Abstract
Avian tibial dyschondroplasia is a disease found in fast growing strains of chickens, ducks, and turkeys worldwide in which growth plate cartilage accumulates in the metaphyseal region of the tibiotarsus; it is similar to mammalian osteochondrosis. Several biochemical and pathologic studies have shown that the growth plate chondrocytes do not reach their expected size in the hypertrophic zone and necroses prematurely. The chondrocytes also produce decreased amounts of extracellular proteins, such as collagen X and fibroblast growth factor-beta, that are necessary for cartilage maturation. This immature cartilage becomes highly cross-linked in the collagen molecules and apparently resistant to resorption and vascularization by the metaphyseal vessels. The dyschondroplastic cartilage remains in the metaphysis for several weeks. Not until the growth rate of the birds slows down is the cartilage able to be resorbed and replaced by trabecular bone. Many conditions have been found to induce tibial dyschondroplasia, including copper deficiency; fusarochromanone, thiram, and antabuse intoxication; excessive dietary levels of cysteine and homocysteine; metabolic acidosis; and bird rearing environment. However, the mechanism(s) by which these various methods induce tibial dyschondroplasia is presently not known. Current research is focusing on understanding the development of the disease and whether or not all these methods work by the same physiological chain of events. Recent biochemical evidence suggests that a copper deficiency might be caused by a different mechanism than genetically and thiram-induced tibial dyschondroplasia.
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