Genetic welfare problems of companion animals

 

Elbow Dysplasia (humeral condylar osteochondrosis [HCO])

 

Breed: Golden Retriever

 

Condition:  Elbow Dysplasia

Related terms: osteochondrosis dissecans. osteochondrosis dessicans, OCD, osteochondritis dissecans (dessicans) of the humeral condyle

Outline: In humeral condylar osteochondrosis, cartilage of the growing elbow joint fails to develop normally and becomes abnormally thickened and damaged. This leads to chronic arthritis of the joint that may be apparent before 6 months of age. It can cause mild to severe chronic pain throughout life and is a common disease of Golden retrievers.

 


 

Summary of Information

(for more information click on the links below)

 

 

1.           Brief description

Humeral condylar osteochondrosis (HCO) is a disease that affects cartilage formation. In HCO, cartilage in one part of the elbow joint becomes abnormally thickened and prone to flaking off from the underlying bone (Schwarz 2000, Hazelwinkel & Nap 2009a), causing osteoarthritis (degenerative joint disease) in the joint. It is one of several types of elbow dysplasia.

HCO is often present in affected dogs by 4-10 months of age, but can show later. It may be treated with rest and pain-killers but treatment may need to be life-long. Surgery is usually recommended and this is often undertaken with keyhole surgery techniques using an arthroscope (Shell 2007, Burton & Owen 2008a).

 

2.           Intensity of welfare impact             

HCO leads to pain and disability associated with the osteoarthritis. This can be mild to severe (Shell 2007).

 

3.           Duration of welfare impact

 

The mild to severe welfare impacts that result from the osteoarthritis seen in this disease can be expected to start during the first few months of life and, without successful treatment, to continue for life. Treatment may help but keeping affected dogs free from pain and avoiding disabilities is often challenging (Shell 2007).

 

4.           Number of animals affected

 

Golden retrievers have long been known to suffer from elbow osteochondrosis as well as from other forms of elbow dysplasia (Grondalen & Grondalen 1981, LaFond et al 2002), and is included among those involved in the British Veterinary Association/Kennel Club Elbow Dysplasia Scheme (Kennel Club 2010). Kirberger & Stander (2007) found ED in 38% of Golden retrievers in South Africa but others have estimated prevalences of 4 - 5% (Clements et al 2006, Coopman et al 2008).

 

5.           Diagnosis

Determination of the type of elbow disease, its extent and the degree of secondary osteoarthritis requires X-rays examination. In dogs with HCO it is particularly important also to check for the presence of fragmented medial coronoid process (FMCP), as these two problems often coexist (Burton & Owen 2008b). Other diagnostic tests are needed to rule out the presence of concurrent FMCP.

 

6.           Genetics

 

There is strong evidence of a genetic component to HCO. The genes responsible have yet to be determined.

 

7.           How do you know if an animal is a carrier or likely to become affected?

Affected dogs should not be used for breeding. Affected puppies can be born to unaffected parents (Hazelwinkel & Nap 2009a). Detecting carriers - those which carry and may pass on the gene(s) but which do not show signs of the disease themselves - is not currently possible.

 

8.          Methods and prospects for elimination of the problem

 

A voluntary scheme for grading the elbows of dogs susceptible to elbow dysplasia has been operating in the UK since 1998, although it has been suggested that breeder uptake has been relatively low (Sampson 2006). In this scheme, elbows are scored for condition when the dog is over one year old.

Like other complex, multi-gene diseases in which environmental factors also play a part, good progress in reducing the prevalence of HCO is likely to be aided by greater knowledge of the underlying genetics. One approach is to breed from dogs that have better breeding value (see below) than is average for the breed (Sampson 2006). This takes account of both the individual being evaluated and its relatives (Malm et al 2008). Out-breeding Golden retrievers with dogs of breeds known to have a much lower prevalence of HCO and elbow dysplasia (ED) in general may lead to fewer dogs being born with a lifetime of painful joint problems before them.

 


 

For further details about this condition, please click on the following:

 

 

 

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1.           Clinical and pathological effects

 

Elbow dysplasia (ED) is a general term that encompasses five distinct anatomical problems that tend to result in malformation of the elbow joint and to early-onset osteoarthritis. Humeral Condylar Osteochondrosis (HCO) is one of these. HCO and the other four are described below:

Fragmented medial coronoid process (FMCP): The medial coronoid process is a piece of bone that should form part of the top of the ulna and part of the elbow joint. In FMCP, during early development, this fails to connect to the ulna.

