorganic minerals remaining forms the framework for the formation of a fully functional new bone tissue.
Diagnosis
In the early stages, bone scribbles and MRIs are the preferred diagnostic tools.
X-ray image of avascular necrosis in the early stages usually appears normal. At a later stage it appears relatively more radio-opaque since nearby living bones become secondary resorbed for reactive hyperemia. The necrotic bone itself does not show increased radiographic opacity, because dead bone can not undergo bone resorption performed by living osteoclasts. The final radiographic signs also include the radiolucent area after subchondral bone collapse (crescent sign) and the ringed region of radiodensity resulting from sapding and calcification of marrow fat after medullary infarction.
Treatment
Various methods can be used to treat the most common is total hip replacement (THR). However, THRs have a number of disadvantages including long recovery times and short life spans (from hip joints). THRs are an effective way of treatment in the older population; However, in younger people they may wear out before the end of one's life.
Other techniques such as metals in metallic coating may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage occurs to the femoral head. Bisphosphonates that reduce the extent of bone damage can prevent collapse (especially in the pelvis) due to AVN.
Core decompression
Other treatments include core decompression, where internal bone pressure is reduced by drilling holes into bone, and live bone chips and electrical devices to stimulate the growth of newly planted blood vessels; and a free vascular fibular graft (FVFG), in which a portion of the fibula, together with its blood supply, is removed and transplanted into the femoral head. A systematic review of Cochrane 2012 notes that no obvious improvement can be found between people who have decompressed the hip core and participated in physical therapy, rather than physical therapy alone. More research needs to look at the effectiveness of pelvic core decompression for people with sickle cell disease.
The progression of this disease may be stopped by transplanting nucleated cells from the bone marrow into avascular necrosis lesions after core decompression, although further research is still needed to establish this technique.
Prognosis
The number of defects resulting from avascular necrosis depends on which part of the bone is affected, how large the area is involved, and how effectively the bone rebuilds itself. The process of bone rebuilding occurs after injury as well as during normal growth. Usually, the bones continue to break and rebuild - old bones are resorbed and replaced with new bone. This process keeps the skeleton strong and helps maintain the mineral balance. However, in the process of avascular necrosis, the healing process is usually ineffective and bone tissue breaks faster than the body can fix it. If left untreated, developing disease, collapsed bones, and joint surfaces are damaged, causing pain and arthritis.
Epidemiology
Avascular necrosis usually affects people between the ages of 30 and 50 years; about 10,000 to 20,000 people develop avascular necrosis of the femoral head in the US each year. When it occurs in children in the femoral head, it is known as Legg-Calvà ©  © -Perthes syndrome.
Society and culture
Cases of avascular necrosis have been identified in some high-profile athletes. This suddenly ended the football career of American Boone run-back Bo Jackson in 1991. Doctors found Jackson had lost all the cartilage that supported his hip as he underwent tests after a hip injury he had on the pitch during the 1991 NFL Playoff game. Avascular necrosis of the hip was also identified in routine medical examinations on quarterback Brett Favre following his trade to the Green Bay Packers in 1991. However, Favre will continue to have a long career in the Packers.
Another high-profile athlete is American road racing biker Floyd Landis, winner of the 2006 Tour De France, the title was subsequently dropped from his notes by the bike governing body after his blood sample was tested positive for a banned substance. During the tour, Landis was allowed to perform cortisone shots to help manage his illness, although cortisone also became a banned substance in professional cycling at the time.
References
External links
- Osteonecrosis/Avascular Necrosis at National Institute of Health
- Osteonecrosis/Avascular necrosis at Merck Manual for patients
- Osteonecrosis/Avascular necrosis at Merck Manual for medical professionals
Source of the article : Wikipedia
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