Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 10, 1997
Publication Date: N/A
Interpretive Summary: Tibial dyschondroplasia (TD) is a leg problem in adolescent, meat-type poultry that is characterized by the presence of a plug of cartilage that prevents normal development of leg bones. TD makes the leg bones fragile and may lead to distortions and infections of bone. We employed biochemical and histochemical methods to understand the problems associated with the cells of the growth plate cartilage that may be responsible for this defect. Our results show that the cartilages of TD-affected birds that may be responsible for their lowered metabolic activities, prevention of bone development, and consequently, to the accumulation of a mass of nonviable cartilage.
Technical Abstract: Tibial dyschondroplasia (TD) is a local defect of growth plate cartilage in fast-growing poultry where the transitional zone chondrocytes fail to undergo hypertrophy, calcification, and subsequent replacement by bone. The cartilage persists as an avascular plug whose metabolic and functional activities are significantly impaired. We investigated the changes associated with the growth plate chondrocytes from TD-affected cartilages using in vitro reduction of MTS (3-(4,5 dimethylthiazol-2-yl)-5- (3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt) by cartilage explants, morphological assessment of isolated cells, and the determination of apoptosis using terminal deoxynucleotide transferase (TdT) mediated 3'-OH labeling of DNA breaks with fluorescein-dUTP. The TD-affected cartilage showed a lower level of MTS reduction while a significant population of cells in the transition-zone exhibited condensation and apoptosis as determined using in situ staining of growth plate sections and in vitro isolated cells from these tissues. Normal growth plates, under similar conditions, showed no specific apoptosis in chondrocytes from hypertrophic and chondrolysing zones but there were many cells in the invading vasculature that were labeled. While the cause of TD is unknown, it appears that reduced metabolic and functional activities of cartilage in this defect may be due to the aberrant death of the chondrocyte in hypertrophic regions of the growth plate.