From Wikipedia, the free encyclopedia
Avascular necrosis (also
osteonecrosis, aseptic (bone)
necrosis, ischemic bone necrosis[1],
and AVN) is a disease resulting from the temporary
or permanent loss of the blood
supply to an area of bone.[1]
Without blood, the bone tissue dies and the bone collapses.[1]
If avascular necrosis involves the bones of a joint, it often leads to destruction of the joint
articular surfaces (see Osteochondritis
dissecans).
Causes
There are many theories about what causes avascular necrosis.
Proposed risk factors include alcoholism,[2]
excessive steroid use,[3] post
trauma,[4][5] caisson disease (decompression
sickness),[6][7]
vascular compression,[8] hypertension, vasculitis, thrombosis, damage from
radiation, bisphosphonates (particularly the mandible),[9] sickle cell anaemia,[10] and Gaucher's Disease.[11] In
some cases it is idiopathic (no cause is found).[12]
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.
Presentation
While it can affect any bone, and half of cases show multiple
sites of damage, avascular necrosis primarily affects the joints at
the shoulder, knee, and hip.
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),[13][14]
knees,[15][16]
shoulders,[13][14]
ankles and the jaw.[17] The
disease may affect just one bone, more than one bone at the same
time, or more than one bone at different times.[18]
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.[19]
Diagnosis
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.
Because in the early stage of the disease x-ray images usually
appear normal, bone scintigraphy[20] and
MRI[21] are
the diagnostic modalities of choice. Both modalities can detect
minimal changes at early stages of the disease. Late radiographic
signs 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,[18]
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. 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 remodelling.[22]
The bone is broken down by osteoclasts and rebuilt by
osteoblasts.[22]
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.[23]
Other treatments include Core Decompression, where internal bone
pressure is relieved by drilling a hole into the bone, and living
bone chip and 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.[24]
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.[25]
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.[22]
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.[22]
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,[1]
and the joint surface breaks down,[12]
leading to pain and arthritis.[12]
Notable individuals
affected
Avascular necrosis cut short the football and baseball careers of star athlete
Bo Jackson.[26]
Other sports stars with this condition are former NFL running back Garrison Hearst, cyclist Floyd Landis, NFL quarterback Brett Favre, professional wrestler "Superstar" Billy Graham,
wrestler Joe Heat, Number one draft pick for the Minnesota Lynx:
Ben Dvorak, NBA
player Jorge
Garbajosa, and gymnast Jade Barbosa.
In addition to the athletes listed, AVN has affected Edward Van Halen, lead guitarist for the
rock band Van Halen, and
Micky Dolenz, the
drummer/singer of the band The Monkees.
See also
Dysbaric osteonecrosis
References
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External
links