In osteochondrosis (OC) the process of endochondral ossification is impaired. Proteoglycans form one of the major components of the extracellular matrix of cartilage and are able to bind calcium. For this reason, proteoglycans are thought to play an important role early in the mineralisation process and may, therefore, be important in the pathogenesis of OC. To investigate possible differences in proteoglycan metabolism, normal and osteochondrotic articular-epiphyseal cartilage was harvested from the hock and stifle joints of 43 foals age 5 and 11 months. The samples were cultured as explants in which 35S-[sulphate]-incorporation, release of newly synthesised and endogenous proteoglycans and content of DNA and proteoglycans were measured ex vivo and after a 4 day period of serum stimulation. In osteochondrotic cartilage of foals age both 5 and 11 months synthesis of proteoglycans was less stimulated by serum than in normal cartilage. Furthermore, only in the foals age 11 months, ex vivo proteoglycan production was decreased and an increase in the turnover of newly synthesised proteoglycans was detected in osteochondrotic cartilage, without a change in release of endogenous proteoglycans. The reduced response to serum stimulation in osteochondrotic cartilage indicates that osteochondrotic chondrocytes are less vital. The increase in turnover of newly synthesised proteoglycans reflects a change in composition of the proteoglycan pool. Considering the late changes in proteoglycan synthesis, an aberrant proteoglycan synthesis pattern is more likely to be a sequence than a primary cause of the impaired endochondral ossification of osteochondrotic lesions.