Support the genetic welfare problems web resource
Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
Rottweiler
Osteochondritis Dessicans of the Hock Joint
Related terms: OCD, osteochondrosis, osteochondrosis dessicans
Outline: Rottweilers are predisposed to a developmental abnormality of the cartilage of the hock (ankle) joint – osteochondritis – that causes pain and which usually leads to osteoarthritis of the joint resulting in further pain and loss of function.
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 – of joints. The joint that is affected in this condition is the canine hock, or tarsus, - the equivalent of the human ankle joint. Dogs with hock OCD often have problems as a direct result of the disease but in many cases the problems develop due to secondary osteoarthritis (degenerative joint disease) of the joint. Typical signs include stiffness after rest, lameness and pain.
In the early stages of the disease, when only the joint cartilage is affected, it is detectable only with direct observation by surgery (usually arthroscopy). Later, as the disease progresses and the bone of the joint becomes diseased too, changes can also be detected on radiography (Baines 2006).
Dogs may suffer directly from the OCD lesions. In these cases, puppies may show lameness with an insidious onset that gradually worsens over weeks to months and with exercise. The joints may become swollen and stiff (Trostel et al 2002). Other affected dogs have their most major problems in later life, as the consequence of osteoarthritis secondary to OCD or secondary to surgical procedures undertaken to treat the condition.
2. Intensity of welfare impact
The effects of osteochondrosis can be mild or severe depending on the size of the OCD lesion, its site and whether one or both hind legs are affected (Trostel et al 2002). The OCD lesion directly causes pain and this can vary from mild to severe. Pain also comes from the secondary osteoarthritis that frequently develops in affected animals. Stiffness, joint swelling and muscle wastage all cause disability and this has welfare implications as mobility may be impaired with difficulties in running and jumping (Trostel et al 2002).
3. Duration of welfare impact
OCD starts in puppyhood (Trostel et al 2002). It usually causes problems for weeks to months and may respond to treatment. One study found that around half of affected dogs have chronic lameness despite surgical and medical treatment in the fours years after presentation (Breur et al 1989). Secondary osteoarthritis often develops post treatment so individuals may be affected throughout their lives. Others may not show any signs for months or years and then develop pain and disability in middle or old age due to the secondary osteoarthritis. Once this starts, it persists throughout the life of the dog although medical treatments may help.
4. Number of animals affected
The Rottweiler is the breed of dog most affected by hock OCD and is about 206 times greater at risk of this disease than mixed breed dogs (Montgomery et al 1994, LaFond et al 2002, Miller & Hulse 2006, Fossum 2007). We are not aware of information onthe proportion of the breed that is affected, however.
5. Diagnosis
OCD may be suspected when a Rottweiler has hind limb lameness with evidence of hock disease. Radiography will usually enable the correct diagnosis to be made (Trostel et al 2002, Fossum 2007, Shell 2007). Arthroscopy can be used as part of the diagnostic procedure (Wisner et al 1990; Gielen et al 2002). Advanced imaging methods such as CT scans are also sometimes used (Gielen et al 2002).
6. Genetics
Rottweilers are predisposed to OCD, and to hock OCD in particular (Montgomery et al 1994, Necas et al 1999, LaFond et al 2002) but the genes involved have not been determined. OCD of a joint is known to have a genetic basis in other breeds. For example, osteochondrosis of the elbow is known to be a polygenic disorder (Padgett et al 1995, Maki et al 2002, 2004, Janutta et al 2006). It is likely that multiple genes, as well as environmental influences are important in causing hock OCD in Rottweilers.
The fact that OCD often affects the hock in Rottweilers, but usually occurs elsewhere in other breeds, is also evidence that there is a genetic component to this condition in this breed (Trostel et al 1990, Fossum 2007).
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
As with other complex, multi-gene diseases in which environmental factors also play a part, good progress in reducing the prevalence of OCD of the hock is likely to be aided by greater knowledge of the genetics that underlie the condition. One approach, taken from recommendations for similar diseases, is to breed from dogs that have a better breeding value than average for the breed (Sampson 2006). Breeding value 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). This is likely to mean avoiding breeding from animals with affected relatives (or which have more than a very few affected relatives), including siblings and siblings of parents (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 - of 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 several breeds of dog, OCD is common in the elbow and shoulder and also in the stifle. In the Rottweiler, it often occurs in the hock (the ankle joint).
In osteochondrosis, trauma, nutritional disturbance or other factors distrupt the process of ossification and the result is that 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 (Schwarz 2000, Trostel et al 2002, Shell 2007).
