Support the genetic welfare problems web resource
Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
Bull Terrier
Shoulder Osteochondrosis
Related terms: OCD, osteochondritis, osteochondritis dissecans, osteochondrosis dissecans, humeral head osteochondrosis
Outline: Shoulder osteochondrosis is a disease of the cartilage of the shoulder joint that causes pain and often leads to the development of chronically painful arthritis. It typically develops within the first year and can cause pain for weeks or throughout life.
Summary of Information
(for more information click on the links below)
1. Brief description
Osteochondrosis of the shoulder is a common disease in large and giant breeds of dog, though certain smaller breed dogs are also affected. English bull terriers (EBT) are predisposed to developing the condition (Woodard 1979). In general, OCD in dogs affects males more commonly than females (Shell 2007).
In affected animals, the articular cartilage of the head of the humerus becomes thickened and diseased – cracking and separating from the underlying bone, so producing a flap of cartilage, which may or may not break off and float around within the joint. These lesions are painful and affected EBTs become lame. Initially, the lameness may improve with rest; however, it tends to worsen over three to four weeks. Without treatment osteoarthritic changes occur within the joint, secondary to the osteochondrosis, and permanent pain and disability may result.
2. Intensity of welfare impact
Osteochondrosis of the shoulder causes significant pain. The osteoarthritis that develops as a secondary consequence of the disease, leads to further pain and disability. This can be mild to severe (Shell 2007).
3. Duration of welfare impact
Commonly starting at five to ten months of age, the lameness associated with the disease may last from weeks to years in severely affected dogs if treatment is not instigated. Development of secondary osteoarthritis leads to permanent pain and disability.
4. Number of animals affected
English bull terriers are predisposed to the condition (Woodard 1979) but we are unaware of any published data on the prevalence of the disease in this breed.
5. Diagnosis
Diagnosis is confirmed by shoulder radiographs (x-rays) and/ or arthroscopy (a fibre optic camera examination of the joint via a keyhole incision).
6. Genetics
There is strong evidence of a genetic component to shoulder osteochondrosis. The genes responsible have yet to be determined. Certain families of English bull terriers are predisposed to shoulder OCD (Woodard 1979).
7. How do you know if an animal is a carrier or likely to become affected?
Affected dogs should not be used for breeding. It is likely that affected puppies can be born to unaffected parents (Hazelwinkel & Nap 2009). 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
In the USA, the Orthopedic Foundation for Animals (OFA) run a voluntary scheme for breeders to register pedigree dogs certified to be free of OCD in the shoulder. Further information can be found about the scheme at http://www.offa.org/shoulder_info.html.
Like other complex, multi-gene diseases in which environmental factors also play a part, good progress in reducing the prevalence of shoulder osteochondrosis is likely to be aided by greater knowledge of the underlying genetics. One approach that is recommended is to breed from dogs that have a better breeding value (see below) than average for the breed (Morgan et al 2000, Bell 2010). This takes account of both the individual being evaluated and its relatives (ideally siblings, parents and grandparents), and compares its likely genetic health to the average for the breed. Out-breeding English bull terriers with dogs of breeds known to have a much lower prevalence of osteochondrosis in general may lead to fewer 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
Osteochondrosis 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 enlarge through growth of cartilage and, as the cartilage layer thickens, the lower, older layers become ossified – that is, they turn into bone.
In osteochondrosis, this process of ossification is disturbed so an area of thickening cartilage develops. As cartilage has no blood supply it cannot function well when it is thicker than normal. The 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 and forms a flap that may break free into the joint, the condition is called osteochondrosis dissecans (OCD), 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 within the joint or becomes trapped elsewhere in the surface of the cartilage (Grondalen & Grondalen 1981, Schwarz 2000, Shell 2007). It is thought that affected animals suffer pain when fissures in the cartilage become large enough to allow synovial fluid to contact the underlying bone (Leighton 1971). In shoulder osteochondrosis, OCD lesions form on the head of the humerus, the long limb bone that articulates with the shoulder of the dog.
The pain is usually manifested as forelimb lameness, which may be gradual in onset, often initially improving with rest, but worsening over weeks (Berzon 1979). Affected dogs may prefer to stand with their shoulders turned out slightly, and move with a shortened stride so as to not fully extend their shoulder joints (Berzon 1979, Shell 2007). Obvious pain is apparent on manipulation of the joint. Muscle wastage is often noticeable over the affected shoulder.
