Prevalence of hip dysplasia, elbow dysplasia and humeral head osteochondrosis in dog breeds in Belgium

Department of Medical Imaging, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium.
The Veterinary record (Impact Factor: 1.49). 12/2008; 163(22):654-8. DOI: 10.1136/vr.163.22.654
Source: PubMed


The official screening results of the Belgian National Committee for Inherited Skeletal Disorders, an affiliate of the Belgian Kennel Club, have been used to estimate the prevalence of hip dysplasia, elbow dysplasia and humeral head osteochondrosis in the dog breeds in Belgium, and these have been compared with reported prevalence data from other countries. In some breeds, the prevalence of hip and elbow dysplasia is very high, both in Belgium and in other countries. Comparisons of the prevalence of hip dysplasia are not always feasible because different systems are used to evaluate the quality of the hips and because there is no strict consensus on what should be considered a diseased hip joint.

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Available from: Frank Coopman, Mar 18, 2014
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    • "The incidence of ED ranges from 0% to 55%, depending on breed, population, and screening technique (Swenson et al., 1997; Hazewinkel et al., 1996; Kirberger and Stander, 2007; Coopman et al., 2008; Temwichitr et al., 2010). The first clinical signs usually occur after the phase of rapid growth at 4–6 months of age, but can also become apparent later in life (Olsson, 1983; Voorhout and Hazewinkel, 1987; van Bruggen et al., 2010). "
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    ABSTRACT: Canine elbow dysplasia encompasses four developmental diseases: ununited anconeal process, osteochondrosis of the medial part of the humeral condyle, fragmented medial coronoid process (FCP), and incongruity of the elbow joint. Four radiographic views per joint were used to evaluate 2693 Labrador Retrievers (LRs), 1213 Golden Retrievers (GRs), and 974 Bernese Mountain Dogs (BMDs) for the presence of elbow dysplasia between 2002 and 2009 in the Netherlands. The views were also graded for signs of osteoarthritis and sclerosis. FCP was diagnosed most frequently in LRs, GRs and BMDs, with an incidence of 6%, 5%, and 15%, and a heritability of 0.17, 0.24, and 0.06, respectively. Heritabilities were estimated using a sire model and all available ancestors. Sclerosis at the base of the medial coronoid process was the radiographic sign most strongly correlated with FCP (r=0.95, 0.92, and 0.95 in LRs, GRs and BMDs, respectively). The sex of the dog was significantly correlated with the presence of osteoarthritis in LRs, but not in GRs and BMDs. Male LRs were 1.7-fold more frequently, but not more severely, affected by osteoarthritis than female dogs. Age at radiographic examination was significantly associated with osteoarthritis in all three breeds. The heritability estimates in Retrievers were high enough to warrant including FCP findings in the breeding policy, but until the biomechanical and genetic background of elbow dysplasia are better understood, correct phenotyping with a sensitive technique is essential.
    The Veterinary Journal 02/2012; 193(2):486-92. DOI:10.1016/j.tvjl.2012.01.001 · 1.76 Impact Factor
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    • "Concerning the prevalences and phenotype distributions of both CHD and CED, it must be kept in mind that because of the lack of population-wide screening for these and other diseases, it is not possible to quantify the role of voluntary exclusion of severe cases from official statistics. It has been shown on the basis of simulated data that selective non-reporting of clear cases of CHD affection, which has been surmised previously (Hamann et al. 2003; Coopman et al. 2008 "
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    ABSTRACT: Results from radiographic screening for canine hip dysplasia (CHD) and elbow dysplasia (CED) of 48 367 German shepherd dogs born in 2001-07 were used for the population genetic analyses. Available information included CHD scores for 47 730 dogs, CED scores for 28 011 dogs and detailed veterinary diagnoses of primary ED lesions for a subsample of 18 899 dogs. Quasi-continuous traits were CHD, CED and cases of CED without radiographically visible primary lesion (CED-ARTH). Binary coding was used for fragmented medial coronoid process of the ulna (FCP), borderline findings and mild to severe signs of dysplasia in hip and elbow joints. Genetic parameters were estimated in univariate threshold and multivariate linear and mixed linear-threshold models using Gibbs sampling. Correlations between