Conditions of bone viability

• Conditions of bone viability

□ Osteonecrosis

hydroxyproline levels

• Virus-like inclusion bodies in osteoclasts— abnormal function of osteoclasts

• Both decreased and increased osteodensities may be present.

  • Depends on phase of disease

    • Active phase

      • Lytic phase: intense osteoclastic bone resorption

    • Mixed phase

      • Sclerotic phase: osteoblastic bone formation

    • Inactive phase

    • Death of bony tissue from causes other than infection

      • Usually adjacent to a joint surface

    • Caused by loss of blood supply as a result of trauma or another event (e.g., SCFE)

    • Idiopathic osteonecrosis of the femoral head and Legg-Calvé-Perthes disease may occur in patients with coagulation abnormalities.

      • Deficiency of antithrombin factors protein C and protein S

      • Increased levels of lipoprotein(a)

    • Commonly affects the hip joint

      • Leads to collapse and flattening of the femoral head, most frequently the anterolateral region

    • Associated with the following conditions:

      • Steroids

      • Heavy alcohol use

      • Blood dyscrasias (e.g., sickle cell disease)

      • Dysbarism (caisson disease)

      • Excessive radiation therapy

      • Gaucher disease

    • Cause

 

• Osteonecrosis may be related to enlargement of space-occupying marrow fat cells, which lead to ischemia of adjacent tissues.

• Vascular insults and other factors may also be significant.

  • Idiopathic (or spontaneous) osteonecrosis is diagnosed when no other cause can be identified.

  • Chandler disease: osteonecrosis of the femoral head in adults

  • Medial femoral condyle osteonecrosis: most common in women older than 60 years

    • Idiopathic, alcohol, and dysbaric forms of osteonecrosis are associated with multiple insults.

    • These may be secondary to a hemoglobinopathy (e.g., sickle cell disease) or marrow disorder (e.g., hemochromatosis).

  • Cyclosporine has reduced the incidence of osteonecrosis of the femoral head among renal transplant recipients.

  • Pathologic changes

    • Grossly necrotic bone, fibrous tissue, and subchondral collapse (Figs. 1.24 and 1.25)

  • Histologic findings

    • Early changes (14–21 days) involve autolysis of osteocytes and necrotic marrow.

    • Followed by inflammation with invasion of buds of primitive mesenchymal tissue and capillaries

    • Newly woven bone is laid down on top of dead trabecular bone.

       

       

      FIG. 1.24 Fine-grain micrograph demonstrating space between articular surface and subchondral bone:

      crescent sign of osteonecrosis.

      From Steinberg ME: The hip and its disorders,

      Philadelphia, 1991, Saunders, p 630.

       

    • Followed by resorption of dead trabeculae and remodeling through creeping substitution

      • The bone is weakest during resorption and remodeling.

      • Collapse (crescent sign on radiographs) and fragmentation can occur.

  • Evaluation

    • A careful history (to discern risk factors) and physical examination (e.g., to discern decreased ROM, limp) should precede additional studies.

    • Other joints (especially the contralateral hip) should be evaluated to identify the disease process early.

    • The process is bilateral in the hip in 50% of cases of idiopathic osteonecrosis and up to 80% of cases of steroid-induced osteonecrosis.

       

  • Treatment

• MRI and bone scanning are helpful for early diagnosis.

  • MRI: earliest study to yield positive results; highest sensitivity and specificity

     

• Resurfacing arthroplasty of the hip is associated with increased risk of implant loosening and failure.

• Total hip arthroplasty is indicated in Ficat stage III or IV.

• Nontraumatic osteonecrosis of the distal femoral condyle and proximal humerus may improve spontaneously without surgery.

• Precise role of core decompression remains unresolved.

  • Results are best when core decompression is performed in early hip disease (Ficat stage I).

    • Osteochondrosis (Table 1.18)

      • Can occur at traction apophyses in children

      • May or may not be associated with trauma, joint capsule inflammation, vascular insult, or secondary thrombosis