Chicken tibial dyschondroplasia: A limb mutant with two growth plates and possible defects of collagen crosslinking

Abstract

In the cartilaginous epiphyseal growth plate, extracellular matrix molecules such as collagens are believed to play important roles during both normal and abnormal development. One defect of the epiphyseal plate occurs in chickens with a condition termed tibial dyschondroplasia (TD). This abnormality occurs in certain strains of juvenile chickens and other rapidly developing animals. It is characterized by the presence of a mass of avascular, uncalcified cartilage which is retained in the proximal metaphysis of the tibiotarsus. To elucidate the developmental events which may be involved in this lesion, we have performed both immunohistochemistry and in situ hybridizations for collagen types II and X, known components of the extracellular matrix of the growth plate. By immunohistochemical analyses, the TD lesion contains both of these collagen types; therefore, the presence of these molecules per se is not sufficient for calcification of vascularization to occur. Since type X collagen is expressed exclusively in hypertrophic cartilage, the chondrocytes in the lesion must have undergone hypertrophy before their developmental arrest. The matrix of the lesion also reacted with a monoclonal antibody which is directed against an epitope in the NH₂‐terminal telopeptide of the α1(II) chain. Our previous data suggest that this epitope is rendered unavailable in type II collagen which has undergone crosslink formation; its availability in the lesion suggests that crosslinking may be abnormal. Lastly, analyses by in situ hybridization failed to detect mRNA for either type II or type X collagen within the lesion, but chondrocytes distal to the lesion do contain mRNAs for these collagens in a spatial pattern suggesting the presence of a second growth plate.