Mineralization of normal and rachitic chick growth cartilage: vascular canals, cartilage calcification and osteogenesis.
This paper reviews recent work in the authors' laboratories that has led to new observations and thoughts concerning the mineralization of normal and rachitic chick growth cartilage. The proximal tibial growth cartilages of normal and rachitic chicks were rapidly frozen and prepared for SEM and biochemical studies. Using a scanning microfluorimetric technique we showed that at the mineralization front of normal and rachitic cartilage there is an abrupt change in chondrocyte metabolism. Thus cells in this region exhibited an increase in NADH and oxidative metabolism. In rickets, there was a decrease in the reduced pyridine nucleotide content of each of the zones. The reversal in chondrocyte metabolism was not due to low oxygen tension. SEM observations indicated that this region of cartilage was well supplied with vascular channels; moreover, mineral was first seen deposited in matrix in close proximity to the blood supply. Indeed these vascular channels appeared to be a basic architectural feature of normal cartilage, although disorganized in the rachitic state. The morphological studies also showed that gaps existed in the continuity of the mineral phase in normal cartilage. Although the rachitic cartilage does mineralize, discontinuities in the mineral distribution are much more severe, with the general failure of fusion of adjacent mineral clusters. These structures would serve as pathways for transport of nutritional factors and gases to chondrocytes that are distant from the vascular channels. Observation of hypertrophic cells reinforced the view that some osteoblasts represented a terminal stage in the maturation of chondrocytes.
D000818:Animals; D001846:Bone Development; D002114:Calcinosis / Q000473:pathology*; D002645:Chickens; D005614:Freeze Fracturing; D006132:Growth Plate / Q000098:blood supply / Q000473:pathology / Q000648:ultrastructure*; D008854:Microscopy, Electron; D010012:Osteogenesis; D012279:Rickets / Q000473:pathology*