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Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
Labrador Retriever
Elbow Dysplasia (Fragmented Medial Coronoid Process)
Related terms: medial compartment disease, medial coronal process disease, elbow disease.
Outline: Fragmented medial coronoid process is a common disease of Labrador retrievers and is thought to affect 17-21% of these dogs. In this disease, part of the surface of the bones of the elbow joint develops abnormally, or is damaged. This results in fragments breaking off into the joint and the development of chronic arthritis of the elbow. The arthritis tends to start within the first year and, unless successfully treated, causes lifelong pain and discomfort. It is difficult to treat.
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Summary of Information
(for more information click on the links below)
1. Brief description
The medial coronoid process is part of the ulna bone which makes up part of the elbow joint of a dog. In this disease, pieces of bone and cartilage may fragment, breaking off into the elbow joint and cause osteoarthritis.
Fragmented medial coronoid process(es) (FMCP) can occur from an early age, and in affected dogsosteoarthritis is often present by 4-6 months of age but can show later. Such dogs may be treated with rest and pain-killers, but treatment often needs to be lifelong. Various surgical procedures have been recommended but there is no clear consensus as to which is best. Some treatments involve major surgery with sections of bone being removed (Burton & Owen 2008b).
2. Intensity of welfare impact
FMCP leads to pain and disability associated with the osteoarthritis. This can be mild or severe.
3. Duration of welfare impact
The mild to severe welfare impacts 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.
4. Number of animals affected
It has been suggested that between 13 and 21% of Labradors are affected with FMCP (Ubbink 2000, Kirkberger & Stander 2007, Coopman et al 2008, Temwichitr 2009). Other authors have suggested that 17 to 21% of Labradors are affected by this and other forms of elbow dysplasia (Studdert et al 1991, Morgan et al 1999).
5. Diagnosis
For dogs showing signs of elbow dysplasia (a general term covering a number of developmental abnormalities of the joint) determination of the cause, its extent and the degree of secondary osteoarthritis requires veterinary examinations including x-rays, CT and MRI scans and exploratory surgery – often using an arthroscope.
6. Genetics
There is strong evidence of a genetic component to FMCP and that genes account for about 45 - 71% of the chance of the disease occurring (Guthrie and Pidduck 1990), but the genes involved 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 produced from unaffected parents (Hazelwinkel and Nap 2009). 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 breeder uptake is suggested to be relatively low (Sampson 2006). Dogs are scored for elbow 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 FMCP 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 Labradors with breeds known to have a much lower prevalence of FMCP 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, outlined below, that tend to result in malformation of the elbow joint that leads to early-onset osteoarthritis, of which fragmented medial coronoid process (FMCP) is one.
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. UAP occurs when this fusion fails to happen.
Osteochondrosis dissecans (OCD): In OCD an area of joint cartilage develops abnormally or becomes damaged leading to thickening, cracking and fragmentation of the cartilage.
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 FMCP in the Labrador retriever but some of the above conditions are referred to in the descriptions (below) about how FMCP may develop.
The elbow is a complicated joint of three bones; the humerus (upper bone of the foreleg/arm bone), 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 humerus. Most of this articular surface is on the radius but two parts of the ulna are involved: the medial (towards the inside of the leg) and lateral (towards the outside) coronoid processes.
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).
Figure 2. A diagram of the upper end of the ulna illustrating the locations of the coronoid and anconeal processes. The medial coronoid process (MCP) is located towards the inside of the leg. (Image property of Phil Witte, to whom we are grateful for permission to reproduce it here).
At birth the medial coronoid process (MCP) is composed of cartilage. In dogs with an FMCP this cartilage does not turn into bone in the normal way (a process called endochondral ossification). There are different theories as to why as outlined below.
For a healthy elbow joint it is vital (among other things) for the ulna and the radius to grow together and create a flat articular surface with the humerus. One theory is that FMCP is caused by the radius not growing in coordination with the ulna, so that the weight passing down from the humerus rests largely and abnormally on the coronoid processes of the ulna. More weight goes medially and this pressure prevents endochondral ossification (Ubbink et al 1999).
