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Osteonecrosis (plural: osteonecroses) is a generic term referring to the ischemic death of the constituents of bone. It has a wide variety of causes and can affect nearly any bone in the body. Most sites of involvement have an eponym associated with osteonecrosis of that area (see list below), and these sites are discussed individually, as each site has unique clinical, etiologic and prognostic features.
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Osteonecrosis vs avascular necrosis
Historically, the terms ischemic and avascular necrosis were typically reserved for subchondral (epiphyseal) osteonecrosis, whereas bone infarct referred to medullary (metaphyseal) osteonecrosis. The term avascular necrosis (and also aseptic necrosis) is usually seen in older publications. Osteonecrosis is a more general and inclusive term, and is now preferably used 10; it is also important to note that necrosis is always avascular. However, often both osteonecrosis and avascular necrosis are often used interchangeably, which can lead to confusion 7.
When osteonecrosis affects bone growth in the skeletally immature population, this is termed osteochondrosis.
There is no single affected demographic as the underlying predisposing factors are varied.
Infarction begins when the blood supply to a section of bone is interrupted. Once an infarct has become established, just as in other tissues, there is a central necrotic core, surrounded by an ischemic zone, the inner portion being "almost dead" and the outer portion being hyperemic. Beyond this is normal viable marrow. Between the normal and the ischemic zone, that demarcation occurs with the development of viable granulation separating dead tissue. This leads to the double line sign on MRI.
When the infarct is subchondral, a wedge of tissue is typically affected, the apex of which points towards the center of the bone.
trauma: fracture or dislocation
corticosteroid excess: both endogenous and exogenous
Mnemonics: STARS, PLASTIC RAGS
Classification by eponymous names
Ahlback disease: medial femoral condyle, i.e. SIFK/SONK
Brailsford disease: navicular (adult)
Buchman disease: iliac crest
Burns disease: distal ulna
Caffey disease: entire carpus or intercondylar spines of the tibia
Dias disease: trochlea of the talus
Freiberg infraction: head of the second metatarsal
Friedrich disease: medial clavicle
Haas disease: humeral head
Iselin disease: base of 5th metatarsal
Kienböck disease: lunate
Köhler disease: patella or navicular (children)
Kümmell disease: vertebral body
Legg-Calvé-Perthes disease: femoral head
Mandl disease: greater trochanter
Mauclaire disease or Dietrich disease: metacarpal heads
Milch disease: ischial apophysis
Mueller-Weiss disease: navicular (adult)
Panner disease: capitellum of the humerus
Pierson disease: symphysis pubis
Preiser disease: scaphoid
Sever disease: calcaneal epiphysis
Siffert-Arkin disease: distal tibia
Thiemann disease: base of phalanges
Classification by location
Radiographic changes alter with the stage of osteonecrosis - see Ficat staging, Steinberg classification, ARCO classification for examples within the femoral head.
Plain radiographs are negative in early disease. In general, there is initial minor osteopenia, followed by variable changes, such as patchy sclerosis and rim calcification. Gradually microfractures of the subchondral bone accumulate in the dead bone, which is unable to repair leading to the collapse of the articular surface and the crescent sign of osteonecrosis. Eventually the cortex collapses and fragments, with superimposed secondary degenerative change.
MRI is the most sensitive (~95%) modality and demonstrates changes well before plain radiographic changes are visible.
reactive interface line: focal serpentine low signal line with fatty center (most common appearance and first sign on MRI)
double line sign: T2WI serpentine peripheral/outer dark (sclerosis) and inner bright (granulation tissue) line is diagnostic (the line usually extends to the subchondral bone plate, which helps to differentiate it from subchondral fracture)
diffuse edema: edema is not an early sign; indeed, studies show that edema occurs in advanced stages and is directly correlated with pain
rim sign: osteochondral fragmentation
secondary degenerative change (i.e. osteoarthritis)
on contrast-enhanced images, non-viable marrow does not enhance
in case of radiation necrosis, there is edema or fatty replacement of the adjacent bone marrow (depending on the interval between the examination and radiotherapy)
Bone scintigraphy is also quite sensitive (~85%) and is the second option after MRI. It is a choice when multiple sites of involvement must be assessed in patients with risk factors, such as sickle cell disease. The findings are different according to the time of the scan:
early disease: often represented by a cold area likely representing the vascular interruption
late disease: may show a "doughnut sign": a cold spot with surrounding high uptake ring (surrounding hyperemia and adjacent synovitis)
Treatment and prognosis
The goal of treatment is to reduce the load on the affected part and to promote revascularization. Treatment varies by location and includes:
conservative: anti-inflammatory, analgesia, and reduced/non-weight bearing
joint replacement for end-stage disease
MRI and bone scintigraphy have high sensitivity, with MRI studies being the first line for the assessment of osteonecrosis
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