Ununited anconeal process (UAP): The anconeal process is a protrusion of the top of the ulna. Developmentally, it starts as a separate bone which should fuse to the ulna. When this fusion fails to happen, the dog suffers from a UAP.

Elbow incongruity (IC): Dogs with IC have malformed articular surfaces of the three bones that make up the elbow and because of this they do not fit together normally. It can affect the weight-bearing surfaces between the humerus and the radius and ulna and also the way in which the upper part of the ulna fits inside the lower end of the humerus (Schwarz 2000).

Ununited medial epicondyle (UME): This is an uncommon condition in which the medial epicondyle, a bone on the end of the humerus, fails to unite with the humerus during development.

Here the focus is on HCO. Other forms of elbow dysplasia can also occur in this breed and HCO is also common in other dogs, particularly those of large body size. More than one form of elbow dysplasia may be seen in the same elbow.

The elbow is a complex joint of three bones: the humerus (upper bone of the foreleg/arm), the ulna and the radius (lower foreleg/arm bones). At their upper ends, the radius and part of the ulna form a flattened surface that bears the load imposed by the condyles of the humerus.


Figure 1. The three bones of the elbow joint separated and in normal alignment. In a healthy canine elbow joint the ulna and radius form a flat surface for articulation with the humerus. (Image property of Phil Witte, to whom we are grateful for permission to reproduce it here).

 

The condyles of the humerus are two fist-like projections on the lower end of the humerus that articulate with the radius and ulna bones at the elbow joint. They are formed of bone covered with joint cartilage. The condyle on the inside (on the side of the humerus adjacent to the body) is the medial condyle, the other is the lateral condyle. 

Figure 2. The anterior (front) view of the humerus, highlighting the location of the humeral condyles.

 

Osteochondrosis (OCD) is a disease process that affects the articular cartilage – the layer of smooth, incompressible cartilage that covers the ends of bones that articulate with one another in joints (Junqueira & Carneiro 1980). Bones grow through growth of cartilage and, as the cartilage layer thickens, the lower, older layers become ossified – that is, they turn into bone.

In osteochondrosis, trauma, nutritional disturbance or other factors disturbs this process of ossification so an area of thickening cartilage develops. As cartilage has no blood supply it cannot function well when it is thicker than normal. Thick cartilage degenerates and an area of diseased cartilage forms. This may crack, cavities may form within it, and it may fragment (Guthrie et al 1992). When cartilage fragments break free into the joint the condition is called osteochondrosis dessicans,and the function of the joint is compromised. This occurs both because of the damage to the cartilage and because the loose piece of cartilage (sometimes called a joint mouse) moves around the joint or becomes trapped elsewhere in the surface of the cartilage (Grondalen & Grondalen 1981, Schwarz 2000, Shell 2007).


Figure 3. A schematic diagram illustrating Humeral Condylar Osteochondrosis (HCO). The deeper layers of articular cartilage (red) covering the surface of the humeral condyles have failed to turn to bone. The result is an abnormally thick layer of cartilage, which can then crack and fragment due to a lack of blood supply, causing discomfort and inhibiting the action of the joint.

 

Dogs with HCO develop osteoarthritis (degenerative joint disease) of the elbow. In osteoarthritis there are progressive changes to the cartilage of the affected joint, varying amounts of inflammation and ongoing damage to other joint structures - the joint capsule, the synovial fluid of the joint and the surrounding bone. These changes are often present by 4-10 months of age but can show later. Typical signs include: stiffness after rest, lameness (which can be worse after exercise) and pain when the leg is straightened or bent. Such signs are indistinguishable from other causes of elbow dysplasia and imaging of the joint (eg by radiography) is usually needed to make a definitive diagnosis (Schwarz 2000, Shell 2007). In the early stages of the disease, when only cartilage is affected, it is detectable only with direct observation by surgery (usually arthroscopy). Later, when bone is diseased too, changes can also be detectedon radiography (Baines 2006).

 

                 Figure 4A                                               Figure 4b

Figures 4a and 4b. Osteoarthritic changes to the shape and structure of the elbow joint. The shaded areas on figure 4a (extended elbow) and 4b (flexed elbow) represent the changes to bone and cartilage as a result of HCO and other forms of elbow dysplasia.

(Images property of the British Veterinary Association Elbow Dysplasia Scheme, to whom we are grateful for permission to reproduce them here).