Figure 3. Uncoordinated growth of the elbow joint. If the radius (blue) is too short relative to the ulna (purple), the humerus (green) applies excessive pressure on to the coronoid processes (blue arrow in the diagram), rather than it being distributed evenly across both radius and ulna. The coronoid processes therefore develop abnormally and are prone to fragmentation (Image property of Phil Witte, to whom we are grateful for permission to reproduce it here).
Another possibility is that abnormal development of the tracheal notch (an aspect of elbow IC) causes abnormal pressure on the medial coronoid processes (MCP) and abnormal endochondral ossification in them (Wind and Packard 1986a, Wind and Packard 1986b, Ubbink et al 1999).
The above theories are those currently favoured (Burton & Owen 2008a) but other possibilities have been considered, as outlined below:
FMCP may arise through damage to the MCP while it is of cartilage, which might be due to unusual stresses through activity in large dogs. The damaged MCP then does not properly undergo the process that should turn its cartilage into bone (endochondral ossification) (Grondalen and Grondalen 1981, Olsson 1993).
Trauma is also a possible cause of the initial damage (Guthrie et al 1992).
Whatever leads to its formation, FMCP is characterised by the MCP breaking up. Pieces of bone and cartilage may break off, with these fragments floating in the joint or becoming embedded elsewhere within it. Holes may also be seen in the cartilage.
Figure 4. In cases of FMCP, the medial coronoid process breaks off from the ulna as shown in this radiograph. (Image property of Southern Counties Veterinary Specialists, to whom we are grateful for permission to reproduce it here).
Figure 5. A Computed Tomography (CT) image shows a cross section of the elbow joint, and illustrates the fracture of the medial coronoid process (blue arrow) from the ulna. (Image property of Southern Counties Veterinary Specialists, to whom we are grateful for permission to reproduce it here).
The pathology may be somewhat different in different breeds. In the Labrador it tends to be the lateral side of the MCP that breaks but this is held in place by the radius (Hazelwinkel 2009).
Associated with FMCP there is often a lesion on the adjacent cartilage of the humerus . It has been suggested that both these changes should be encompassed within the term medial compartment disease (Kramer et al 2006).
Dogs with FMCP develop osteoarthritis (degenerative joint disease) in the elbow. In osteoarthritis there are progressive changes to the joint cartilage, varying amounts of inflammation and ongoing damage to other joint structures - the joint capsule, joint fluid and surrounding bone. These changes are often present by 4-6 months of age and lead to clinical signs later. Typical signs include: stiffness after rest, lameness (which can be worse after exercise) and reduced mobility of the joint, with the leg tending to be held twisted outwards (abducted and suppinated). Such signs are indistinguishable from those shown in other forms of elbow dysplasia and imaging of the joint is usually needed to make a definitive diagnosis (Schwarz 2000).
Affected dogs may be treated with rest and pain-killers, and often treatment needs to be life long. Various surgical procedures have been recommended but there is no clear consensus as to which is best. Some of these procedures involve major surgery, including removing whole sections of the ulna in order to shorten it (Burton and Owen 2008b).
In general, FMCP is seen more commonly in males than females and the problem is often bilateral (Guthrie and Pidduck 1990, Schwarz 2000, Burton and Owen 2008a, Tamwichitr 2009). The male bias may be associated with the greater weight of males (Hazelwinkel 2009).
2. Intensity of welfare impact
MCPF 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.
Figure 6a Figure 6b
Figure 6a and b. Osteoarthritic changes to the shape and structure of the elbow joint secondary to FMCP. The shaded areas on figures 6a (extended elbow) and 6b (flexed elbow) represent secondary changes to the bones as a result of FMCP. (Images property of the British Veterinary Association/ Kennel Club Elbow Dysplasia Scheme and we are grateful to the BVA for permission to reproduce them here).
3. Duration of welfare impact
The mild to severe pain and disability 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 not possible
4. Number of animals affected
The Labrador has long been known to suffer from elbow dysplasia (Grondalen and Grondalen 1981, Grondalen & Lingaas 1991, Studdert et al 1991, LaFond et al 2002) and it is included in the breeds involved in the British Veterinary Association/Kennel Club Elbow Dysplasia Scheme (Kennel Club 2010)
FMCP is the most common of the causes of elbow dysplasia in dogs (van Ryssen and van Bree 1997, Burton and Owen 2008a).
