Considerations of copper metabolism in osteochondrosis of suckling foals.

The research article focuses on studying the potential link between copper metabolism and the development of osteochondrosis in recently weaned Thoroughbred foals. The study discovered that most foals suffering from osteochondrosis had reduced serum copper and ceruloplasmin concentrations, with a few showing evidence of zinc toxicosis.

Research process and findings

• The study involved a group of 8 Thoroughbred foals in which osteochondrosis, a joint condition interrupting the normal development of cartilage, developed before the weaning stage. In 7 of these foals, serum copper and ceruloplasmin concentrations were below the normal range.
• Within this group, 3 foals were found to have considerably high serum zinc content, leading to the suspicion of zinc toxicosis. These same foals also had abnormally high concentrations of zinc in their liver.
• The remaining four foals from the second farm exhibited extremely low serum copper levels while maintaining normal serum zinc levels. No signs of possible environmental exposure to excess zinc were identified on both farms.

Copper metabolism and osteochondrosis

• This study demonstrated an apparent correlation between copper deficiency and the occurrence of osteochondrosis in young foals, leading to the conclusion that copper metabolism could potentially play a crucial role in the development of the condition.
• Further comparison of this phenomenon was made with similar conditions found in other animal species. Such conditions include molybdenum-induced copper deficiency and inhibition of the function of copper-dependent lysyl oxidase by beta-aminopropionitrile. The latter is a toxic component found in Lathyrus odoratus, known to cause osteolathyrism – a condition that affects the connective tissues in animals.
• The lesions present in the zones of endochondral ossification (the process of forming bone from cartilage) of these foals showed many similarities with those observed in animals suffering from the aforementioned conditions, reinforcing the link drawn between copper metabolism and osteochondrosis.