Access Keys:
Skip to content (Access Key - 0)

  • Some of the more common abnormalities seen include
    • IgG anti-cardiolipin antibodies
    • Stimulated plasminogen activator
    • Plasminogen activator inhibitor-1
  • Similar results have been reported in other studies

  •  

  • Other predisposing factors may include
    • Mutations in a multidrug resistance gene
    • Genetic variation in alcohol-metabolizing enzymes
    • Abnormal type II collagen
  • ...

    • MRI is the modality of choice for diagnosing and monitoring stage I disease (99% sensitivity and specificity)

  • Once the disease has progressed to stage II, plain films are typically the preferred imaging modality
  • ...

    • At least 17 classification systems have been used
    • The majority are branches of the Ficat and Arlet System outlined below
    • Ficat and Arlet classification system outlines the natural progression of the disease

     

    Image RemovedJones LC, Hungerford DS, 2007. "The pathogenesis of osteonecrosis." Instr Course Lect 56: 179-96 [PubMed]
    [ a b ]Image RemovedCui Q, Wang GJ, Balian G, 1997. "Steroid-induced adipogenesis in a pluripotential cell line from bone marrow." J Bone Joint Surg Am 79 (7): 1054-63 [PubMed]
    [ a b ] 

  • Alcohol abuse
    • Up to 29% of patients with ON have a history of alcohol abuse
    • However, only 5% of patients with a history of alcohol abuse develop ON

  • The
      •  

  • The pathophysiolgy of corticosteroid and alcohol-related ON has been studied extensively and the strongest evidence is in support of increased adipogenesis as a major underlying mechanism
    • It has been shown that corticosteroids and ethanol can induce the pluripotent bone marrow cell line to preferentially differentiate into adipocytes in vitro
    • Increased adipogenesis causes venous sinusoidal compression which leads to venous congestion, intraosseous hypertension, impaired arterial flow and ultimately infarction

  • Osteonecrosis

    Versions Compared

    Key

    • This line was added.
    • This line was removed.
    • Formatting was changed.

    ...

    • ON is certainly a multifactorial process that is not clearly defined as of yet
    • Most would argue that it is caused by a combination of
      • Metabolic factors
      • Local factors that affect blood supply (e.g., vascular damage)
      • Increased intraosseous pressure
      • Mechanical stresses
    • Majority of osteonecrosis cases are related to
      • Idiopathic disease
      • High dose of corticosteroid
        • Up to 38% of patients with ON have a history of high dose corticosteroid use (~2 grams of prednisone within 2-3 months)
        • However, only 5% of patients with a history of high dose corticosteroid use develop osteonecrosis

    Footnote
    Anchor
    17472306
    Footnote
    Anchor
    9234882
    Footnote

    Image Removed Jones LC, Hungerford DS, 2007. "The pathogenesis of osteonecrosis." Instr Course Lect 56: 179-96 [PubMed]
    [ a b ]

    Footnote

    Laroche M, 2002. "Intraosseous circulation from physiology to disease." Joint Bone Spine 69 (3): 262-9 [PubMed]

    Footnote

    Wang GJ, Sweet DE, Reger SI, Thompson RC, 1977. "Fat-cell changes as a mechanism of avascular necrosis of the femoral head in cortisone-treated rabbits." J Bone Joint Surg Am 59 (6): 729-35 [PubMed]

  • However, as stated earlier, only 5% of patients with a history of high-dose corticosteroid use or alcohol abuse develop ON
  • Corticosteroid use and excessive alcohol intake have been speculated to contribute to vascular compromise through
    • Elevations in lipid levels resulting in microemboli
    • Increased bone marrow fat cell size that leads to venous flow obstruction
    • Alterations in venous endothelial cells causing stasis and increased intraosseous pressure
  • Many groups are researching genetic traits that may predispose to the development of ON
  • There is increasing evidence for the role of clotting disorders in the development of this disease
    • One study reported 82% of patients with osteonecrosis had at least one clotting disorder vs. 30% of controls

  • Footnote

    Jones LC, Mont MA, Le TB, Petri M, Hungerford DS, Wang P, Glueck CJ, 2003. "Procoagulants and osteonecrosis." J Rheumatol 30 (4): 783-91 [PubMed]

