TYPE-X COLLAGEN BIOSYNTHESIS AND EXPRESSION IN AVIAN TIBIAL DYSCHONDROPLASIA

Objective: Tibial dyschondroplasia (TD) is an abnormality of growth pl ate cartilage characterized by the presence of non-vascularized, non-m ineralized tissue. The objective of this study was to examine structur al and functional alterations of the growth plate-specific type X coll agen in TD cartilage. Design: Collagen biosynthesis was examined in or gan cultures and in cultured chondrocytes from normal growth plate and TD cartilage. Thermal stability of type X collagen extracted from nor mal and TD cartilage organ cultures to protease digestions by trypsin plus chymotrypsin or bacterial collagenase was determined. The express ion of collagen genes was examined in cultured normal and TD chondrocy tes. Results: Synthesis of total collagen and of type X collagen was g reater than threefold higher in organ cultures from the TD lesion comp ared with normal growth plate. The increase in type X collagen synthes is in the lesion was compensated by a reduction in the relative propor tions of types II and XI collagens. The thermal denaturation and colla genase cleavage properties of purified types TI and X collagens from T D cartilage were normal. The expression of type X collagen gene was th reefold higher in cultured TD chondrocytes compared to chondrocytes fr om normal growth plate. Normal growth plate chondrocytes in primary cu ltures synthesized predominantly type X collagen (80% of total collage n). In contrast, TD chondrocytes synthesized mainly types I and Il col lagens and type X collagen represented only 22% of total collagen. TD cells initiated the synthesis of type I collagen within 5 days of prim ary culture, whereas normal chondrocytes did not synthesize this colla gen during the same culture period. Although type X collagen synthesis was reduced in TD chondrocytes, the mRNA levels for type X collagen w ere substantially higher than in normal chondrocytes. Conclusion: Accu mulation of type X collagen in TD cartilage results from its increased biosynthesis which is due largely to increased expression of the gene for this collagen, although, the chondrocyte culture studies suggest the possibility of postranscriptional defect in type X collagen synthe sis or processing in TD lesion. Moreover, the TD chondrocytes in contr ast with normal chondrocytes display evidence of prompt loss of their specific phenotype during short-term primary cultures.