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Osteonecrosis (ON)

ON refers to death of the cellular component of bone (osteocytes) and contiguous bone marrow resulting from ischemia. Although inciting factors for such ischemia are varied, their end results are clinically indistinguishable.

  • Osteonecrosis (ON) most commonly involves the femoral head.
  • The most common risk factors for ON are glucocorticoid (GC) use and alcohol abuse.
  • Nonoperative therapy for early disease include protected weight-bearing, bisphosphonates, statins, and anticoagulants.
  • Operative therapy includes core decompression with or without grafting and total joint replacement

Bones are most vulnerable in those areas having both limited vascular supply and restricted collateral circulation, which are areas that are also typically covered by articular cartilage. The area most frequently affected is the femoral head. At risk areas include: femoral head, carpal bones (scaphoid, lunate), humeral head, talus, femoral condyles, tarsal navicular, proximal tibia, and metatarsals.

Conditions Associated With Osteonecrosis

Nontraumatic

JUVENILE

Slipped capital femoral epiphysis, Legg–Calvé–Perthes

ADULT

Corticosteroid administration (Cushing’s disease), Alcohol abuse, Sickle cell anemia, Hemoglobinopathies (thalassemia, hemoglobin C disease [Hgb C]), Dysbaric ON, Gaucher’s disease/Fabry’s disease, Radiotherapy/chemotherapy, Cushing’s disease, Diabetes mellitus, Hyperlipidemia, Hypercoagulable states/thrombophilia/disseminated intravascular coagulation (DIC), Pancreatitis, Pregnancy, Oral contraceptive use, Systemic lupus erythematosus (SLE), primary antiphospholipid syndrome (PAPS), Organ transplantation, Fat embolism, Severe acute respiratory syndrome (SARS), Carbon tetrachloride/lead poisoning, Tumor infiltration of marrow, Arteriosclerosis/vaso-occlusive disorders, Others: human immunodeficiency virus (HIV)/highly active antiretroviral therapy (HAART), smoking, idiopathic

Traumatic

Fracture of the femoral neck, Dislocation or fracture of the hip, Hip trauma without fracture or dislocation, Hip surgery

Pathogenesis of ON

Etiologic factors initiate hemostasis directly or trigger a cascade resulting in hemostasis. Histologic findings indicate that the final common pathway for the various inciting factors involves local intravascular coagulation and resultant tissue ischemia. The end result is that of cancellous bone and bone marrow death. With subchondral cancellous bone death, collapse of the articular surface may or may not occur, depending on the extent of involvement.

Pain, the earliest symptom of ON, may occur in the early stages of involvement, before any radiographic changes are noted. In some individuals, no symptoms develop until the late stages of the disease process when collapse of the articular surface occurs and secondary degenerative changes develop. Others, in whom the area of infarction is small enough that collapse does not occur, may never develop symptoms. Radiographs in these patients reveal sclerotic areas often referred to as “bone islands” or “bone infarcts.”

University of Pennsylvania (Steinberg) System of Staging of Osteonecrosis of the Femoral Head

STAGE

PLAIN RADIOGRAPHIC FINDINGS

MRI

0

Normal

Normal

I

Normal

Abnormal

II

Osteopenia, bony sclerosis, cystic changes

Abnormal

III

Subchondral collapse (“crescent sign”) without articular surface flattening

Abnormal

IV

Flattening of the articular surface without joint-space narrowing

Abnormal

V

Flattening of the articular surface with joint-space narrowing and/or acetabular involvement

Abnormal

VI

Advanced degenerative changes


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Femurkopfnekrose - Ärzteblatt (German)