Avascular necrosis (also osteonecrosis, bone infarction, aseptic necrosis,ischemic bone [2] necrosis, and AVN) is a disease where

there is cellular death (necrosis) of bone components due to [3] [2] interruption of the blood supply. Without blood, the bone tissue dies and the bone collapses. If avascular necrosis involves the bones of a joint, it often leads to destruction of the joint articular surfaces. (see Osteochondritis dissecans).
Contents
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1 Causes 2 Cell death and repair 3 Presentation 4 Diagnosis 5 Treatment 6 Prognosis 7 See also 8 References 9 External links

Causes[edit source | editbeta]

There are many theories about what causes avascular necrosis. Proposed risk factors include, [4] [5] [6][7] chemotherapy, alcoholism, excessive steroid use, post trauma, caisson disease (decompression [8][9] [10] sickness), vascular compression, hypertension, vasculitis,arterial embolism and thrombosis, [11] damage from radiation, bisphosphonates (particularly the mandible), sickle cell [12] [13] [14] anaemia, andGaucher's Disease,. In some cases it is idiopathic (no cause is found). Rheumatoid arthritis and lupus are also 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.

Cell death and repair[edit source | editbeta]

The hematopoietic cells are most sensitive to anoxia and are the first to die after reduction or removal of [1] the blood supply, usually within 12 hours. Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 1248 hours, and that bone marrow fat cells die [1] within 5 days. Upon reperfusion, repair of ischemic bone occurs in 2 phases; First, there is angiogenesis and movement of undifferentiatedmesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, [1] as well as entry of macrophages that degrade dead cellular and fat debris. Second, there is cellular [1] differentiation of mesenchymal cells into osteoblasts or fibroblasts. Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone [1] tissue.

Presentation[edit source | editbeta]

While it can affect any bone, and half of cases show multiple sites of damage, avascular necrosis primarily affects the joints at theshoulder, 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 [15][16] [17][18] [15][16] [19] the humerus (the bone of the upper arm), knees, shoulders, ankles and the jaw. The disease may affect just one bone, more than one bone at the same time, or more than one bone at [20] different times. 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 [21] it occurs in children at the femoral head, it is known as Legg-Calv-Perthes syndrome.

Diagnosis[edit source | editbeta]

Front X-ray of right knee of anadolescent (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
[22]

and MRI

[23]

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 [1] hyperemia. The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot [1] undergo bone resorption which is carried out by living osteoclasts. 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.

Radiography of total avascular necrosis of right humeral head. Woman of 81 years old with diabetes of long evolution.

Radiography of avascular necrosis of left femoral head. Man of 45 years old with AIDS.

Nuclear magnetic resonance of avascular necrosis of left femoral head. Man of 45 years old with AIDS.

Treatment[edit source | editbeta]

Avascular necrosis is especially common in the hip joint. A variety of methods are now used to treat [20] avascular necrosis, 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 patient, bone is always undergoing change or [24] [24] remodelling. The bone is broken down by osteoclasts and rebuilt by osteoblasts. Some doctors also

prescribe bisphosphonates (e.g. alendronate) which reduces the rate of bone breakdown by osteoclasts, thus preventing