There is evidence that the incidence of FMCP varies between lines of Labradors (Ubbink 2000). It has been suggested that between 13 and 21% are affected (Ubbink 2000, Kirkberger and Stander 2007 and Coopman et al 2008). Morgan et al (1999) found 17% of Labradors to have this and other forms of elbow dysplasia and Studdert et al (1991) found 21% of Labradors to be lame due to elbow dysplasia. The Orthopaedic Foundation for Animals (OFA) records state that 10.8% of Labradors examined under their scheme between 1974 and 2010 had elbow dysplasia http://www.offa.org/stats_ed.html.
In their studies of inheritance of elbow dysplasia, Guthrie and Pidduck (1990) found that 1.25% of male and 0.57% of female guide dogs had clinical signs of elbow dysplasia, but pointed out that this low prevalence compared with other surveys of Labrador retrievers, Golden retrievers and crosses between the two, was because lame animals would be removed from the training programme. In a similar study of guide dogs in The Netherlands, Temwichitr (2009) found that 15% suffered from FMCP
5. Diagnosis
FMCP will be suspected by a veterinary surgeon when presented with a Labrador showing forelimb pain and elbow disease. Determining the type of elbow disease, its extent and the degree of secondary osteoarthritis requires further diagnostic procedures. This may include x-rays but, because the MCP is difficult to visualise, FMCP is found in only 62% of cases carefully imaged. In other cases there are typical secondary changes of osteoarthritis than lead to FMCP being suspected (Burton and Owen 2008a).
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. This surgery may be via an arthroscope (a small fibre optic instrument to look directly into the joint through a small key-hole incision) (van Ryssen and van Bree 1997). It has been suggested that the best combination of diagnostic tests is CT plus arthroscopy (Moores et al 2008).
6. Genetics
There is strong evidence of a genetic component to FMCP with 45 to 71% of the variation in incidence in guide dogs (comprising Labrador retrievers, Golden retrievers and crosses between the two) being attributable to genes (Guthrie and Pidduck 1990). Maki et al (2002) gave a figure of 0.1 for the heritability of elbow dysplasia in Labradors (ie estimating that 10% of variation in incidence was attributable to genes) but Malm et al (2008) findings indicated a greater heritability at 0.34-0.38. The heritability probably varies according to the breeding line of the individual; Ubbink et al (2000) found heritability varied from 0.07 – 0.41.
Multiple genes are involved in the condition (Padgett et al 1995). Efforts to identify the genes involved in FMCP are underway but, as with other forms of elbow dysplasia, these are complicated by the difficulty of identifying animals that are definitely free of the disease (Clements 2006, Salg 2006).
Although different forms of elbow dysplasia sometimes occur together in some individuals sometimes (Meyer-Lindenberg et al 2006) they are probably not linked genetically (or pathogenically) so should be considered separately when searching for genetic causes (Innes 2006).
It is known that the father and mother contribute equally to the likelihood of the development of elbow dysplasia (Maki et al 2002).
There are genetic influences both on the occurrence of FMCP and on whether, and to what degree, osteoarthritis occurs in an individual with FMCP (Clements et al 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 produced from apparently normal parents (Hazelwinkel and Nap 2009). 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 for grading the elbows of dogs susceptible to elbow dysplasia (all forms) has been operating in the UK since 1998 although it has been suggested that breeder uptake is relatively low (Sampson 2006). Details of this 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 the higher of the 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 is reducing elbow dysplasia in the Labrador. A comparable scheme, run in Sweden since 1990, requires that all Labradors are screened in order to be allowed onto the breeding register (Hedhammar and Malm 2008). This scheme has reduced the prevalence of elbow dysplasia in Bernese Mountain dogs (Swenson et al 1997, Malm et al 2008) but data are not available on its impact in Labradors. A similar scheme is run in the USA by OFA.