OCD typically affects large dogs and their rapid growth rate has been implicated in this predisposition (Trostel et al 2002, Shell 2007).
Dogs with OCD develop osteoarthritis (degenerative disease) of the joint. 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 5-7 months of age but can show later (Trostel et al 2002). Typical signs include: reduced willingness to exercise, lameness (often with the leg being held off the ground) and pain when the leg is straightened or flexed. The joint may be swollen. Such signs are difficult to distinguish from other causes of hock 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, it is detectable only with direct observation by surgery (usually arthroscopy). Later, when bone is diseased too, changes can also be detected on radiography (Baines 2006).
Some dogs have OCD in both hocks (Robins et al 1983, Basher et al 1988, Beale et al 1991). The lesions are usually found on the large bony prominence at the top of the hock – the trochlear process of the tibial tarsal bone (talus) (Wisner et al 1990) and most commonly in Rottweilers on the lateral ridge of this structure (Robins et al 1983, Basher et al 1988, van Ee et al 1988, Wisner et al 1990, Beale et al 1991). In other breeds it is usually the medial ridge of the talus that is affected (Beale et al 1991, Trostel et al 2002). Sometimes multiple lesions occur in a single hock joint (Wisner et al 1990, Beale et al 1991, Van Ryssen & van Bree 1992).
Dogs may suffer directly from the effects of the OCD lesions. In these cases, puppies show lameness with an insidious (gradual) onset that worsens over weeks to months and with exercise. The joints may become swollen and stiff (Trostel et al 2002). In other cases, the main problems develop later in life as the consequence of osteoarthritis secondary to OCD or secondary to surgical procedures undertaken to try to correct the condition.
There is a possible association between OCD of the hock in and fracture of the lower end of the tibia associated with osteoarthritis (Newell et al 1990).
2. Intensity of welfare impact
The welfare effects of osteochondrosis can be mild or severe depending on the size of the OCD lesion, its site and whether one or both hind legs are affected (Trostel et al 2002). The OCD lesion directly causes pain which can vary from mild to severe. Pain also comes from the secondary osteoarthritis that frequently develops in affected animals. Stiffness, joint swelling and muscle wastage all cause disability which has welfare implications as the mobility of the dog may be impaired, with it having difficulty in running and jumping (Trostel et al 2002), or it may be discouraged or restrained from doing so by the veterinary surgeon and owner in order to decrease pain and secondary damage to a diseased joint.
The diagnostic procedures and treatments necessary with this disease may also have negative welfare effects. The major surgery sometimes required when trying to treat the condition is not always effective and can have adverse side effects. Medical treatments may also have adverse side effects. For example non-steroidal anti-inflammatory drugs may cause gastrointestinal damage (Ramsey 2011).
3. Duration of welfare impact
OCD starts in puppyhood (Trostel et al 2002). It usually causes problems for weeks to months and may respond to treatment. One study found that around half of affected dogs have chronic lameness despite surgical and medical treatment in the four years after presentation (Breur et al 1989). Secondary osteoarthritis often develops post treatment so individuals may be affected throughout their lives. Others may not show any signs for months or years and then develop pain and disability in middle or old age due to the secondary osteoarthritis. Once this starts, it persists throughout the life of the dog although medical treatments may help.
4. Number of animals affected
The Rottweiler is the breed of dog most affected by hock OCD and is about 206 times greater at risk of this disease than mixed breed dogs (Montgomery et al 1994, LaFond et al 2002, Miller & Hulse 2006, Fossum 2007). We are not aware of information on the proportion of the breed that is affected, however.
5. Diagnosis
OCD may be suspected when a Rottweiler has hind limb lameness with evidence of hock disease. Radiography will usually enable the correct diagnosis to be made (Trostel et al 2002, Fossum 2007, Shell 2007). Arthroscopy can be used as part of the diagnostic procedure (Wisner et al 1990, Gielen et al 2002). Advanced imaging methods such as CT scans are also sometimes used (Gielen et al 2002).
6. Genetics
Rottweilers are predisposed to OCD and to hock OCD in particular (Montgomery et al 1994, Necas et al 1999, LaFond et al 2002) but the genes involved have not been determined. OCD of a joint is known to have a genetic basis in other breeds. For example, osteochondrosis of the elbow is known to be a polygenic disorder (Padgett et al 1995, Maki et al 2002, 2004, Janutta et al 2006). It is likely that multiple genes, as well as environmental influences are important in causing hock OCD in Rottweilers.
