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Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
Labrador Retriever
Osteochondritis Dessicans of the Stifle
Related terms: OCD, osteochondrosis, osteochondrosis dessicans
Outline: Osteochondrosis of the stifle is a disease in which the cartilage lining the joint surfaces of the bones of the knee develops abnormally and may become pitted, cracked or fragmented. It causes pain and some loss of function and affected joints develop osteoarthritis which leads to further pain and loss of function. Labrador retrievers are predisposed to the disease but the genes involved have not been determined. To avoid perpetuating the disease, it would seem sensible not to use affected dogs (or those with close relatives that are affected) for breeding but as far as we are aware there is no organised scheme yet for tackling this disease.
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Summary of Information
(for more information click on the links below)
1. Brief description
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. The canine stifle is the equivalent of the human knee joint. Dogs with stifle OCD often have pain and some loss of joint function due to the disease itself but these problems can worsen due to the secondary osteoarthritis (degenerative joint disease) that also usually develops in dogs affected with this condition. Typical signs include: stiffness after rest, lameness (which can be worse after exercise) and pain.
In the early stages of the disease, when only cartilage is affected, these changes can only be seen by direct observation involving surgery (usually arthroscopy). Later, when bone is diseased too, changes can also be detected on radiography (Baines 2006).
Affected puppies may show lameness that has a gradual onset that worsens over weeks to months and with exercise. The stifle joints may become swollen and stiff (Trostel et al 2002). In other cases, signs develop later as a consequence of the osteoarthritis secondary to OCD (or to surgical procedures undertaken to tackle it).
2. Intensity of welfare impact
Osteochondrosis causes pain, this may be mild or severe. It leads to the development of osteoarthritis and this also causes pain. The stiffness, joint swelling and muscle wastage associated with the disease affect normal movement and this has welfare implications as the dog may be unable to express all its natural behaviours such as running and jumping (Trostel et al 2002). .
3. Duration of welfare impact
Osteochondrosis starts in puppyhood (Trostel et al 2002). It usually causes problems for weeks to months but may respond to treatment. However, the development of secondary osteoarthritis may cause adverse welfare effects for the remainder of their lives. In other cases there may be a period of months to years without problems before pain and disability develop in middle or old age due to the secondary osteoarthritis. Once secondary osteoarthritis starts it will persist for life, although medical treatments may help.
4. Number of animals affected
Labrador retrievers are predisposed to stifle osteochondrosis (Necas et al 1999, LaFond et al 2002) but we are unaware of data on the proportion of animals that are affected.
5. Diagnosis
The condition may be suspected when a puppy of a predisposed breed, such as the Labrador retriever, shows hind limb lameness with evidence of stifle disease. Radiography will usually enable the correct diagnosis. Arthroscopy can be used as part of the diagnostic procedure (Bertrand et al 1997, McCarty 2005).
6. Genetics
Although it is known that Labrador retrievers are predisposed to the disease (Necas et al 1999, LaFond et al 2002), the genes involved have not been determined. It is likely that multiple genes, as well as environmental influences, have an important role in the development of the disease.
7. How do you know if an animal is a carrier or likely to become affected?
Affected dogs should not be used for breeding. 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
In contrast to the situation with the more common forms of osteochondrosis, which occur in the shoulder or elbow, there are no schemes, as far as we are aware, aimed at reducing the prevalence of stifle OCD. The recommended approach for some similar diseases is to breed from dogs that have better than average breeding values for the breed (Sampson 2006). Breeding values take account of the health of both the individual and its relatives (Malm et al 2008, Bell 2010).
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 (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 interfere with the process of ossification so that, as the cartilage continues to grow but does not become ossified, a region of thickened cartilage develops. As cartilage has no blood supply, it cannot function properly when it becomes thicker than normal and affected regions of cartilage degenerate. Cracks or cavities may form within this diseased cartilage and it may fragment (Guthrie et al 1992). If the cartilage has fragmented the condition is called osteochondrosis dessicans, and when this occurs the function of the joint is compromised. Joint function is affected both because of the damage to the cartilage and because loose pieces of cartilage (sometimes called joint mice) may move around within the joint or become trapped elsewhere in the surface of the cartilage (Schwarz 2000, Trostel et al 2002, Shell 2007).
