A large-scale epidemiological study was conducted to determine breeds at risk for 12 developmental orthopedic diseases (DODs). Developmental orthopedic diseases investigated included canine hip dysplasia (CHD); craniomandibular osteopathy (CMO); fragmented coronoid process; hypertrophic osteodystrophy; Legg-Calve-Perthes disease; osteochondrosis of the medial humeral condyle, caudal humeral head, femoral condyles, and talar trochlear ridges; panosteitis; patella luxation; and ununited anconeal process. Dogs that were diagnosed with any one of the diseases of interest at any of 10 veterinary teaching hospitals participating in the Veterinary Medical Database from 1986 to 1995 were included as cases. Odds ratios and corresponding 95% confidence intervals were calculated to determine risk. Frequency of diagnosis during the 10-year period ranged from 35 cases (CMO) to 10,637 cases (CHD). The number of breeds at increased risk for a disease ranged from one (CMO) to 35 (CHD). Breed susceptibility for a DOD may suggest a genetic component in the disease etiology. The results of this study serve to increase veterinarians' awareness of breeds susceptible to DODs and may facilitate the control of such diseases by identifying breeds that might benefit from breeding programs or environmental intervention such as dietary modification.

Breed susceptibility for developmental orthopedic diseases in dogs.

Creatinine is the analyte most frequently measured in human and veterinary clinical chemistry laboratories as an indirect measure of glomerular filtration rate (GFR). Although creatinine metabolism and the difficulties of creatinine measurement have been reviewed in human medicine, similar reviews are lacking in veterinary medicine. The aim of this review is to summarize information and data about creatinine metabolism, measurement, and diagnostic significance in the dog. Plasma creatinine originates from the degradation of creatine and creatine phosphate, which are present mainly in muscle and in food. Creatinine is cleared by glomerular filtration with negligible renal secretion and extrarenal metabolism, and its clearance is a good estimate of GFR. Plasma and urine creatinine measurements are based on the nonspecific Jaffe reaction or specific enzymatic reactions; lack of assay accuracy precludes proper interlaboratory comparison of results. Preanalytical factors such as age and breed can have an impact on plasma creatinine (P-creatinine) concentration, while many intraindividual factors of variation have little effect. Dehydration and drugs mainly affect P-creatinine concentration in dogs by decreasing GFR. P-creatinine is increased in renal failure, whatever its cause, and correlates with a decrease in GFR according to a curvilinear relationship, such that P-creatinine is insensitive for detecting moderate decreases of GFR or for monitoring progression of GFR in dogs with severely reduced kidney function. Low sensitivity can be obviated by determining endogenous or exogenous clearance rates of creatinine. A technique for determining plasma clearance following IV bolus injection of exogenous creatinine and subsequent serial measurement of P-creatinine does not require urine collection and with additional studies may become an established technique for creatinine clearance in dogs.

Creatinine in the dog: a review.

Osteochondrosis is a disorder of epiphyseal cartilage about which there is considerable confusion in the literature, largely because it has been studied mainly in its chronic stages. Based on recent studies in pigs and horses, and supported by observations in dogs and cats, local ischemia, secondary to defects in cartilage canal blood supply, is a key factor in the inititation of lesions of osteochondrosis and explains many of the features of this disease.

The Pathophysiology of Osteochondrosis

Hip dysplasia is a common developmental problem affecting the canine population. Despite extensive research into the condition, many questions remain unanswered and numerous misconceptions are present among the general public. The purpose of this paper is to review the current knowledge on the development of hip dysplasia, factors modifying its development, and current diagnostic techniques.A computerized literature search was conducted for the period of January 1983 to April 1985 using the MEDLINE and CAB databases, and the keywords hip dysplasia, hip, dog, and canine. Other articles,wherever possible original research articles, published before 1983 were also reviewed. Animals affected by hip dysplasia are born with normal hips, but quickly develop subluxation of the femoral head. Degenerative joint disease follows. Hip dysplasia is a complex, inherited, polygenic trait. Selective breeding of only normal dogs with normal littermates, parents, and grandparents is there commended method of reducing the incidence in the general population.Gene expression in affected individuals may be modified by a number of environmental factors. These factors do not cause hip dysplasia, but they alter manifestations of the trait and its severity. Nutrition is a major environmental factor. Excess energy consumption increases the frequency and severity of hip dysplasia in genetically predisposed dogs. Food intake should be regulated to maintain a slender figure with the ribs and dorsal vertebral spines easily palpable, but not visible. Excess dietary calcium and vitamin D contribute to hip dysplasia in genetically predisposed individuals and should be avoided. High dose vitamin C supplementation ingrowing puppies does not prevent hip dysplasia, and this practice should be discontinued. Animals must be 2 years old before they can be certified as normal, but the disease may be diagnosed earlier. Earlier diagnosis of the condition would be very useful for the selection of breeding stock, but palpation techniques and the standard extended view radiographs have unacceptably high rates of error in young puppies. Stress radiography techniques may improve the accuracy of early diagnosis in the future.

The pathogenesis and diagnosis of canine hip dysplasia: a review.

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.

Effect of diets with different calcium and phosphorus contents on the skeletal development and blood chemistry of growing great danes

Feeding a dog of a large breed with a diet exceeding the National Research Council (1974) recommendations for energy, protein, calcium, phosphorus and vitamin D may result in disturbances of skeletal development. The effects of excess energy and various calcium:phosphorous ratios per se have been reported by others. The role of dietary protein, especially with regard to calcium metabolism and skeletal development, in large breed-dogs is reported in this article. Seventeen Great Dane pups, 7 wk of age, were divided into three groups. During 18 wk each group received isoenergetic dry food (approximately 15 kJ metabolizable energy/g) containing 31.6, 23.1 or 14.6% protein on dry matter basis. No differences were found among the high (H-Pr), normal (N-Pr) and low protein (L-Pr) groups for the height at the shoulder. Significant differences were found between the H-Pr and L-Pr groups for body weight and plasma albumin and among all three groups for plasma urea. The differences in protein intake per se had no demonstrable consequences for calcium metabolism and skeletal development. A causative role for dietary protein in the development of osteochondrosis in dogs is unlikely.

Growth and skeletal development in great dane pups fed different levels of protein intake

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Growth and skeletal development in great dane pups fed different levels of protein intake