Avascular necrosis

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Avascular necrosis
File:Head of femur avascular necrosis.jpg
Femur head showing a flap of cartilage (osteochondritis dissecans) due to avascular necrosis. Specimen from total hip replacement surgery.
Classification and external resources
Specialty Orthopedics
ICD-10 M87
ICD-9-CM 733.4
DiseasesDB 1174
MedlinePlus 007260
eMedicine med/2924
Patient UK Avascular necrosis
MeSH D010020
[[[d:Lua error in Module:Wikidata at line 863: attempt to index field 'wikibase' (a nil value).|edit on Wikidata]]]

Avascular necrosis (AVN), also called osteonecrosis, bone infarction,[1] aseptic necrosis, and ischemic bone necrosis,[2] 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).

Signs and symptoms

While it can affect any bone, about half of cases show multiple sites of damage, avascular necrosis primarily affects the joints at the shoulder, knee, and hip. The classical sites are: head of femur, neck of talus and waist of scaphoid.

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),[4][5] knees,[6][7] shoulders,[4][5] ankles and the jaw.[8] The disease may affect just one bone, more than one bone at the same time, or more than one bone at different times.[9]

Causes

There are many theories about what causes avascular necrosis. Proposed risk factors include, chemotherapy, alcoholism,[10] excessive steroid use,[11] post trauma,[12][13] caisson disease (decompression sickness),[14][15] vascular compression,[16] hypertension, vasculitis, arterial embolism and thrombosis, damage from radiation, bisphosphonates (particularly the mandible),[17] sickle cell anaemia,[18] and Gaucher's Disease,.[19] In some cases it is idiopathic (no cause is found).[20] Lupus is also a 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.

Pathophysiology

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 (osteocytes, osteoclasts, osteoblasts 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]

Diagnosis

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

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[21] and MRI[22] 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 hyperaemia.[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.

Treatment

Avascular necrosis is especially common in the hip joint. A variety of methods are now used to treat avascular necrosis,[9] 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 (of the hip joints). 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 resurfacing or 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 patien and bone is always undergoing change or remodelling.[23] The bone is broken down by osteoclasts and rebuilt by osteoblasts.[23] 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.[24]

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.[25]

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.[26][27]

Prognosis

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 reabsorbed 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,[2] and the joint surface breaks down,[20] leading to pain and arthritis.[20]

Epidemiology

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.[28]

See also

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 eMedicine Specialties > Bone Infarct Author: Ali Nawaz Khan. Coauthors: Mohammed Jassim Al-Salman, Muthusamy Chandramohan, Sumaira MacDonald, Charles Edward Hutchinson
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  3. eMedicine Specialties > Avascular Necrosis Author: Jeanne K Tofferi, MD, MPH, FACP; Coauthor: William Gilliland, MD, MPHE, FACP, FACR. Updated: Dec 17, 2009
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  9. 9.0 9.1 National Institute of Arthritis and Musculoskeletal and Skin Diseases (March 2006). "Osteonecrosis". Food and Drug Administration. Archived from the original on 23 May 2009. Retrieved 25 May 2009.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
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  19. Steinberg, Marvin E. (March 2008). "Osteonecrosis". Merck Manual of Diagnosis and Therapy. Archived from the original on 12 May 2009. Retrieved 25 May 2009.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
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  23. 23.0 23.1 23.2 23.3 Hall, B., The Osteoblast and Osteocyte. Vol. 1. 1990: The Telford Press. 494.
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  27. Lieberman JR, Conduah A, Urist MR. Treatment of osteonecrosis of the femoral head with core decompression and human bone morphogenetic protein. Clin Orthop Relat Res. 2004;429:139–45
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External links