Stifle OCD, as with OCD in other joints, typically affects large or giant breeds of dog and their predisposition to the disease may be associated with the growth rates of these dogs (Trostel et al 2002, Shell 2007).
Dogs with stifle OCD develop osteoarthritis (degenerative joint disease) of the joint. In osteoarthritis there are progressive changes to the cartilage of the affected joint, with varying degrees 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 4-9 months of age but can show later. Typical signs of osteoarthritis 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 stifle disease and imaging of the joint (eg by radiography) is usually needed to make a definitive diagnosis (Trostel et al 2002, Shell 2007, Fossum 2007). In the early stages of the disease, when only cartilage is affected, the condition is detectable only by direct observation involving surgery (usually arthroscopy). Later, when osteoarthritis has developed, changes can also be detected on radiography (Baines 2006).
Some dogs develop OCD in both stifles (Denny & Gibbs 1980). One report suggested that this occurs in about three out of four affected dogs (Montgomery et al 1989). The regions of cartilage affected are usually on the femoral condyles, the fist-like protuberances on the far end of the thigh bone that form the upper part of the stifle joint (Denny & Gibbs 1980, Fossum 2007) and most commonly occur on the inner side of the lateral condyle (Trostel et al 2002). They have also been recorded in the inter-condylar fossa, the 'valley' between the condyles (Kulendra et al 2008).
Affected puppies may show lameness, that has a gradual onset and that worsens over weeks to months and with exercise. The stifle joints may become swollen and stiff (Trostel et al 2002). In other cases, signs develop later as a consequence of the osteoarthritis secondary to OCD (or to surgical procedures undertaken to tackle it). A further complication is that some dogs with the disease develop a tear in a meniscus, the C-shaped cartilage found in the stifle joint (Langley-Hobbs 2001). This requires further surgical treatment.
Surgical treatment is suggested for young animals that are lame but which have not yet developed osteoarthritis, in the hope that the onset of osteoarthritis will be delayed or its severity reduced. It may also be recommended for older dogs that have responded poorly to medical treatment (Fossum 2007). Knee replacement may be an option in severe cases (Liska & Doyle 2009). Medical treatment aimed partly at alleviating chronic pain is likely to be necessary throughout life once secondary osteoarthritis has developed (Bertrand et al 1997).
2. Intensity of welfare impact
Osteochondrosis causes pain, this may be mild or severe. It leads to the development of osteoarthritis and this also causes pain. The stiffness, joint swelling and muscle wastage associated with the disease affects normal movement and this has welfare implications as the dog may be unable to express all its natural behaviours such as running and jumping (Trostel et al 2002). Treatment may involve the need to restrict activity in order to reduce pain and slow the development of secondary damage to the diseased joint.
The diagnostic procedures and treatments can themselves have adverse welfare effects. Major surgery is sometimes necessary in order to enable the chances of normal activity and to control pain. However, surgery is not always effective and can have side effects of its own. Medical treatments can also have side effects. For example, non-steroidal anti-inflammatory drugs administered to help control the condition may cause gastrointestinal damage (Ramsey 2011).
3. Duration of welfare impact
Osteochondrosis starts in puppyhood (Trostel et al 2002). It usually causes problems for weeks to months but may respond to treatment. However, the development of secondary osteoarthritis may cause adverse welfare effects for the remainder of their lives. In other cases there may be a period of months to years without problems before pain and disability develop in middle or old age, due to the secondary osteoarthritis. Once secondary osteoarthritis starts it will persist for life although medical treatments may help to alleviate some of its effects.
4. Number of animals affected
Labrador retrievers are predisposed to stifle osteochondrosis (Necas et al 1999, LaFond et al 2002) but we are unaware of data on the proportion of animals that are affected.