Like other complex, multi-gene diseases in which environmental factors also play a part, good progress in reducing the prevalence of FMCP 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 Labradors with breeds known to have a much lower prevalence of FMCP 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
Burton N and Owen M (2008a) Canine elbow dysplasia 1. Aetiopathogenesis and diagnosis. In Practice 30: 508-512
Burton N and Owen M (2008b) Canine elbow dysplasia 2. Treatment and prognosis. In Practice 30: 552-557
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: 654-658
Grondalen J and Grondalen T (1981) Arthrosis in the elbow joint of young rapidly growing dogs. Nordisk Veterinaermedicin 31: 1
Grondalen J and Lingaas F (1991) Arthrosis in the elbow joint of young rapidly growing dogs: a genetic investigation. Journal of Small Animal Practice 32: 460-464
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 (2009) Preamble. Proceedings of 24th Annual Meeting of International Elbow Working Group. pp 2
Hazelwinkel HAW and Nap RC (2009) Preamble. Proceedings of 24th Annual Meeting of International Elbow Working Group. pp 2
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
Kennel Club (2010) (On-line) The BVA /KC Elbow Dysplasia Scheme. Available at http://www.thekennelclub.org.uk/item/309. Accessed 1st December 2010
Kirberger RM and Stander N (2007) Incidence of canine elbow dysplasia in South Africa.
Journal of the South African Veterinary Association 78: 59-62
Kramer A, Holsworth IG, Wisner ER, Kass PH and Schulz KS (2006) Computed tomographic evaluation of canine radioulnar incongruence in vivo. Veterinary Surgery 35: 24-29
LaFond E, Breur GJ and Austin CC (2002) Breed susceptibility for developing orthopaedic diseases in dogs. Journal of the American Animal Hospital Association 38: 467-77
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
Olsson SE (1993) Pathophysiology, morphology, and clinical signs of osteochondrosis in the dogs. In; Disease Mechanisms in Small Animal Surgery. Editor M.J. Bojrab. Lea & Febiger, Philadelphia. pp 777
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
Salg KG, Temwitchitr J, Imholz S, Hazewinkel HA and Leegwater PA (2006) Assessment of collagen genes involved in fragmented medial coronoid process development in Labrador Retrievers as determined by affected sibling-pair analysis. American Journal of Veterinary Research 67: 1713-8
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 J.D. Bonagura. WB Saunders, Philadelphia. pp 1004
Studdert VP, Lavelle RB, Beilharz RG and Masont TA (1991) Clinical features and heritability of osteochondrosis of the elbow in Labrador retrievers. Journal of Small Animal Practice 32: 557-563
Swenson L, Audell L and Hedhammar A (1997) Prevalence and inheritance 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
Tamwichitr J (2009) The genetic defect of fragmented coronoid process in Labrador Retrievers and other skeletal diseases in dogs. PhD thesis. http://igitur-archive.library.uu.nl/dissertations/2009-0630-200820/temwichitr.pdf
Ubbink GJ, Hazewinkel HA, van de Broek J and Rothuizen J (1999) Familial clustering and risk analysis for fragmented coronoid process and elbow joint incongruity in Bernese mountain dogs in the Netherlands. American Journal of Veterinary Research 60: 1082-1087
Ubbink GJ, Broek J van de, Hazewinkel HAW, Wolvekamp WTC and Rothuizen J (2000) Prediction of the genetic risk for fragmented coronoid process in Labrador Retrievers. Veterinary Record 147: 149-152
van Ryssen B and van Bree H (1997) Arthroscopic findings in 100 dogs with elbow lameness.Veterinary Record 140: 360-362
Wind AP and Packard ME (1986a) Elbow incongruity and developmental elbow disease in the dog: part I. Journal of the American Animal Hospital Association 22: 711-24
Wind AP and Packard ME (1986b) Elbow incongruity and developmental elbow disease in the dog: part II Journal of the American Animal Hospital Association 22: 725-30
http://www.offa.org/stats_ed.html (accessed 6.5.2011)
http://www.thekennelclub.org.uk/item/309 (accessed 6.5.2011)
© UFAW 2012
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