The cause of humeral head osteochondrosis has not been fully determined, however, it is clear that genetics play a major role. Other factors which may be involved include rapid growth rates (also under genetic control to some extent), over-nutrition – excessive intake of nutrient beyond what is needed by the animal, excess dietary calcium, and hormonal influences (Trostel et al 2002, Shell 2007). Males are two to three times more likely to be afflicted than females (Shell 2007), why this is the case is unknown.
The condition affects both shoulders in 20-85% of affected dogs (Trostel et al 2002). However, only 20% of dogs with radiographic signs of bilateral disease show lameness in both legs (Trostel et al 2002).
Dogs with humeral head osteochondrosis develop osteoarthritis (degenerative joint disease) of the shoulder over time (usually years); those with more severe OCD being most affected (Griffiths 1968, Vaughan & Jones 1968). In osteoarthritis, there are progressive changes to the cartilage of the affected joint and, varying amounts of inflammation and ongoing damage to other joint structures - the joint capsule, the synovial fluid of the joint and the surrounding bone. Typical signs of osteoarthritis include: stiffness after rest, lameness (which can be worse after exercise) and pain when the leg is straightened or bent.
Usually, surgical removal of the OCD cartilage flap/ joint mouse is recommended to relieve pain, to prevent the embedding of a free joint mouse elsewhere in the joint and to decrease future development of osteoarthritis, although osteoarthritis may still develop in middle age in these cases (Trostel et al 2002, McKee & Macias 2004). Some mild cases spontaneously resolve with rest.
Occasionally, signs are not seen until secondary osteoarthritis has developed in the joint during middle-age (http://www.willows.uk.net/specialist-services/pet-health-information/orthopaedics/osteochondrosis).
2. Intensity of welfare impact
English bull terriers with shoulder osteochondrosis can suffer significant pain for weeks to months, which, without surgical treatment, is likely to initiate secondary permanent pain and disability from the osteoarthritis that develops. This pain 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 for the disease (for example: through the side effects of non-steroidal anti-inflammatory drugs on the gastrointestinal tract). Restricted activity may be recommended, for a period of time, to facilitate tissue repair and this reduced activity may constrain the dog’s capacity for normal life and behaviour (Shell 2007).
3. Duration of welfare impact
Most dogs are between five and ten months of age when signs of lameness first occur with humeral head osteochondrosis (Trostel et al 2002, McKee & Macias 2004), although some may be over 12 months old. Lameness and pain may last for weeks to months or years in severely affected individuals (Griffiths 1968, Vaughan & Jones 1968). If no treatment is sought permanent osteoarthritis is likely to develop leading to a lifetime of pain and disability. Surgery is often successful in relieving current discomfort although osteoarthritis often occurs in the joint over time.
4. Number of animals affected
English bull terriers are predisposed to the condition (Woodard 1979) but we are unaware of any published data on the prevalence of the disease in this breed.
5. Diagnosis
Young English bull terriers can suffer from a number of conditions causing forelimb lameness. Thorough veterinary examination may be needed to determine if the shoulder is involved. Osteochondrosis can be confirmed from radiographs (x-rays) of the shoulder joints. Arthroscopy (examination of the joint with a fibre optic camera via a keyhole incision) may also be used to view potential OCD lesions.
6. Genetics
English bull terriers are recognised as being predisposed to shoulder OCD (Shell 2007) and certain families are especially affected (Woodard 1979). This familial predisposition has been reported in Border collies also (Knecht et al 1977) and these strong breed and family dispositions indicate a genetic cause (Morgan et al 2000). An unpublished analysis of shoulder osteochondrosis in Bernese mountain dogs in the UK reported a heritability of between 0.55 and 0.7 (Guthrie & Pidduck 1990). These are the proportions of the disease considered to be due to genetic rather than environmental influences such as nutrition. The study by Morgan et al (1999) also suggested that the disease has high heritability in Labrador retrievers. The heritability of the condition has not been investigated in English bull terriers as far as we are aware.
Humeral condyle osteochondrosis is known to be a polygenic disorder in Labrador retrievers and other breeds (Padgett et al 1995, Maki et al 2002, Maki et al 2004, Janutta et al 2006) and this is likely to be the case also for humeral head osteochondrosis. However, the genes responsible are unknown.
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).
7. How do you know if an animal is a carrier or likely to become affected?
Affected dogs should not be used for breeding. It is likely that affected puppies can be born to unaffected parents – this is certainly the case for humeral condyle osteochondrosis (Hazelwinkel & 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
It has been suggested that development of a breeding program aimed at controlling or eliminating shoulder osteochondrosis would be worthwhile because, its relatively high heritability, suggests that it would be possible to make good progress in this way (LaFond et al 2002).