 

Affected dogs may be treated with rest and pain-killers, and often treatment needs to be life-long.  Removal of the diseased cartilage is often recommended. This can be performed using open joint surgery or with an arthroscope (an endoscope designed for joints) via key-hole incisions. The condition affects both elbows in 30-80% of affected dogs (Schwarz 2000). 

When it occurs with Fragmented Medial Coronoid Process (one of the other forms of elbow dysplasia) HCO is described as being part of ‘medial compartment disease’ – disease of both the proximal and distal aspects of the medial side of the joint.

There is some evidence that HCO is more common and more severe in males than females (Guthrie & Pidduck 1990, Lang et al 1998, Janutta et al 2006).

 

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2.               Intensity of welfare impact

HCO causes pain and disability associated with osteoarthritis. This can vary from mild to severe. Welfare may also be affected as a result of the veterinary investigations (from visits to veterinary practices, examinations, anaesthetics and surgery) and treatments of the disease (for example: the side effects of non-steroidal anti-inflammatory drugs on the gastrointestinal tract). Restricted activity will often be recommended in order to prevent further joint damage and this reduced activity may constrain the dog’s capacity for normal life and behaviour (Shell 2007).

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3.           Duration of welfare impact

 

The mild to severe pain and disability that result from the osteoarthritis seen in this disease can be expected to start during the first few months of life and, without successful treatment, to continue for life. Some puppies are affected from six weeks (Guthrie & Pidduck 1990). Treatment may help. Surgery is effective in 40-70% of affected dogs (Burton & Owen 2008a) but keeping affected dogs free from pain and avoiding disabilities is often challenging (Shell 2007).

 

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4.           Number of animals affected

 

Golden retrievers have long been known to suffer from elbow osteochondrosis as well as from other forms of elbow dysplasia (Grondalen & Grondalen 1981, LaFond et al 2002), and the breed is included among those involved in the British Veterinary Association/Kennel Club Elbow Dysplasia Scheme (Kennel Club 2010). Kirberger & Stander (2007) found ED in 38% of Golden retrievers in South Africa but others have estimated prevalence to be 4 - 5% (Clements et al 2006, Coopman et al 2008).

 

The incidence of elbow dysplasia has been shown to vary in Labrador retrievers, being much more prevalent in some families than in others (Ubbink et al 1998, Hazewinkel & Nap 2009) and it is likely that the same applies in other breeds, such as the Golden retriever.

 

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5.           Diagnosis

 

HCO will be suspected by a veterinary surgeon when presented with a Golden retriever showing forelimb pain. Determining the type of elbow dysplasia, its extent and the degree of secondary osteoarthritis requires further diagnostic investigations. The disease may also be suspected when the typical secondary changes of osteoarthritis are seen on an X-ray (Burton & Owen 2008a). HCO can usually be diagnosed using radiography (van Bree & Gielen 2008, Chanoit et al 2010) but other techniques are needed in order to rule out the concurrent presence of other forms of elbow dysplasia, particularly FMCP. Magnetic resonance imaging (MRI) or computerised tomography (CT) scanning are more sensitive methods of detection and are increasingly being used (Burton & Owen 2008a). Exploratory surgery is used to find fragments of bone, this is both diagnostic and can be therapeutic. It has been suggested that the best combination of diagnostic tests is CT plus arthroscopy (Moores et al 2008).

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6.           Genetics

Humeral condyle osteochondrosis is known to be a polygenic disorder in Golden retrievers (Maki et al 2002, Maki et al 2004) as it is in other breeds (Padgett et al 1995, Janutta et al 2006). The heritability of the disease in Golden retreivers was found by Maki et al (2002) to be around 0.26, but Guthrie & Pidduck (1990) found that considering HCO and FMCP together, there was a heritability of 0.45. These are the proportions of the disease considered to be due to genetic rather than environmental influences.

 

Efforts are underway to investigate the genes involved in HCO, particularly the genetics of aberrant proteins that have been found to be associated with abnormal ossification of cartilage (Pead & Ruaux-Mason 2006).

 

There may also be genetic factors which affect the degree of osteoarthritis that develops in an individual, independent of the genetics of the underlying cause for the initial joint disease (Clements et al 2006).

 

A genetic link between the presence of ED and hip dysplasia has been found but the genes involved have not been determined (Cachon et al 2010).

 

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7.           How do you know if an animal is a carrier or likely to become affected?

Affected dogs should not be used for breeding. Affected puppies can be born to unaffected parents (Hazelwinkel & Nap 2009a). Determining carriers - those which carry and may pass on the gene(s) but which do not show signs of the disease themselves - is not currently possible.

