A quantitative histologic study of avian osteopetrotic bone demonstrating normal osteoclast numbers and XXXX .

@entity1 @entity778 @entity66 @entity19 @entity5 @entity1573 @entity79 @entity2915 @entity74 @entity2525
@entity66 caused by @entity2915 are poorly understood partially because a suitable animal model is not available for their study. In contrast, a @entity74 caused by defective osteoclasts ( @entity1 @entity2525 ) is better understood, largely because of advances made with a @entity19 model of the disease. The avian form of @entity2525 is caused by RNA @entity5 viruses, but the role of osteoblasts and osteoclasts is not clear. We have performed a morphometric analysis of osteopetrotic avian bone to provide basic information about changes in the cells of bones from animals developing the disease. @entity1573 embryos were injected at 12 days of incubation with a @entity778 (MAV-2(0)) that induces @entity2525 at a high frequency. Changes in bone volume were detected 14 days after @entity778 injection. By 3 weeks of age, the bone volumes of osteopetrotic chicks were 4.7-fold larger than controls. The mean caliper diameter of an osteoclast was the same in osteopetrotic and normal bone. The number of osteoclasts per tibia increased in osteopetrotic animals, but the density of osteoclasts decreased. The presence of an increased number of osteoclasts of a normal size rules out the possibility that the @entity778 causes @entity2525 by selectively killing osteoclasts. The total bone-nonbone interface increased in @entity2525 , and greater than 90 per cent of interface surface was devoted to bone deposition. These results indicate that avian @entity2525 is an osteoblastic, proliferative @entity79 and may serve as an excellent animal model for @entity1 diseases in which osteoblasts increase in number.
