Ununited anconeal process in the dog.
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This article discusses principles of corrective osteotomy and describes operative plans for specific growth deformities such as premature closure of the distal ulna, asynchronous growth of the radius and ulna in achondroplastic breeds, retarded growth of the distal radius, retarded growth of the proximal radius, and synostosis of the radius and ulna.
Five patients with polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLO-SL) were investigated using bone scintigraphy. Abnormal findings were detected in hands, wrists, knees, ankles and feet of all five patients.
All members of a weimaraner litter had clinical and radiographic signs of hypertrophic osteodystrophy shortly after weaning. Three dogs were necropsied. Radiographic metaphyseal densities, which are used to make a clinical diagnosis of hypertrophic osteodystrophy, were found to result from elongation of the calcified cartilage lattice of the primary spongiosa. Intertrabecular acute inflammation was associated with necrosis, failure to deposit osseous tissue on the calcified-cartilage lattice, and trabecular microfractures. This process led to metaphyseal infraction and separation of the epiphysis. Defective bone formation (osteodystrophy) was considered a secondary process resulting from inflammation of osteochondral complexes, marrow, and periosteum. Enamel hypoplasia also was found to be associated with inflammation of the dental crypt, and abnormal enamel matrix was observed in the developing teeth. The histopathology of the bones and teeth was different from alterations which occur in infantile scurvy or congenital syphilis, although these diseases of man have radiographic similarities to canine hypertrophic osteodystrophy. Because the radiologic lesion is nonspecific, a clinical diagnosis of hypertrophic osteodystrophy is not necessarily diagnostic of a specific disease due to a single etiologic agent. Liver levels of ascorbic acid were within the normal range. Although an infectious agent could not be identified, the conditions may have an infectious origin with systemic manifestations.
Craniodiaphyseal dysplasia is a rare, sporadic form of craniotubular bone dysplasia, characterized by massive generalized hyperostosis and sclerosis, particularly of the skull and facial bones, leading to severe deformity. The clinical course is typically characterized by progressive encroachment of the craniofacial foramina and brain by the relentless deposition of bone. Compression of cranial nerves, the foramen magnum, and intracranial contents commonly leads to blindness, loss of hearing, and death. This report describes a unique case of craniodiaphyseal dysplasia manifesting with asymmetric craniofacial and axial hyperostosis. The tubular bones demonstrated the characteristic diaphyseal endostosis, undertubulation, and relative overgrowth on the involved side. Significant brain compression with signs and symptoms of increased intracranial pressure was managed successfully with decompressing craniectomy at age 12 years, enlarging the anterior and middle fossae. Calvarial thickness measured nearly 4 cm. Further calvarial, midfacial, and mandibular recontouring were performed 6 and 22 months later. Follow-up in our case indicates that close observation is mandatory to manage further progression of the disease.
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Skin disorders in which a radiograph may detect associated bony changes or abnormalities of calcification are discussed. They are grouped into eight categories: (1) inherited diseases (e.g., alkaptonuria, neurofibromatosis); (2) congenital disorders (e.g., Sturge-Weber and Proteus syndromes); (3) inflammatory conditions (e.g., dermatomyositis, sarcoidosis); (4) infections (e.g., dental sinus, syphilis); (5) neoplasias (e.g., histiocytosis, mastocytosis); (6) drug- and environment-induced (e.g., acroosteolysis, retinoid toxicity); (7) calcinosis cutis; and (8) osteoma cutis. Part I of our review discusses the first two categories.
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Limb angulation in foals may be due to defects in epiphyseal growth plates. The present state of knowledge concerning rate of growth in foals and differences in growth of different epiphyseal plates is reviewed and the importance of accurate knowledge of these parameters in treatment of angulation by unilateral retardation of an epiphyseal growth plate is stressed. Retardation of epiphyseal plate growth by compression wiring is described and its advantages in comparison with staplings are suggested. Compression wiring was used in 3 cases in which age, bone width and the degree of angulation were known so that the probable rate of bone growth could be assessed and the necessary unilateral bone increment could be calculated. It is suggested that further measurements of these parameters prior to growth plate retardation would give a more accurate comparison of the benefits of stapling and compression wiring.
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.