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Equine dyschondroplasia (osteochondrosis)--histological findings and type VI collagen localization
F M Henson1, M E Davies, L B Jeffcott
1Department of Clinical Veterinary Medicine, University of Cambridge, UK.
Abstract:
This study describes (1) the histological appearance of dyschondroplasia, the primary lesion of osteochondrosis, in articular cartilage of the horse and (2) the localization of type VI collagen which is an important constituent of the extracellular matrix (ECM). Dyschondroplastic cartilage was identified on the basis of the presence of cartilage cores (i.e., cartilage extending into the subchondral bone) and confirmed with subsequent histological examination. Full-thickness cartilage samples from 57 horses were collected and paraffin embedded. Histological examination was used to examine the normal architecture of equine growth cartilage and to determine the presence of various pathological changes in dyschondroplastic lesions. Immunolocalization was used to identify type VI collagen in normal and dyschondroplastic lesions. The abnormalities observed in the dyschondroplastic cartilage fell into two groups. In Group A (n = 18) the lesions were associated with a disruption in the normal sequential transition of the chondrocytes through proliferation and maturation resulting in an accumulation of large numbers of small, rounded chondrocytes. A decrease in type VI collagen immunoreactivity compared with normal animals was detected except around chondrocyte clusters. Group B lesions (n = 9) were characterized by an alteration in the staining pattern of the mineralized cartilage and underlying bone. In these lesions type VI collagen immunoreactivity was increased. In both groups the presence of retained blood vessels, chondrocyte clusters, chondronecrosis and fissure formation was detected. These two histologically-distinct groups suggest that equine dyschondroplasia may be comprised of different pathological entities and that it is associated with alterations in the pattern of distribution of an ECM protein.