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The clinical, radiological and pathological findings in a natural outbreak of rickets affecting 82 pigs are described. An interesting feature was the presence of gross articular abnormalities including resorption of subchondral bone with folding and ulceration of the articular cartilage. The diet was deficient in calcium and vitamin D. A diagnosis of rickets complicated by nutritional secondary hyperparathyroidism was made. The results of treatment and the economics of the outbreak are discussed.
Vet Rec 1978 Jul
PMID:Rickets in growing pigs and response to treatment. 67 16

The most commonly encountered nutritional bone disease is nutritional secondary hyperparathyroidism. This is primarily of importance in the dog but is occasionally seen in kittens, particularly of the Siamese breed, and is often associated with the feeding of owner compiled, meat-rich diets. Classic rickets is now a rare clinical entity. Hypertrophic osteodystrophy is regularly seen in the larger breeds of dog and the aetiology remains obscure. Hypervitaminosis A associated with liver-rich diets is often encountered in the cat. Hypovitaminosis A has been described but its true clinical significance is unknown.
Vet Rec 1976 Apr 17
PMID:Nutrition and bone disease in the dog and cat. 77 53

Type X collagen is a prominent component of the extracellular matrix in cartilage destined to mineralize during endochondral ossification, yet its role is only now being determined. As a prelude to determining what, if any, alterations occur in the distribution of type X collagen in growth plates of poultry with rickets or tibial dyschondroplasia, our objective in the current study was to determine the distribution of type X collagen in the proximal tibiotarsi of broiler chickens and turkeys from 1 day of age through physeal closure. Proximal tibiotarsi from five male broiler chickens, five female broiler chickens and five male turkeys were collected at 1, 7, 14, 28, 56, and 98 days of age and processed for immunohistochemistry; a monoclonal antibody for type X collagen was used to demonstrate type X collagen distribution. Our findings indicate that type X collagen is produced in the prehypertrophic and early hypertrophic zones of the avian growth plate and is incorporated into the extracellular matrix in these zones. Furthermore, intracellular type X collagen is markedly decreased in more mature areas of the growth plate, although type X collagen remains a prominent component of the extracellular matrix until the matrix is completely resorbed. In addition, the distribution of type X collagen is similar in the proximal tibiotarsi of broiler chickens and turkeys at comparable stages of endochondral ossification and distribution of type X collagen in the secondary center of ossification parallels that in the physis.
Anat Rec 1990 Jul
PMID:Immunohistochemical localization of type X collagen in the proximal tibiotarsi of broiler chickens and turkeys. 169 95

The morphology of the metaphyseal microvasculature at the epiphysis was examined at both the light and electron microscopic level in rickets and rachitic reversal. The animals studied were normal, rachitic, and rachitic reversed at 8, 24, and 96 hours post-vitamin D administration. The overall architecture of the metaphyseal vessels was significantly altered throughout the intervals examined. In the rachitic animal, arterioles, venules, and capillaries were found adjacent to the growth plate, either directly apposed to the hypertrophic chondrocytes or separated from them by bone-forming cells. These vessels are in many ways similar to the larger arterioles and venules that normally supply the metaphyseal capillary sprouts, but in the normal growing animal are usually located 350-500 microns from the epiphyseal cartilage. The rachitic capillaries appear relatively well differentiated with a partial basement membrane and a perivascular cell lining. In early rachitic reversal, small vascular projections are induced to grow from the large diameter venules that border upon the hypertrophic chondrocytes. These vascular sprouts that invade the epiphyseal cartilage are quite undifferentiated, with no basement membrane or pericyte lining at the sprout apex and occasional abluminal endothelial cell projections. Within 96 hours, the metaphyseal microvasculature has returned to an apparently normal state with only capillaries at the cartilage-vascular interface and larger vessels (arterioles and venules) located several hundred microns deeper into the metaphysis. The sequential processes of differentiation and cessation of capillary growth followed by dedifferentiation and reinitiation of microvascular growth make the rachitic system a unique one in which to study angiogenesis.
Anat Rec 1991 Apr
PMID:Rearrangement of the metaphyseal vasculature of the rat growth plate in rickets and rachitic reversal: a model of vascular arrest and angiogenesis renewed. 171 Aug 78

