Key points are not available for this paper at this time.
Reduced enzyme activities and elevated phosphate in TD cartilage suggest impaired turnover; leaves open mechanistic drivers in avian skeletal disease.
Comparative differences between tibial dyschondroplastic (TD) and age-matched control turkey epiphyseal cartilages were studied using cellular, metabolic, and extracellular matrix characteristics. Alkaline phosphatase and aryl sulfatase activities were measured as variables of calcification and cartilage degradation, respectively. There was a decrease in the activities of both enzymes in TD tissues. An increase in tissue phosphate concentrations was noted in the TD tissue whereas neither tissue calcium nor serum calcium and phosphorous concentrations were affected. Profiles of noncollagenous and collagenous proteins from normal and TD-affected tissues were compared following in vitro biotinylation of epiphyseal cartilage followed by a sequential extraction using 4 M guanidine HCl and pepsin digestion, respectively. Electrophoretically separated proteins from both extracts were analyzed on Western blots and compared for any prominent differences between normal and TD cartilages. Biotinylation enhanced the detectability of extracted proteins. There were, however, no major differences in the patterns of noncollagenous or collagenous proteins between the two groups of tissues. Tibial dyschondroplastic lesions further exhibited a large number of dead chondrocytes, which increased with severity of lesion. There appears to be no significant difference in the pattern of extracellular-matrix-associated proteins. However, enzyme and metabolic activities of TD-affected cartilages were significantly reduced, and this may be due to premature death of chondrocytes in the process of development.
No takes yet. Share an insight, caveat, or question.
Rath et al. (1994) studied this question.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: