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Legg-Calvé-Perthes Disease—Pathogenesis and Evolution Failure of Treatment with L-Triiodothyronine
Ignacio V. Ponseti; Ralph L. Cotton
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Department of Orthopaedic Surgery, State University of Iowa, Iowa City
1961 by The Journal of Bone and Joint Surgery, Incorporated
The Journal of Bone & Joint Surgery.  1961; 43:261-274 
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Abstract

We suspect that the primary lesion in Legg-Calvé-Perthes disease is a weakening and disruption of the upper femoral epiphyseal plate. Aseptic necrosis of the femoral head results from the interruption of the retinacular vessels when they cross the cartilage at the edge of the disrupted plate.

Early clinical signs of Legg-Calvé-Perthes disease are related to synovitis, which usually follows total femoral-head necrosis and collapse of the center of ossification.

The speed of recovery of the necrotic epiphysis is related to the severity of the epiphyseal-plate lesion and of bone collapse.

No evidence of thyroid dysfunction was discovered in our patients. Administration of large doses of l-triiodothyronine during periods of from six to eighteen months did not alter the speed of reconstruction of the necrotic femoral head.

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    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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