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Royal National Orthopaedic Hospital, London, W.1
Anna-Klinick voor Orthopaedie, Leiden, Holland
This excerpt was created in the absence of an abstract.
Although many theories have been advanced in an attempt to explain the aetiology of Perthes' disease, the precise nature of the condition has yet to be established. In support of the concept that the disease could be due to a circulatory disturbance, it is of interest to recall that Legg (1910) believed that injury could interfere with the epiphyseal circulation. Amongst those who supported the concept of a vascular disturbance, Burrows (1941) appears to have been the first to consider the possibility of the lesion occurring as a sequel to occlusion of the venous return. He suggested that in cases of coxa plana preceded by transient arthritis, the effusion may exert pressure on the veins draining the epiphysis, so that they become obstructed.
More recently, experimental work has been presented supporting this vascular concept (Bassett, Wilson, Allen and Azuma, 1969). Other experimental studies have shown that tamponade, at pressures producing transient venous occlusion, lead to a raised intramedullary pressure, causing a stagnant anoxia which will induce osteocyte and osteoblast death (Kemp, 1969).
If this concept that the disease is due to transient venous anoxia is correct, it would be logical to anticipate that the lesion could occur more than once in the same epiphysis during growth.
Amstutz and Carey (1966) quoted two cases of recurrent necrosis occurring in Gaucher's disease, though both their cases were older than the usual age group in which Perthes' disease normally occurs.
Received for publication January 1, 1971.
Revision received May 1, 1971.
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