Avascular Necrosis (AVN) Specialist Clinic

Avascular Necrosis (AVN) is a disease where there is cellular death (necrosis) of bone components due to 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).

Avascular Necrosis

Causes of Avascular Necrosis?

There are many theories about what causes avascular necrosis. Proposed risk factors include alcoholism,excessive steroid use,post trauma,caisson disease (decompression sickness),vascular compression, hypertension, vasculitis, arterial embolism and thrombosis, damage from radiation, bisphosphonates (particularly the mandible),sickle cell anaemia,Gaucher’s Disease,and deep diving.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.

Diagnosis of Avascular Necrosis

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 scintigraphyand MRI 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 hyperemia.The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot 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.

Treatment for Avascular Necrosis:

Avascular necrosis is especially common in the hip joint. A variety of methods are now used to treat 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. 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.  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 remodelling.

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.

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.

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