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8.          Methods and prospects for elimination of the problem

A voluntary scheme for grading the elbows of dogs susceptible to elbow dysplasia (all forms) has been in operation in the UK since 1998 although it has been suggested that breeder uptake has been relatively low (Sampson 2006). Details of the scheme can be found at: http://www.thekennelclub.org.uk/item/309.

In this scheme, dogs are scored once when over one year old. Radiographs taken by a local veterinary surgeon are forwarded to veterinary radiologists on the scheme panel for assessment. Each elbow is graded 0-3, with zero meaning that no evidence of elbow dysplasia was seen. If the two elbows have different grades, then the higher of the two grades is the one used for the dog. The scheme recommends that dogs used for breeding should have grades of zero or one and that those with higher scores are not bred from.

No evidence has yet been published as to whether this scheme has reduced the prevalence of elbow disease in the Golden retriever but a comparable scheme, run in New Zealand is suggested to have helped (Worth et al 2010) and a similar scheme in Sweden run since 1990, has led to a marked reduction in its incidence in other breeds (Swenson et al 1997, Hedhammar & Malm 2008, Malm et al 2008, Hazelwinkel & Nap 2009b).

Like other complex, multi-gene diseases in which environmental factors also play a part, good progress in reducing the prevalence of HCO is likely to be aided by greater knowledge of the underlying genetics. Treating the different forms of ED as separate entities is also likely to be helpful (Innes 2006). One approach is to breed from dogs that have a better breeding value (see below) than average for the breed (Sampson 2006). This takes account of both the individual being evaluated and its relatives and compares its likely genetic health to the average for the breed (Malm et al 2008). It has been found that ED is more likely to occur in animals with hip dysplasia and both conditions should be screened for and considered in breeding programmes (Cachon et al 2010). Out-breeding Golden retrievers with dogs of breeds known to have a much lower prevalence of HCO and elbow dysplasia (ED) in general may lead to fewer being born with a lifetime of painful joint problems before them.

 
 

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9.          Acknowledgements

UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section and to Stephanie Kaufman for assistance in illustrating it.

 

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10.          References

Baines E (2006) Clinically significant developmental radiological changes in the skeletally immature dog: 2. Joints. In Practice 28: 247-254

 

Burton N and Owen M (2008a) Canine elbow dysplasia 2. Treatment and prognosis. In Practice 30: 552-557

 

Burton N and Owen M (2008b) Canine elbow dysplasia 1. Aetiopathogenesis and diagnosis. In Practice 30: 508-512

 

Cachon T, Genevois JP, Remy D, Carozzo C, Viguier E, Maitre P, Arnault F and Fau D (2010) Risk of simultaneous phenotypic expression of hip and elbow dysplasia in dogs. Veterinary Comparative Orthopedics and Traumatology 23: 28–30

 

Chanoit G, Singhani NN, Marcellin-Little DJ and Osborne JA (2010) Comparison of five radiographic views for assessment of the medial aspect of the humeral condyle in dogs with osteochondritis dissecans. American Journal of Veterinary Research 71: 780-3

Clements DN, Carter SD, Innes JF and Ollier WER (2006) Genetic basis of secondary osteoarthritis in dogs with joint dysplasia. American Journal of Veterinary Research 67: 909-19

Coopman F, Verhoeven G, Saunders J, Duchateau L and van Bree H (2008) Prevalence of hip dysplasia, elbow dysplasia and humeral head osteochondrosis in dog breeds in Belgium. Veterinary Record 163: 654-8

Grondalen J and Grondalen T (1981) Arthrosis in the elbow joint of young rapidly growing dogs. V. A pathoanatomical investigation. Nordisk Veterinaermedicin 31: 1

Guthrie S and Pidduck HG (1990) Heritability of elbow osteochondrosis within a closed population of dogs. Journal of Small Animal Practice 32: 460-464

Guthrie S, Plummer JM and Vaughan LC (1992) Aetiopathogenesis of canine elbow osteochondrosis: a study of loose fragments removed at arthrotomy. Research in Veterinary Science 52: 284

 

Hazelwinkel HAW and Nap RC (2009a) Elbow dysplasia; a definition and known aetiologies. Proceedings of 24th Annual Meeting of International Elbow Working Group. pp 6-18

 

Hazelwinkel HAW and Nap RC (2009b) Screening programme for elbow dysplasia. Proceedings of 24th Annual Meeting of International Elbow Working Group. pp 28-30

