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Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
Labrador Retriever
Elbow Dysplasia (Humeral Condylar Osteochondrosis)
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 quite a common disease of Labrador retrievers.
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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 and Nap 2009), causing osteoarthritis (degenerative joint disease) in the joint.
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 using keyhole surgery techniques using an arthroscope (Shell 2007, Burton and 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
Morgan and others (1999) found elbow dysplasia (of all types – see below) in 18% of Labrador retrievers. More recent estimates put the level at 4 - 5% (Clements et al 2006, Coopman et al 2008). From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are Labrador retrievers (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 1 million. It may be, therefore, that there are about 50,000 with this form of elbow dysplasia in the UK.
5. Diagnosis
For dogs showing signs of elbow dysplasia (a general term covering a number of developmental abnormalities of the joint) determination of cause, its extent and the degree of secondary osteoarthritis requires veterinary examination, including X-rays. In dogs with HCO it is particularly important to check also for the presence of fragmented medial coronoid process (FMCP), as these two problems often coexist (Burton and 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 and that genes account for about 45% to 77% of the chance of the disease occurring. 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 and 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.
8. Methods and prospects for elimination of the problem
A voluntary scheme to grade 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). For this scheme, dogs elbows are scored for condition when over one year old and this is only performed once.
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 Labrador retrievers with 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:
(these link to items down this page)
- Clinical and pathological effects
- Intensity of welfare impact
- Duration of welfare impact
- Number of animals affected
- Diagnosis
- Genetics
- How do you know if an animal is a carrier or likely to become affected?
- Methods and prospects for elimination of the problem
- Acknowledgements
- References
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, 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 in the Labrador retriever. Other forms of elbow dysplasia can also occur in this breed (especially FMCP) 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 and 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 compromises the function of the joint. 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 and 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).
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’.
There is some evidence that HCO is more common in males (Guthrie and Pidduck 1990).
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 and treatments of the disease. 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).
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 and Pidduck 1990). Treatment may help. Surgery is effective in 40-70% of affected dogs (Burton and Owen 2008a) but keeping affected dogs free from pain and avoiding disabilities is often challenging (Shell 2007).
4. Number of animals affected
Labrador retrievers have long been known to suffer from elbow osteochondrosis as well as from other forms of elbow dysplasia (Grondalen and Grondalen 1981, Studdert et al 1991, Baines 2006), and it is included among the breeds involved in the British Veterinary Association/Kennel Club Elbow Dysplasia Scheme (Kennel Club 2010). Morgan and others (1999) found elbow dysplasia (of all types – see below) in 18% of Labrador retrievers. More recent estimates put the level at 4 - 5% (Clements et al 2006, Coopman et al 2008). From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are Labrador retrievers (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 1 million. It may be, therefore, that there are about 50,000 with this form of elbow dysplasia in the UK. The incidence of elbow dysplasia varies among lines of Labradors, being much more prevalent in some families than in others (Ubbink et al 1998, Hazewinkel and Nap 2009).
5. Diagnosis
HCO will be suspected by a veterinary surgeon when presented with a Labrador 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 and Owen 2008a). HCO can usually be diagnosed using radiography (van Bree and 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 Fragmented Medial Coronoid Process (FMCP). Magnetic resonance imaging (MRI) or computerised tomography (CT) scanning are more sensitive methods of detection and are increasingly being used (Burton and 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).
6. Genetics
Humeral condyle osteochondrosis is known to be a polygenic disorder in Labrador retrievers (Guthrie and Pidduck 1990, Padgett et al 1995, Maki et al 2002, Maki et al 2004). The heritability of the disease in male Labradors was shown to be 0.77, that is, 77% of the variation in its incidence being attributable to genes. The heritability in females was found to be 0.45 (Guthrie and Pidduck 1990).
Efforts are underway to investigate the genetics of HCO, particularly the genetics of aberrant proteins that have been found to be associated with abnormal ossification of cartilage (Pead and Ruaux-Mason 2006).
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 and 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.
8. Methods and prospects for elimination of the problem
A voluntary scheme to grade 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 Labrador retriever but a comparable scheme, run in Sweden since 1990, has led to a marked reduction in its incidence in other breeds (Swenson et al 1997, Hedhammar and Malm 2008, Malm et al 2008, Hazelwinkel and 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. One approach is to breed from dogs that have better breeding value (see below) than average for the breed (Sampson 2006). This takes account of both the individual being evaluated and its relatives (Malm et al 2008). Out-breeding BMDs with 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.
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
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 (2006) Gene Expression in Normal and Diseased Elbows. Proceedings of the British Veterinary Orthopaedics Association Autumn Meeting 2006. 6-7
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
Denny HR and Butterworth SJ (2001) The elbow. In: A Guide to Canine and Feline Orthopaedic Surgery, 4th edn. Bodmin, Blackwell Science, MPG Books. pp 363-388
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
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 December 2010
Mäki 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
Mäki 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
Meyer-Lindenberg A, Fehr M and Nolte I (2006) Co-existence of ununited anconeal process and fragmented coronoid process of the ulna in the dog. Journal of Small Animal Medicine 47: 61-5
Morgan JP, Wind A and Davidson AP (1999) Bone dysplasias in the Labrador retriever: a radiographic study. Journal of the American Animal Hospital Association 35: 332-40
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
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
Studdert VP, Lavelle RB, Beilharz RG and Masont TA (1991) Clinical features and heritability of osteochondrosis I of the elbow in labrador retrievers. Journal of Small Animal Practice 32: 557-563
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
van Ryssen B and van Bree H (1997) Arthroscopic findings in 100 dogs with elbow lameness. Veterinary Record 140: 360-362
© UFAW 2011
Credit for main photo above:
By Erikeltic at English Wikipedia [CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons
