Morphological observations concerning the pattern of mineralization of the normal and the rachitic chick growth cartilage

Publisher Website
Google Scholar
Abstract
The entire calcified layer of the chick growth cartilage is penetrated by canals that contains blood vessel complexes: some of these canals pass through all the layers of the cartilage from the resorptive zone at the metaphysis, through the mineralizing, hypertrophic, proliferative and resting regions. This study aimed to provide more details of the 3-D microanatomy of this region and to establish whether there are differences in the process and progress of mineralization compared with the established mammalian “model”. Proximal tibial heads from 6 to 8 weeks old normal and vitamin D deficient chickens were rapidly frozen and prepared for scanning electron microscopy using freezefracture, freeze-drying, plasma ashing, and chemical deproteinization techniques. Cartilage samples were also embedded in PMMA and polished for BSE imaging. Other samples were prepared for light microscopy. Zones of (mineralized) cartilage several cells thick separate adjacent canals. At the mineralizing front, calcification of the matrix is most advanced close to the canals, but the matrix adjacent to the canal lumens does not calcify. Mineralisation of the cartilage matrix is incomplete and small fenestrae of unmineralized matrix connect chondrocyte lacunae. These discontinuities in matrix calcification could serve as a route for diffusion of nutrients, metabolites and dissolved gases. The calcified cartilage is more mineralized than the contiguous developing bone. Osteoblasts surrounded by bone were seen to occupy the lacunae of hypertrophic chondrocytes. We tentatively suggest that some osteoblasts represent a terminal stage in the differentiation of hypertrophic chondrocytes. The rachitic cartilage was disorganised. It was penetrated by irrugular vascular canals and exhibited a greatly expanded hypertrophic zone. The matrix was mineralized and mineral particles and clusters were spread throughout the matrix. However, these centres did not become continuous with adjacent or contiguous mineral. The results indicate that an absence of vitamin D affects crystal growth rather than initiation.