CELL-DEATH IN AVIAN TIBIAL DYSCHONDROPLASIA

Tibial dyschondroplasia (TD) is a local defect of growth plates in fas tgrowing poultry where the transitional zone cartilage fails to resorb and persists as an avascular plug that prevents endochondral bone for mation. We compared the differences in the cartilages from normal and TD-affected growth plates using the reduction of MTS to assess cartila ge viability. Chondrocyte apoptosis was determined using biochemical m easurement of DNA fragmentation, and in situ labeling of nuclei with f luorescein-dUTP using terminal deoxynucleotide transferase (TdT)-media ted nick end labeling (TUNEL) of isolated chondrocytes and growth plat e sections. The TD-affected cartilage showed a significantly lower lev el of MTS reduction and a decrease in trichloroacetic acid (TCA)-preci pitable DNA content. The TD cartilages had a higher percentage of frag mented DNA, which was also evident with agarose gel electrophoresis. A significantly higher number of chondrocytes isolated from TD-affected cartilages had condensed morphology, shrunken nuclei with little cyto plasm, and were TUNEL positive as identified by the incorporation of f luorescein-dUTP into the nuclei. In vivo results similarly showed a si gnificant population of chondrocytes in transition zones undergoing co ndensation and apoptosis as determined by in situ TUNEL staining of gr owth plate sections. Normal growth plates, under similar conditions, s howed no significant apoptosis of chondrocytes from hypertrophic and c hondrolyzing zones. The condensation and apoptotic cell death may be r esponsible for the reduction of growth plate viability as well as the reduction in DNA content and increased DNA fragmentation. While the ca use of the pathogenesis of TD is unknown, it appears that the aberrant death of chondrocytes in hypertrophic regions of growth plates may be responsible for the accumulation of cartilage and the arrest of endoc hondral bone formation.