 

Hedhammar A and Malm S (2008) Genetic aspects of elbow dysplasia and efficacy of breeding programmes. Proceedings of 23th Annual Meeting of International Elbow Working Group. 24-5

 

Innes JF (2006) Is elbow dysplasia a syndrome? Proceedings of the British Veterinary Orthopaedics Association Autumn Meeting 2006. 10-11

 

Janutta V, Hamann H, Klein S, Tellhelm B & Distl O (2006) Genetic analysis of three different classification protocols for the evaluation of elbow dysplasia in German shepherd dogs. Journal of Small Animal Practice 47: 75-82

 

Junqueira LC and Carneiro J (1980) Cartilage. In: Basic Histology, 3rd edition. Lange Medical Publications. pp121

Kennel Club 2010 The BVA /KC Elbow Dysplasia Scheme.  http://www.thekennelclub.org.uk/item/309. accessed 1st June 2011

Kirberger RM and Stander N (2007) Incidence of canine elbow dysplasia in South Africa. Journal of the South African Veterinary Association 78: 59-62

 

LaFond E, Breur GJ & Austin CC (2002) Breed susceptibility for developmental orthopedic diseases in dogs. Journal of the American Animal Hospital Association 38:467-477

 

Lang J, Busato A, Baumgartner D, Flückiger M and Weber UT (1998) Comparison of two classification protocols in the evaluation of elbow dysplasia in the dog. Journal of Small Animal Practice 39:169-74

 

Maki K, Groen AF, Liinamo-E and Ojala M (2002) Genetic variances, trends and mode of inheritance for hip and elbow dysplasia in Finnish dog populations. Animal Science 75: 197-207

 

Maki K, Janss LLG, Groen AF, Liinamo A-E and Ojala M (2004) An indication of major genes affecting hip and elbow dysplasia in four Finnish dog populations. Heredity 92: 402–408

 

Malm S, Fikse WF, Danell B and Stanberg E (2008) Genetic variation and genetic trends in hip and elbow dysplasia in Swedish Rottweiler and Bernese mountain dogs. Journal of Animal Breeding and Genetics 125: 403-12

 

Moores AP, Benigni L and Lamb CR (2008) Computed tomography versus arthroscopy for the detection of canine elbow dysplasia lesions. In Proceedings of the 35th Annual Veterinary Orthopaedic Society 51

 

OFA no date Elbow dysplasia statistics. http://www.offa.org/stats_ed.html accessed 3.6.11

 

Padgett GA, Mostosky UV, Probst CW, Thomas MW and Krecke CF (1995) The inheritance of osteochondritis dissecans and fragmented coronoid process of the elbow joint in Labrador retrievers. Journal of the American Animal Hospital Association 31: 327-30

 

Pead M and Ruaux-Mason C (2006) Protein expression in elbow development and dysplasia. Proceedings of the British Veterinary Orthopaedics Association Autumn Meeting 2006. 8-9

 

Sampson J (2006) What is required for breeding programmes or molecular technologies to make impact on the prevalence and incidence of elbow dysplasia in dogs? Proceedings of the British Veterinary Orthopaedics Association Autumn Meeting 2006. 4-5

 

Schwarz PD (2000) Canine elbow dysplasia. In; Kirks Current Veterinary Therapy XIII editor JD Bonagura. WB Saunders, Philadelphia. pp 1004

Shell L (2007) Osteochondrosis. VIN Associate. Accessed 20.12.2010

Swenson L, Audell L and Hedhammar A (1997) Prevalence and heritance of and selection for elbow dysplasia in Bernese mountain dogs in Sweden and benefit: cost analysis of a screening and control programme. Journal of the American Veterinary Medical Association 210: 215-221

Ubbink GJ, van de Broek J, Hazewinkel HAW and Rothuizen J (1998) Cluster analysis of the genetic heterogeneity and disease distributions in purebred dog populations. Veterinary Record 142: 209-213

van Bree H and Gielen I (2008) Diagnostic imaging in elbow dysplasia: including scintigraphy, radiography, ultrasound, CT and MRI. Proceedings of 23th Annual Meeting of International Elbow Working Group 13-17

 

Worth AJ, Bridges JP and Jones G (2010) Reduction in the incidence of elbow dysplasia in four breeds of dog as measured by the New Zealand Veterinary Association scoring scheme. New Zealand Veterinary Journal 58: 190-5

 

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