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Year |
2001 |
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Question Number |
227. |
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Category |
Select |
Question
The process of host repair following osteonecrosis is referred to as
1. haversian remodeling.
2. osteogensis.
3. osteoinduction.
4. fracture healing.
5. creeping substitution.
Figures
Answer (click for answer)
Answer: 5
Osteonecrosis, or bone death, occurs as a result of either impaired blood supply (eg. due to trauma) or severe marrow and bone cell damage. The hip joint is commonly affected, causing eventual collapse and flattening of the femoral head. Other susceptible sites include the femoral condyles, head of humerus, capitulum, scaphoid, lunate and talus.
It is associated with steroids and heavy alcohol consumption (both causing fatty infiltration and capillary compression), and also with blood dyscrasias (such as Sickle-cell Disease), decompression sickness (Caisson Disease), vasculitis, excessive radiation therapy, and Gaucher’s Disease (abnormal accumulation of glucocerebride in the reticuloendothelial system causes pressure on bone sinusoids, thus necrosis).
The etiology of osteonecrosis is uncertain, but various factors have been implicated. These include vascular insults, and the enlargement of space-occupying marrow fat cells, causing ischemia of adjacent tissues.
Pathologic Changes that occur are divided into four overlapping stages:
1) Bone death without structural change – Within 24 hours after infarction there is autolysis of osteocytes and necrosis of marrow.
2) Repair and early structural failure – Inflammation occurs, with a vascular reaction. New bone is laid down upon the dead trabeculae (visible on X-ray as increased bone density).
3) Major structural failure – A process of "creeping substitution" occurs, with resorption of necrotic trabeculae and remodeling. The bone is weakest during this phase, and collapse (crescent sign) and fragmentation may occur.
4) Articular destruction – Cartilage, deriving nourishment from synovial fluid, is preserved even in advanced osteonecrosis. However, severe distortion of the surface eventually results in cartilage destruction.
Detailed history-taking and physical examination (eg.? range of movement, pain, stiffness) are obvious first lines of evaluation. Other joints should be examined in order for early diagnosis of the disease process. In 50% of cases of idiopathic osteonecrosis, and in 80% of cases of steroid-induced osteonecrosis, disease is bilateral.
Diagnosis is aided by MRI and bone scans, as well as radiography which shows distinctively increased bone density due to reactive new bone formation in the surrounding viable tissue. Femoral head pressure measurements may also be done – pressure greater than 30 mm Hg, or an increase of over 10 mm Hg with injection of 5ml of saline is considered abnormal.
Treatment should aim to eliminate the cause if possible. Nontraumatic osteonecrosis of the proximal humerus and femoral condyle may show spontaneous improvement. In stages 1 and 2, weight-relief, splintage and surgical decompression of the bone may prevent bone collapse. If in stage 3 (ie. bone collapse has occurred), realignment osteotomy to shift stress to an undamaged area may relieve pain and prevent further bony injury. If in stage 4, treatment is the same as for osteoarthritis.
Reference: Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemont, IL, American Acaemy of Orthopaedic Surgeons, 2000, pp 372-399.
http://www.worldortho.com/database/etext/basicsci.html