The fact that OCD often affects the hock in Rottweilers but usually occurs elsewhere in other breeds is also evidence that there is a genetic component to this condition in this breed (Trostel et al 1990, Fossum 2007).
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 more common forms of OCD affecting the shoulders or elbows of dogs of some breeds, there are no organised breeding schemes, as far as we are aware, aimed at to reducing the prevalence of hock OCD in Rottweilers.
As with other complex, multi-gene diseases in which environmental factors also play a part, good progress in reducing the prevalence of OCD of the hock is likely to be aided by greater knowledge of the underlying genetics. One approach, taken from recommendations for similar diseases, is to breed from dogs that have a better breeding value than average for the breed (Sampson 2006). Breeding value 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). This is likely to mean avoiding breeding from animals with affected relatives (or which have more than a very few affected relatives), including siblings and siblings of parents (Bell 2010).
9. Acknowledgements
UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section.
10. References
Baines E (2006) Clinically significant developmental radiological changes in the skeletally immature dog: 2. Joints. In Practice 28: 247-254
Basher AWP, Doige CE and Presnell KR (1988) Subchondral bone cyst in a dog with osteochondrosis. Journal of the AmericanAnimalHospital Association 24: 321-326
Beale BS, Goring RL, Herrington J et al (1991) A prospective evaluation of four surgical approaches to the talus of the dog used in the treatment of osteochondritis dissecans. Journal of the AmericanAnimalHospital Association 27: 221-229
Bell JS (2010) Genetic Testing and Genetic Counseling in Pet and Breeding Dogs. 35th World Small Animal Veterinary Association World Congress Proceedings2-5th June 2010, Geneva, Switzerland.
http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2010&Category=&PID=56159&O=Generic. Accessed 28.9.2011
Breur GJ, Spaulding HA and Braden TD (1989) Osteochondritis dissecans of the medial trochlear ridge of the talus in the dog. Veterinary and Comparative Orthopaedics and Traumatology 41: 168-176
van Ee RT, Gibson K and Roberts ED (1988) Osteochondritis dissecans of the lateral ridge of the talus in a dog. Journal of the American Veterinary Medical Association 193: 1284-1286
Fossum TW (2007) Management of Joint Disease. In: Small Animal Surgery, Mosby, St Louis 993-98
Gielen I, van Bree H, Van Ryssen B, Clercq T De and Rooster H De (2002) Radiographic, computed tomographic and arthroscopic findings in 23 dogs with osteochondrosis of the tarsocrural joint. Veterinary Record 150:442-447
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
Junqueira LC and Carneiro J (1980) Cartilage. In: Basic Histology, 3rd edition. Lange Medical Publications, California 121
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
Miller A and Hulse D (2006) The tarsus. In: BSAVA Manual of Canine and Feline Musculoskeletal Disorders edited by JEF Houlton, JL Cook and JF Innes. British Small Animal Veterinary Association, Gloucester 396-405
Montgomery RD, Hathcock JT, Milton JL and Fitch RB (1994) Osteochondritis dissecans of the canine tarsal joint. The Compendium on Continuing Education for the Practicing Veterinarian 16: 835-844
Necas A, Dvorak M and Zatloukal J (1999) Incidence of osteochondrosis in dogs and its late diagnosis. Acta Veterinaria Brno 68: 131-139
Newell SM, Mahaffey, MB and Aron DN (1994) Fragmentation of the medial malleolus of dogs with and without tarsal osteochondrosis. Veterinary Radiology & Ultrasound 35: 5–9
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 54-5
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. 4-5
Robins GM, Read RA, Carlisle CH et al (1982) Osteochondritis dissecans of the lateral ridge of the trochlear of the tibial tarsal bone in the dog. Journal of Small Animal Practice 24: 675-685
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 28.9.2011
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 28.9.2011
Van Ryssen B and van Bree H (1992) Arthroscopic evaluation of osteochondrosis lesion in the canine hock: a review of two cases. Journal of the AmericanAnimalHospital Association 28: 295-299
Wisner ER, Berry CR, Morgan JP, Pool RR, Wind AP and Vasseur PB (1990) Osteochondrosis of the Lateral Trochlear Ridge of the Talus in Seven Rottweiler Dogs. Veterinary Surgery 19: 435–439
© UFAW 2011
Credit for main photo above:
By rostdi (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html), CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/) or CC-BY-2.5 (http://creativecommons.org/licenses/by/2.5)], via Wikimedia Commons