    Footnote

    Glueck CJ, Freiberg RA, Wang P, 2008. "Heritable thrombophilia-hypofibrinolysis and osteonecrosis of the femoral head." Clin Orthop Relat Res 466 (5): 1034-40 [PubMed]

    Footnote

    Lieberman JR, Berry DJ, Mont MA, Aaron RK, Callaghan JJ, Rajadhyaksha AD, Urbaniak JR, 2003. "Osteonecrosis of the hip: management in the 21st century." Instr Course Lect 52: 337-55 [PubMed]

    Footnote

    Mont MA, Marulanda GA, Jones LC, Saleh KJ, Gordon N, Hungerford DS, Steinberg ME, 2006. "Systematic analysis of classification systems for osteonecrosis of the femoral head." J Bone Joint Surg Am 88 Suppl 3: 16-26 [PubMed]

    Stage

    Imaging Findings

    I

    Evidence seen on MRI only

    II

    Diffuse sclerosis, subchondral cysts. No femoral head collapse

    III

    Subchondral fracture ("Crescent sign") with or without collapse

    IV

    Collapse of the femoral head and secondary degenerative joint disease

    ...

    • The main complication of conservative management is disease progression to subchondral bone collapse and joint destruction
    • The most common complication of core decompression, reported in 0-18% of cases, is hip fracture
    • Vascularized fibular grafting
      • It is a more complicated procedure than other bone grafts, so it has related morbidity consequences; all of which must be considered especially in older patients
      • Disadvantages
        • Longer recovery
        • Less complete analgesia
        • Variable success rate
        • Decreased effectiveness in advanced osteonecrosis
      • Complications
        • Ankle pain
        • Great-toe flexion contracture
        • Foot motor weakness and sensory loss
        • Femoral fracture
        • Deep vein thrombosis
        • Pin migration
        • Hematoma
        • Trochanteric bursitis
      • The overall complication rate for vascularized fibular grafting was found to be 17% at an average of 8 years
      • 4% of total cases required additional surgery or chronic pain management
    • Total hip replacement
      • Deep vein thrombosis (3-5%)
      • Dislocation (1-5%)
      • Infection (1-2%)

    References

    Display Footnotes

    Jones LC, Hungerford DS, 2007. "The pathogenesis of osteonecrosis." Instr Course Lect56: 179-96 [PubMed]

     Cui Q, Wang GJ, Balian G, 1997. "Steroid-induced adipogenesis in a pluripotential cell line from bone marrow." J Bone Joint Surg Am 79 (7): 1054-63 [PubMed]

     Jones LC, Hungerford DS, 2007. "The pathogenesis of osteonecrosis." Instr Course Lect 56: 179-96 [PubMed]

     Laroche M, 2002. "Intraosseous circulation from physiology to disease." Joint Bone Spine69 (3): 262-9 [PubMed]

     Wang GJ, Sweet DE, Reger SI, Thompson RC, 1977. "Fat-cell changes as a mechanism of avascular necrosis of the femoral head in cortisone-treated rabbits." J Bone Joint Surg Am59 (6): 729-35 [PubMed]

     Jones LC, Mont MA, Le TB, Petri M, Hungerford DS, Wang P, Glueck CJ, 2003. "Procoagulants and osteonecrosis." J Rheumatol 30 (4): 783-91 [PubMed]

     Glueck CJ, Freiberg RA, Wang P, 2008. "Heritable thrombophilia-hypofibrinolysis and osteonecrosis of the femoral head." Clin Orthop Relat Res 466 (5): 1034-40 [PubMed]

     Lieberman JR, Berry DJ, Mont MA, Aaron RK, Callaghan JJ, Rajadhyaksha AD, Urbaniak JR, 2003. "Osteonecrosis of the hip: management in the 21st century." Instr Course Lect 52: 337-55 [PubMed]

     Mont MA, Marulanda GA, Jones LC, Saleh KJ, Gordon N, Hungerford DS, Steinberg ME, 2006. "Systematic analysis of classification systems for osteonecrosis of the femoral head." J Bone Joint Surg Am 88 Suppl 3: 16-26 [PubMed]