5. Diagnosis
The condition may be suspected when a puppy of a predisposed breed, such as the Labrador retriever, shows hind limb lameness with evidence of stifle disease. Radiography will usually enable the correct diagnosis, although other tests may be required to rule out other diseases of the stifle, some of which are more common – for example rupture of the cranial cruciate ligament (Trostel et al 2002, Fossum 2007, Shell 2007). Arthroscopy can be used as part of the diagnostic procedure (Bertrand et al 1997, McCarty 2005).
6. Genetics
Although it is known that Labrador retrievers are predisposed to the disease (Necas et al 1999, LaFond et al 2002), the genes involved have not been determined. It is likely that multiple genes, as well as environmental influences, have an important role in the development of the disease.
The occurrence of OCD in other joints is known to have significant genetic influences. For example, osteochondrosis of the elbow is known to be a polygenic disorder in Labradors (Padgett et al 1995) and in other breeds (Maki et al 2002, Maki et al 2004, Janutta 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. 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
In contrast to the situation with the more common forms of osteochondrosis, which occur in the shoulder or elbow, there are no schemes, as far as we are aware, aimed at reducing the prevalence of stifle OCD. 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. The recommended approach for some similar diseases is to breed from dogs that have better than average breeding values for the breed (Sampson 2006). Breeding values take account of the health status of both the individual and its relatives (Malm et al 2008, Bell 2010). Until such time as a breeding strategy is developed to tackle this disease of the stifle joints, the best approach is simply not to use affected animals for breeding, nor any that have affected relatives (or which have more than a very few affected relatives) (Bell 2010).
9. Acknowledgements
UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section.
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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
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/proceedings/Proceedings.plx?CID=WSAVA2010&Category=&PID=56159&O=Generic. Accessed 23.9.2011
Bertrand SG, Lewis DD, Madison JB, de Haan JH, Stubbs WP and Stallings JT (1997) Arthroscopic examination and treatment of osteochondritis dissecans of the femoral condyle of six dogs. Journal of the American Animal Hospital Association 33: 451-5
Denny HR and Gibbs C (1980) Osteochondritis dissecans of the canine stifle joint. Journal of Small Animal Practice 21: 317–322
Fossum TW (2007) Disease of the joints. In: Small Animal Surgery, Elsevier, Oxford, UK pp 1299-1303
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
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, California pp121
Kulendra E, Lee K, Schoeniger S and Moores AP (2008) Osteochondritis dissecans-like lesion of the intercondylar fossa of the femur in a dog. Veterinary and Comparative Orthopedics and Traumatology 21: 152-5
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
Langley-Hobbs (2001) Lateral meniscal tears and stifle osteochondrosis in three dogs. Veterinary Record 149: 592-4
Liska WD and Doyle ND (2009) Canine total knee replacement: surgical technique and one-year outcome. Veterinary Surgery 38: 568-82
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
McCarthy TC (2005) Treating Osteochondritis Dissecans of the Stifle with Arthroscopic Surgery. Veterinary Medicine 100: 196
Montgomery RD, Milton JL, Henderson RA et al (1989) Osteocondrosis dessicans of the canine stifle joint. Compendium of Continuing Education for the Practising Veterinarian 11: 1199-1205
Necas A, Dvorak M and Zatloukal J (1999) Incidence of osteochondrosis in dogs and its late diagnosis. Acta Veterinaria Brno 68: 131-139
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
Ramsey I (2011) Carprofen Small Animal Formulary 7th Ed. British Small Animal Veterinary Association: Gloucester, UK pp54-5
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. pp4-5
Schwarz PD (2000) Canine elbow dysplasia. In Bonagura JD (ed) Kirks Current Veterinary Therapy XIII. WB Saunders, Philadelphia. pp 1004
Shell L (2007) Osteochondrosis. VIN Associate. Accessed 20.9.2011
Trostel CT, McLaughlin RM and Pool RR (2002) Canine lameness caused by developmental orthopaedic diseases: osteochrondrosis. Compendium 24: 836-854 http://www.compendiumvet.com/Media/PublicationsArticle/PV_24_11_836.pdf accessed 23.9.2011
© UFAW 2011
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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
