Tibial dyschondroplasia (TD) is a disorder of endochondral ossification characterized by the presence of an avascular, non-mineralized cartilage lesion extending from the growth plate into the metaphysis. Cells within the TD growth plate fail to differentiate to full hypertrophy, and instead appear to maintain a 'pre-hypertrophic' or 'transitional' status. The synthesis and distribution of aggrecan, biglycan, decorin, and collagen types II and X in the growth plates of normal and tibial dyschondroplastic chickens have been investigated using in situ hybridization and immunolocalization. Marked reductions in the amount of aggrecan and biglycan core protein mRNAs were observed in the tibial dyschondroplastic lesion by in situ hybridization. Reduction in mRNA production seemed to be specific to the extracellular matrix components since total mRNA expression showed no significant difference between normal and dyschondroplastic cartilage. In addition, expression of collagen type II and decorin did not differ significantly between normal and TD cartilage. Distribution of aggrecan biglycan, decorin, type II and X collagens were examined using immunohistochemistry. Normal hypertrophic cartilage showed a strong matrix labelling for aggrecan and biglycan. Type X collagen in the normal hypertrophic cartilage showed strong pericellular and matrix distribution, whereas in TD cartilage labelling for aggrecan, biglycan and collagen X was located intracellularly with a very low level of signal in the matrix. In contrast, collagen type II was found to be present throughout the extracellular matrix of both the normal growth plate and the TD lesion, suggesting that the differences observed in aggrecan, biglycan and type X collagen distribution are specific to these proteins and not a general disturbance of matrix macromolecular metabolism. The reduced deposition of these macromolecules may have implications in normal and pathological bone development.