To examine whether either of the two known active vitamin D metabolites 1,25(OH)2D3 or 24,25(OH)2D3 could reverse the mineralization defect induced by 1-hydroxyethylidene-1,1-bis phosphonate (EHDP), a model of EHDP-induced rickets was used. Rats at the age of 31 days were injected for 10 consecutive days with EHDP (10 mg/kg). Other littermates were treated with a combination of EHDP and either 1,25(OH)2D3 or 24,25(OH)2D3 or were treated following 10 days of EHDP, with either of the vitamin D metabolites for an additional 72 hr. Samples of cartilage fluid (Cfl) and of blood were removed prior to sacrifice for biochemical studies of some parameters of calcification. These parameters were correlated with the results of light and electron microscope studies of growth plate cartilage and bone. EHDP-treated rats revealed signs of typical rickets, manifested by widened growth plates and impaired bone mineralization. Transmission electron microscope (TEM) examination revealed matrix vesicles distributed throughout the growth plate; however, there appeared to be an arrest of the spread of the crystals at the provisional zone of calcification. Treatment with either 1,25(OH)2D3 or 24,25(OH)2D3 failed to reverse the rachitic condition of the animals. Serum calcium blood levels were elevated in the 1,25(OH)2D3 and EHDP-treated group. 1,25(OH)2D3 and 24,25(OH)2/D3 further increased the already elevated serum alkaline phosphatase levels observed in EHDP rats, although the increase observed with 1,25(OH)2D3 was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
Anat Rec 1988 Jan
PMID:EHDP-induced rachitic syndrome in rats is not reversed by vitamin D metabolites. 312 78

An outbreak of rickets in sheep under a year old (hoggs) appeared clinically as stiffness and rotation of the carpal joints. Histological studies confirmed the diagnosis and biochemical analyses of blood demonstrated a primary vitamin D deficiency.
Vet Rec 1988 Apr 16
PMID:Rickets associated with vitamin D deficiency in young sheep. 339 20

A biomechanical model of endochondral ossification (Frost and Jee, 1994. Anat. Rec., 240:435-446) can help to explain: (1) some differences in fracture patterns in children and adults, (2) increased fractures during the human adolescent growth spurt, (3) localization of stress fractures and pseudofractures to cortical instead of trabecular bone, (4) increased bone mass in adult-acquired and childhood obesity, (5) subchondral bone densification and osteopenia in some arthroses, (6) why and where mammals lose spongiosa with aging, (7) why, as percents of the original bone stock, metaphyseal trabecular bone losses with aging usually exceed cortical bone losses, (8) why osteochondritis dissecans and aseptic necroses of bone localize in epiphyses instead of metaphyses, (9) some features of growth plate histology in rickets and the chondrodystrophies, (10) why spontaneous fractures in osteoporotic patients affect vertebral more than metaphyseal spongiosa, (11) why osteopenias develop in most chronic, debilitating diseases, and (12) why histomorphometric values can differ in iliac bone biopsies obtained by the "vertical" Jamshidi and "horizontal" Bordier-Meunier techniques.
Anat Rec 1994 Dec
PMID:Perspectives: applications of a biomechanical model of the endochondral ossification mechanism. 787 97

The skeletal development of three groups of great dane dogs, fed a diet composed according to the published nutritional requirements for dogs (controls) or with increased calcium or calcium and phosphorus content, was examined radiographically, histologically and biochemically. The diets were fed from the time the dogs first began eating food in addition to their dam's milk, until they were 17 weeks old. Thereafter, the calcium and phosphorus intakes of the dogs in the high calcium groups were normalised for a further 10 weeks. The dogs fed the high calcium diet without a proportionally high phosphorus intake became hypercalcaemic and hypophosphataemic, and had severe disturbances in skeletal development, growth, and mineralisation which were typical for rickets. After their calcium intake was normalised the lesions of rickets resolved but osteochondrotic lesions became apparent. The dogs fed the high calcium and phosphorus diet became slightly hypophosphataemic, their growth was retarded, and they had disturbances in skeletal development resembling osteochondrosis, which had only partly resolved after 10 weeks on the normal calcium and phosphorus diet.
Vet Rec 2000 Dec 02
PMID:Effects of diets with different calcium and phosphorus contents on the skeletal development and blood chemistry of growing great danes. 1113 52