Studies on the pathogenesis of avian rickets. I. Changes in epiphyseal and metaphyseal vessels in XXXX and @entity12146 .

@entity3747 @entity1184 @entity5886 @entity14645 @entity460 @entity12146
Growth plate morphometry and measurements of serum chemistry were correlated to clarify the pathogenesis of @entity14645 and @entity12146 . Accumulation of proliferating and maturing cartilage in @entity14645 chicks is accompanied by increased length and increased variation in length of perforating epiphyseal vessels, decreased number and abnormal arrangement of marrow spaces, an increased proportion of cells to blood vessels in marrow spaces, and a change in the distribution but not the total number of DNA-synthesizing chondrocytes per unit width of growth plate. Accumulation of @entity1184 cartilage in @entity12146 is accompanied by no change in length, distribution, or number of perforating epiphyseal vessels, elongation but no change in number or arrangement of marrow spaces, an increase in the relative proportion of blood vessels to cells in the marrow spaces, and no change in distribution but a decrease in total number of DNA-synthesizing chondrocytes per unit width of growth plate. Both types of rickets have decreased amounts of calcified cartilage. These results provide further evidence that @entity3747 and @entity5886 cause morphologically distinct types of rickets in birds. The data indicate that the thickness of the proliferating and maturing region and hence the distance of the @entity1184 zones from the epiphysis are anatomically and temporally related to length of perforating epiphyseal vessels and serum @entity460 levels. They indicate that in @entity14645 of proliferating and maturing cartilage is unlikely to be the result of increased chondrocyte replication and that the relative rates of chondrocyte @entity1184 and resorption of @entity1184 cartilage by marrow are equal. They support the concept that delayed chondrocyte @entity1184 is the major cause of growth plate thickening in @entity14645 . Data presented in this study, when considered together with data from the literature on @entity12146 , support the long-held concept that growth plate thickening in this disease is caused primarily by a decreased rate of resorption of @entity1184 cartilage by marrow relative to the rates of chondrocyte proliferation, maturation, and @entity1184 . The data further support the concepts that growth of cartilage into marrow is a biphasic process including longitudinal growth effected mainly by blood vessels, and resorption of the lateral walls of marrow spaces effected mainly by marrow cells, and that it is the latter phase that is defective in @entity5886 .
