Many factors must be considered in the pathogenesis of ischemic necrosis of bone. Etiologic considerations deal with the heterogeneous disease categories that are associated with bone necrosis; these may affect bone circulation either directly or indirectly on either the arterial or the venous side. Moreover, the compartmental nature of bone makes it vulnerable to the direct effects of pathologic processes on the cellular elements of the intraosseous extravascular compartment. Once ischemia has been initiated, whether directly through influence on the circulatory tree or indirectly by the elevation of bone marrow pressure, the effects of ischemia are likely to be further potentiated because of the compartmental nature of bone blood flow. Once a critical level of ischemia is surpassed, it is possible that the condition becomes self perpetuating through increased bone marrow pressure leading to further ischemia. Interruption of this cycle by core decompression can be successful if extensive tissue death has not already occurred at the time of the intervention.
|Original language||English (US)|
|Number of pages||8|
|Journal||Canadian Journal of Surgery|
|State||Published - Dec 1 1981|
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