![]() Diarrhea and/or upper respiratory disease has been frequently reported in the literature prior to clinical signs of H.O.D. History may range from a mild limp to peracute onset of refusal to stand, anorexia, malaise, depression and dehydration. ![]() This corresponds to HOD developing in giant breed dogs during their time of most rapid growth (3-5 months of age), especially if nutritionally stimulated to grow rapidly.Īge is typically 3 - 5 months (range 2-8 months occurs only in dogs with open physes), any large breed can be affected, and the sex ratio is 1:1. Slow blood flow reduces oxygen supply to these cells during a time of extremely rapid growth and high metabolism. Vascular supply does not cross the cartilaginous physis, and laminar flow dynamics cause the blood flow in the zone of necrosis to be stagnant. Later in the course of the disease dystrophic periosteal bone formation in the metaphyseal area frequently occurs that radiographically is similar to a fracture callus. In some cases their may also be irregular widening of the physis (zone of hypertrophy - presumably due to disruption of metaphyseal blood supply), and subperiosteal hemorrhage. This band corresponds to the pathognomonic radiolucent line (pseudophysis) seen radiographically. Large multiple foci of resorption of the metaphyseal trabeculae occurs and may be accompanied by neutrophil infiltration similar to that seen with osteomyelitis. A history of overnutrition of vitamin D, minerals and/or calories is not present in the majority of cases and correction of nutrition (if needed) does not result in cure.Ī band of metaphyseal bone immediately adjacent to the physis consist of disrupted trabeculae, hemorrhage, hemosiderin deposits, necrotic trabeculae and inflammatory cells. ![]() has as many differences from human scurvy as it does similarities. Abnormal metabolism of vitamin C is a possibility. Since only primates and guinea pigs require dietary vitamin C, then a lack in the dogs diet is not a problem. ![]() Previous theories of etiology that have been disproven include deficient dietary vitamin C, excessive dietary vitamin D, excessive dietary minerals and excessive calories. Exercise should be encouraged.Ĭanine skeletal scurvy, idiopathic osteodystrophy, Barlow's disease, Moller-Barlow disease, metaphyseal osteopathy. The forelimbs should not be splinted or cast. Radiographs do not image abnormalities.Įxercised puppies have been reported to spontaneously recover in 7-10 days, while confined puppies recover in about 6 weeks. Owners note carpal hyperextension or hyperflexion, on one or both carpii.Ĭarpal hyperextension or hyperflexion, unilaterally or bilaterally, with mild to moderate lameness. The condition has been reported in a puppies 2 - 5 months of age. The condition is self-limiting and permanent pathology rarely occurs. Poor muscle tone allows hyperextension or hyperflexion of the carpus (carpii). If elbow subluxation is present then progressive degenerative joint disease can be expected. Mild lameness without apparent pain is present that worsens with exercise. Subluxation of the elbow is also a potential finding. Radiography will demonstrate agenesis and malformation of the phalanges, metacarpus and carpus. Two of the 17 reported cases had bilateral involvement. Obvious deformity of the manus is present, but is not painful. Mixed and pure breed dogs have been afflicted, without breed predisposition. It has been reported in 17 dogs, of which 15 were large dogs. The deformity is inherited in cats, horses and people probably inherited in dogs.Īgenesis and malformation of the phalanges, metacarpal and carpal bones in utero is the basic pathology, and is occasionally accompanied by subluxation of the elbow.
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