Abstract

Within the diaphyseal cortex, the primary resorption phase of Paget's disease is often limited either to the endosteum or to the central layers of the cortex. This results in primary resorption fronts that are usually discrete, both radiologically and scintigraphically. The subsequent activation of the subperiosteal cortex may be delayed, leading to secondary expanding fronts associated with subperiosteal new bone formation. Sequential radiographs of 19 untreated patients followed 6.4 +/- 1.2 years showed that the mean extension rate of the lesions within cortical bone was 8 +/- 0.5 mm/year per advancing front. This extension rate showed no significant change in 15 patients treated with calcitonin (CT) and/or ethane-1-hydroxy-1,1-diphosphonate (EHDP), but was significantly decreased in 14 patients treated with 3-amino-1-hydroxypropilidene-1,1-diphosphonate (APD). The increased remodeling rate of pagetic bone magnifies the radiologic changes due to mechanical, dystrophic, and metabolic interferences. Thus, a sclerotic pattern of the disease may rapidly change into a mixed or even a lytic pattern under the influence of any rarefying factor. Conversely, lytic pagetic bone may transform into dense bone through the administration of antiosteoclastic medications such as CT and APD. The reconstructive action of any new therapeutic regimen should be monitored radiologically.

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