univariately predicted breeding values (BV) indicated genetic differences between borderline and affected disease status for both CHD (r(BV) = 0.5) and CED (r(BV) = 0.3). Multivariate genetic analyses with separate consideration of borderline findings revealed moderate heritabilities of 0.2-0.3 for the quasi-continuous traits with positive additive genetic correlation of 0.3 between CHD and both CED and CED-ARTH. For FCP, heritability of 0.6 and additive genetic correlations of +0.1 to CHD and -0.1 to CED-ARTH were estimated. Results supported the relevant genetic determination of CHD and CED, argued for both diseases against interpretation of borderline findings as healthy and implied genetic heterogeneity of CED. Accordingly, future breeding strategies to reduce the prevalences of CHD and CED in the German shepherd dog should be most efficient when based on BV from multivariate genetic evaluation for CHD, CED-ARTH and FCP with use of the whole scale of categories for classification of CHD and CED.
    Journal of Animal Breeding and Genetics 06/2011; 128(3):219-29. DOI:10.1111/j.1439-0388.2010.00901.x · 1.57 Impact Factor
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    ABSTRACT: Fragmented medial coronoid process (FCP) is the main component of elbow dysplasia (ED) in dogs, which also includes osteochondrosis of the humeral condyle (OCD), elbow incongruity (INC), and ununited anconeal process (UAP). FCP is recognized as a hereditary disease in many breeds and is a major concern in working dog breeds such as the Labrador Retriever. Different aspects of FCP were described in this thesis, such as the development of the elbow joint, possible pathogeneses of FCP, and different types of genetic investigations that could be carried out to identify the gene causing FCP. Because mal-development of bone and cartilage could cause FCP, we speculated that collagen genes could play an important role in the pathogenesis of FCP. Microsatellite markers were developed that were closely situated to different genes encoding various collagen proteins including COL1A1 (for collagen type I, subunit alpha-1), COL1A2, COL2A1, COL3A1, COL5A1, COL5A2, COL6A3, COL9A1, COL9A2, COL9A3, COL10A1, COL11A1, COL11A2, and COL24A1. We found that none DNA marker alleles was shared significantly more than expected by FCP-affected sibling pairs. We concluded that the collagen genes investigated were unlikely to play an important role in the pathogenesis of FCP. We also found that COL9A1, COL9A2 and COL9A3 were unlikely to be involved in the pathogenesis of cruciate ligament rupture in Boxers. In addition, research was performed to identify FCP-genes using genome-wide, model-free linkage analysis with 320 microsatellite markers and 1536 SNP markers in parallel. These markers were evenly spread along the genome. Results identified potential FCP loci on CFA01 and CFA13, but the gene for FCP was not elucidated. Research of candidate genes at these loci is currently in progress. We investigated chondrodysplasia in Labrador Retrievers and evaluated the involvement of the genes encoding cartilage oligomeric matrix protein (COMP), COL9A1, COL9A2, and COL9A3, Matrilin-3, and solute carrier family 26 member 2 (SLC26A2) in affected dogs and their relatives. Although we did not find yet the gene responsible for chondrodysplasia in these Labrador Retrievers, we created a solid base for further investigation. We also documented hereditary radial subluxation in Bouvier des Flandres for the first time. This abnormality manifests as disproportionately short front legs with valgus deformity and disturbed configuration of the elbow. We hypothesized that the radial head subluxation in these Bouviers was the consequence of angulation of the radial bone, possibly aggravated by forces resulting from the supinatus muscle and laxity of the annular ligament. The concomitantly occurring cranial bending of the olecranon could be caused by force originating from the triceps brachii muscle. Angulation of the radius occurs at birth or soon thereafter and was seen at the mid-diaphysis of the radius, at the insertion of interosseous ligament. Genealogical analysis indicated that most affected Bouviers, originating from the Netherlands and Sweden, were closely related, but the mode of inheritance is not clear. Heredity based on genomic instability is a possible but yet unproven explanation. The molecular genetic studies as described in this thesis to identify the gene involved in FCP, could serve as a model for the investigation of other diseases of importance in companion animal orthopedics, such as chondrodysplasia and radial head subluxation.
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