A number of nutrients and chemicals have now been identified as consistent inducers of tibia dyschondroplasia (TD). Thiram, Antabuse, and fusarochromanone induce TD when fed at 30 to 75 ppm. Cysteine, cystine, homocysteine, and histidine induced TD when fed at .5 to 3% of the diet. Cation: anion imbalances resulting in acidotic diets also induced TD. Even though prevention of TD induced by these chemicals and nutrients has been established, reversal of the spontaneous TD lesion has not been clearly demonstrated. Thus, the etiology of the spontaneous lesion awaits elucidation. These model systems all suggest that TD is the result of decreased growth plate cartilage degradation. Recent work has shown that increased collagen cross-links in the accumulated cartilage, which makes collagen less susceptible to degradation. Cysteine-induced TD seems to decrease growth plate collagenase activity and production. A role of growth plate macrophages in paracrine signaling of collagenase production by chondrocytes has been presented.