In the USA, the Orthopedic Foundation for Animals (OFA) runs a voluntary scheme for breeders to register pedigree dogs certified to be free of shoulder OCD. To gain this certification a dog needs to be over a year in age and to have x-rays of both their shoulder joints certified as free of the condition by a recognised veterinary radiologist. Further information can be found about the scheme at http://www.offa.org/shoulder_info.html.
Like other complex, multi-gene diseases in which environmental factors also play a part, good progress in reducing the prevalence of shoulder osteochondrosis is likely to be aided by greater knowledge of the underlying genetics. One approach that is recommended is to breed from dogs that have a better breeding value (see below) than average for the breed (Morgan et al 2000, Bell 2010). This takes account of both the individual being evaluated and its relatives (ideally siblings, parents and grandparents), and compares its likely genetic health to the average for the breed. Out-breeding English bull terriers with dogs of breeds known to have a much lower prevalence of osteochondrosis in general may lead to fewer 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.
10. References
Bell JS (2010) Genetic Testing and Genetic Counseling in Pet and Breeding Dogs.35th World Small Animal Veterinary Association World Congress Proceedings. 2-5th June 2010, Geneva, Switzerland. http://www.vin.com/Members/Proceedings/Proceedings.plx?CID=wsava2010&PID=pr56159&O=VIN accessed 19.8.2011
Berzon JL(1979) Osteochondritis dissecans in the dog: Diagnosis and therapy. Journal of American Veterinary Medicine Association 175: 796-799
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
Griffiths RC (1968) Osteochondritis dissecans of the canine shoulder. Journal of American Veterinary Medicine Association 153: 1733-1735
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 (2009) Elbow dysplasia; a definition and known aetiologies. Proceedings of 24th Annual Meeting of International Elbow Working Group. pp 6-18
Janutta V, Hamann H, Klein S, Tellhelm B and 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
Knecht CD, van Sickle DC, Blevins WC, Avolt MD, Hughes RB and Cantwell HD (1977) Osteochondrosis of the shoulder and stifle in 3 out of 5 Border Collie littermates. Journal of American Veterinary Medicine Association 170: 58-60
LaFond E, Breur GJ and Austin CC (2002) Breed susceptibility for developmental orthopedic diseases in dogs. Journal of the American Animal Hospital Association 38: 467-477
Leighton RL (1971) Osteochondritis dissecans of the shoulder joint of the dog. Veterinary Clinics of North America 1: 391-401
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
McKee M and Macias C (2004) Orthopaedic conditions of the shoulder in the dog. In Practice 26: 118-129
Morgan JP, Wind A and Davison AP (1999) Bone dysplasias in the labrador retriever: a radiographic study. Journal of the American Animal Hospital Association 35: 332-340
Morgan JP, Wind A and Davison AP (2000) Hereditary Bone and Joint Disease in the Dog. Schlütersche: Hannover, Germany. pp14
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
Schwarz PD (2000) Canine elbow dysplasia. In; Kirks Current Veterinary Therapy XIII editor JD Bonagura. WB Saunders, Philadelphia. pp 1004
Shell L (2007) Osteochondrosis. On-line. VIN Associate. http://www.vin.com/Members/Associate/Associate.plx?DiseaseId=1274. Accessed 10.11.2011
Trostel CT, McLaughlin RM and Pool RR (2002) Canine lameness caused by developmental orthopaedic conditions: Osteochondrosis. Compendium of Continuing Education for the Practising Veterinarian 24 (11) http://cp.vetlearn.com/Media/PublicationsArticle/PV_24_11_836.pdf. accessed 22.8.11.
Vaughan LC and Jones DGC (1968) Osteochondritis dissecans of the head of the humerus in dogs. Journal of Small Animal Practice 9: 283-294
Woodard DC (1979) Osteochondritis dissecans in a family of bull terriers. Veterinary Medicine Small Animal Clinician 74: 936
http://www.offa.org/shoulder_info.html accessed 23.8.2011
http://www.willows.uk.net/specialist-services/pet-health-information/orthopaedics/osteochondrosis accessed 23.8.2011
© UFAW 2012
Credit for main photo above:
http://depositphotos.com/26569239/stock-photo-bull-terrier.html
©Depositphotos.com/f8grapher
