Avian tibial dyschondroplasia. I. Ultrastructure

• Published in: The American journal of pathology Vol. 119; no. 2; pp. 175 - 190
• Main Authors: Hargest, TE, Leach, RM, Gay, CV
• Format: Journal Article
• Language: English
• Published: Bethesda, MD ASIP 01.05.1985; American Society for Investigative Pathology
• Subjects: Animals; Biological and medical sciences; Cell Nucleus - ultrastructure; Chickens; Diseases of the osteoarticular system; Malformations and congenital and or hereditary diseases involving bones. Joint deformations; Medical sciences; Necrosis; Osteochondrodysplasias - etiology; Osteochondrodysplasias - pathology; Tibia - ultrastructure; Pathology; Vertebrata; Experimental disease; Tibia; Chondrodysplasia; Diseases of the osteoarticular system; Aves; Osteochondrodysplasia
• ISSN: 0002-9440; 1525-2191

Tibial dyschondroplasia is an abnormality of the growth cartilage that occurs in chickens and other rapidly growing animals. The disease is characterized by a mass of avascular opaque cartilage, which is continuous with the growth plate of the proximal tibia and extends into the metaphysis. In this study electron micrographs revealed that chondrocytes in the hypertrophic zone of the growth plate were normal in appearance with the exception that the cells did not undergo complete hypertrophy. In the proximal region of the lesion, cells began to undergo necrotic changes suggestive of an energy depletion. These changes included dilatation and vesiculation of the endoplasmic reticulum, enlargement of the paranuclear space, mitochondrial swelling with dilatation of the intracristal spaces and the appearance of electron-dense, flocculent material in the mitochondrial matrix, chromatin margination, and dilatation of the Golgi saccules. Chondrocytes also occurred with rarefied cytoplasm and atrophic Golgi saccules. A few cartilage cells in the proximal region of smaller lesions contained crescentic caps of condensed chromatin in the nuclei, which is indicative of apoptosis. These cells also exhibited dilated endoplasmic reticulum and lamellar bodies; and sometimes, in the proximal region of the lesion, they appeared to be condensed and convoluted. This process continued in the mid and distal regions. The condensed necrotic cells appeared as amorphous osmiophilic masses with karyorrhexic and pyknotic nuclei. Matrix vesicles were observed at all levels of the lesion, but calcified only at the distal edge of the lesion, where mineralization of both matrix and cells occurred. The resulting shell of mineral may act as a diffusion barrier.