Hypertrophic osteodystrophy, which was first reported in the 1930s, is a developmental systemic disease of rapidly growing young dogs.1–13 Clinical manifestation of HOD ranges from mild, self-limiting disease4,14,15 to severe multisystemic life-threatening illness.5,9,13,16 Clinical signs include recurrent episodes of pyrexia and malaise, often accompanied by signs of pain and soft tissue swelling over a metaphyseal region. Affected dogs have variable degrees of lameness, from a mild limp to full recumbency. Additional clinical signs that may precede the onset of ostealgia include ocular and nasal discharge, skin pustules or nodules, diarrhea, hematochezia, vulvovaginitis, and pathological respiratory sounds.1,4,7,17 Age of onset ranges between 7 weeks6 and 8 months,18 and the highest incidence is reported for dogs between 3 and 4 months of age.16 Relapse is common and may occur until closure of the physes.7
Nonspecific hematologic findings include leukocytosis characterized by neutrophilia and monocytosis as well as mild nonregenerative anemia, thrombocytosis, or thrombocytopenia.9,10,12 Serum biochemical analysis may reveal hyperphosphatemia and an elevated alkaline phosphatase activity, which is characteristic of juvenile animals,19,20 together with nonspecific findings such as hypoalbuminemia and low BUN and creatinine concentrations.9,10,12
Diagnosis of HOD is made on the basis of the medical history, clinical signs, and signalment and by ruling out infectious causes. Radiography and histologic evaluation of bone sections reveal characteristic lesions2,4,5,18 in the metaphysis of the long bones, but lesions in the vertebrae, ribs, and mandible6 as well as the scapulae, humeri, and femurs12,21 and the optic foraminae2 have also been reported. Radiographic changes include metaphyseal sclerosis, widening of the metaphyseal region, and appearance of transverse radiolucent lines in the metaphysis with or without paracortical mineralization and periosteal proliferation.1,7,14 Dogs with severe HOD may develop secondary angular limb deformities.1,7 Histologically, necrotic trabeculae and infiltrations of polymorphonuclear cells are evident in the affected metaphyses and are accompanied by hemorrhage, hemosiderin deposits, and fibrosis.1,2,7,13
Despite extensive clinical characterization of HOD, the pathogenesis remains unknown. Suggested causes, such as vitamin C deficiency6 and excess dietary supplementation with vitamins and minerals,22 have been excluded on the basis of results of controlled studies.3 Infection with canine distemper virus has also been considered as a cause of HOD22–25; however, an attempt to transmit HOD from affected to nonaffected dogs failed, and experimental canine distemper virus infection did not cause HOD lesions in the infected dogs.3 In 1 study,17 investigators found Escherichia coli bacteremia in a single HOD-affected dog, but they speculated that the infection was a secondary condition and not the cause of HOD.
Hypertrophic osteodystrophy has been diagnosed in 40 breeds of dogs16 as well as in mixed-breed dogs.8,26 A specific breed predisposition has been reported for Great Danes, Boxers, German Shepherd Dogs, Irish Setters, and Weimaraners; therefore, it is likely that an inherited factor plays a role in the pathogenesis of the disease.8,16 The Weimaraner is the only breed in which entire litters and closely related animals are reported to be affected,4,5,10,16 which indicates a strong heritable component for the disease in that breed.8 Although Weimaraners are continuously mentioned in relation to HOD, to the authors’ knowledge, there has not been a case series of a large number of HOD-affected Weimaraners from multiple litters. The purpose of the study reported here was to determine the response of Weimaraners with HOD to treatment and to determine the vaccination history, clinical signs, clinical findings, treatment protocols used, and clinical outcome for Weimaraners with HOD.
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