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Osteonecrosis
Overview
Osteonecrosis (aka aseptic necrosis, avascular necrosis (AVN)) occurs from both traumatic and non-traumatic ischemia to the bone and bone barrow, causing infarction (necrosis). It manifests with joint destruction and ultimate skeletal instability/mechanical failure. It typically presents with pain.
Osteonecrosis most commonly impacts the femoral head. Trauma is the leading cause due to vascular interruption. Glucocorticoids and alcohol are the leading non-traumatic causes (>75% of non-traumatic cases). The pathological mechanism of non-traumatic osteonecrosis is multifactorial but abnormal lipid accumulation, adipogenesis (fat cell accumulation), and occlusive ischemia are important factors.
Causes
Trauma
- Bone fracture with/without joint dislocation is the most common cause of osteonecrosis. Most often from femoral head fracture with associated hip dislocation.
- In femoral neck fracture avascular necrosis primarily occurs from injury to the lateral and medial femoral circumflex arteries.
- The medial and lateral femoral circumflex arteries branch from the profundal femoris artery (aka the deep femoral artery), which originates from the femoral artery.
- In humeral head fracture avascular necrosis primarily occurs from posterior humeral circumflex artery injury (the anterior humeral circumflex artery also contributes).
- Glucocorticoid dose and duration are the key factors in inducing osteonecrosis but patients on low-doses of glucocorticoids are still at risk for the disease. Note that there is evidence that the initial dose of glucocorticoid (higher being worse) is more substantial of a factor than duration.
- High alcohol intake can lead to osteonecrosis. The complex underlying pathology has not been fully elucidated but relates to various mechanisms: especially lipid accumulation and adipocyte hypertrophy, as well as fat emboli, cortisol increases, and poor circulation via venous stasis.
- Legg-Calvé-Perthes disease
- Legg-Calvé-Perthes disease is an idiopathic juvenile avascular necrosis of the femoral head. It is considered an osteochondrosis because it impacts the growth plate.
- Slipped capital femoral epiphysis
- Slipped capital femoral epiphysis occurs when the femoral head (at the epiphysis) slips off the neck of the femur. It usually occurs spontaneously in adolescents during periods of rapid growth (growth spurts).
- Systemic Lupus Erythematosus - especially in those who've been taking glucocorticoids.
- Bisphosphonate and antiresportive agent induction of osteonecrosis of the jaw (particularly in patients with malignancies (eg, multiple myeloma).
- Genetic diseases - Sickle cell disease, Gaucher's disease, etc...
- Radiation therapy (especially jaw osteonecrosis)
- Decompression disease ("the bends")
Focused Mnemonic
CASTLS
- Corticosteroids
- Alcoholism
- Trauma
- Sickle cell disease & Systemic lupus erythematosus (SLE)
- Legg-Calvé-Perthes disease
- Slipped capital femoral epiphysis
Broader Mnemonic
CASTS Bend LEGS
Corticosteroids (glucocorticoids)
Alcohol
Sickle cell disease
Trauma, especially medial femoral circumflex artery injury from femoral neck fracture
Systemic lupus erythematosus
Bend
LEgg-Calvé-Perthes
Gaucher disease
Slipped capital femoral epiphysis
Symptoms
Pain is the most common presenting symptom. Look for groin pain (femoral head disease), activity or weight-bearing induced pain, but pain at rest is also common.
Diagnosis
MRI is the gold standard imaging modality for diagnosing osteonecrosis. X-Ray and CT scans can be used but MRI is the most reliable methodology.
Treatment
Supportive care treatments include bedrest, crutches, NSAIDs.
Surgical interventions, such as joint-preserving procedures vs joint replacement (arthroplasty) are sometimes required.
Pharmacological agents may be incorporated to try to combat the ischemia but are generally considered unproven.