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Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
Yorkshire Terrier
Avascular Necrosis of the Femoral Head
Related terms: Legg-Calve-Perthes disease, Coxa plana, Coxa magna, Perthes disease, Legg-Perthes Disease
Outline: In this disease, failure of the blood supply to the head of the femur during growth causes death of bone tissue resulting in distortion of the femoral head. This in turn leads to chronic painful arthritis of the affected hip. The genetic basis of this disease has not been determined but, since a recessive gene may be involved, it is sensible to avoid breeding from affected animals or those with close relatives that are affected.
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Summary of Information
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1. Brief description
Dogs affected with this disease experiences a temporary disruption of the blood supply to the top part of the femur during bone growth. This causes the death of tissue in the affected part of the bone and results in collapse and deformation of the femoral head and hip joint leading to arthritis, pain and disability.
2. Intensity of welfare impact
Avascular necrosis of the femoral head is very painful. Dogs often hold the affected hind-leg off the ground due to the intense pain they experience when it supports any weight.
3. Duration of welfare impact
Dogs affected by avascular necrosis of the femoral head will show symptoms during puppyhood and, once present, the condition causes pain and disability throughout life. Veterinary treatment may reduce the pain and disability experienced by this condition, however, treatment can itself cause some welfare problems.
4. Number of animals affected
The number and proportion of Yorkshire terriers affected is not known but it is considered a significant problem in this breed (Lafond et al 2002).
From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are Yorkshire terriers (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 250,000.
5. Diagnosis
Avascular necrosis will be suspected by a veterinary surgeon when presented with a young, small-breed dog with a hind leg limp. Confirmation requires radiography (x-rays) of the hips.
6. Genetics
A range of factors may be involved in the development of this but it is thought likely that a recessive gene has an important role, although this has yet to be confirmed.
7. How do you know if an animal is a carrier or likely to become affected?
At present there is no method for detecting carriers of the disease (which may show no signs of the condition itself but who are capable of passing the disease on to their offspring), whether such carriers exist, or which puppies are likely to develop the condition later in life. The onset of the condition is always before breeding age.
8. Methods and prospects for elimination of the problem
It is not possible, at present, to determine which individuals may produce affected offspring. The best advice for conditions where the genetic basis of a condition is strongly suspected, but unknown, is not to breed from affected individuals and, generally, to avoid breeding from animals that have affected relatives.
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
At the top of the femur (thigh bone) is the femoral head, which forms the ball of the ball-and-socket hip joint. In avascular necrosis of the femoral head there is a failure of the blood supply to the femoral head during growth that results in death of the femoral bone tissue. The reason for the failure of the blood supply is unknown but there is evidence of a genetic component. The condition affects both sexes of small breed dogs when they are between 3 -13 months old and most often affects only one of the hind legs. Less then 20% of affected dogs have both hind legs affected (Ljunggren 1966, Lee and Fry 1969).
It has been suggested that the disease is due to infarction (death of an area of the body when its blood supply is obstructed (Shell 2007)). The affected bones certainly show signs of lack of blood supply and consequent death but it may be that the loss of supply is a temporary problem during the time that the bone is growing that may or may not lead to death of the bone depending on its degree and duration (Gambardella 1993, Brenig et al 1999).
As the femoral head dies, its shape changes and some parts of the bone collapse. Small fractures in the bone occur and are a source of pain (Lee 1970). Later in the disease process, the femoral head will exhibit both areas where partial repair to the affected bone tissue has occurred and of osteoarthritis (degenerative joint disease). In addition, affected animals also suffer a chronic progressive disease of the joint cartilage, soft tissue and underlying bone (Gambardella 1993).
In humans affected with a similar condition (true Legg-Calves-Perthes disease), the disease is associated with excessive blood clotting but this has been shown not to be the case in dogs (Brenig et al 1999) and the reason for the disease occurring in dogs is unknown (Boss and Misselevich 2003).
Affected puppies show lameness in a hind leg, that has an insidious (gradual) onset and that worsens over a number of weeks until the leg is held off the ground. The affected leg may be shorter than the normal leg. As use of the leg declines, muscle wastage occurs (Gambardella 1993, Piek et al 1996, Shell 2007). The dog continues to avoid using the leg for the rest of its life unless there is successful treatment.
2. Intensity of welfare impact
Avascular necrosis of the femoral head is very painful (Gambarella 1993). The pain is sufficient for the dog to not want to weight bear on the affected leg. Surgery and removal of the affected femoral head is usually required in order to relieve the pain and this surgery itself can cause significant welfare problems related to travel to and from the veterinary practice, examinations, hospitalisations, anaesthesias and major surgery. Total hip replacement surgery is another method of treatment of the disease. Some dogs are treated with long-term pain killers rather than surgery but this is effective in only around 25% of dogs (Piek et al 1996, Demko and McLaughlin 2005).
3. Duration of welfare impact
Dogs affected by avascular necrosis of the femoral head will show symptoms during puppyhood and, once present, the condition causes pain and disability throughout life. Although veterinary treatment usually is successful in reducing the pain and disability experienced by individuals with this condition, treatment and some dogs are left with life-long pain and disability (Piek et al 1996).
4. Number of animals affected
The number and proportion of Yorkshire terriers affected is not known but it is considered a significant problem in this breed (Lafond et al 2002).
From data on estimates of total dog population in the UK and on the percentage of all micro-chip registered dogs that are Yorkshire terriers (Lucy Asher, 2011, personal communication), we estimate that the UK population size of this breed may be around 250,000.
5. Diagnosis
The diagnosis is suspected when a veterinary surgeon sees a young, small-breed dog with a hind leg limp. The condition is confirmed by finding typical changes on radiographs (x-rays) of the hip joint (Gambardella 1993, Piek et al 1996, Baines 2006).
6. Genetics
A strong breed predisposition is seen for various small breed dogs, especially terriers (Ljunggren 1966, Lee and Fry 1969, Lafond et al 2002). Yorkshire terriers were the most commonly affected breed in a long-term study of treatment outcomes in dogs with avascular necrosis of the femoral head (Piek et al 1996). Avascular necrosis has been shown to be a multifactorial inherited disease in other small dogs (Pidduck and Webbon 1978, Vasseur et al 1989) and there is evidence of a recessive gene being important (Robinson 1992, Demko and McLaughlin 2005). Investigations are underway into the genetic components but currently there is no further information.
7. How do you know if an animal is a carrier or likely to become affected?
At present there is no method for detecting carriers of the disease (who may show no signs of the condition itself but who are capable of passing the disease on to their offspring), whether such carriers exist, or which puppies are likely to develop the condition later in life. However, assuming that there is a significant genetic component to this disease, and that it is recessive, then individuals who inherited two recessive genes would be affected whilst individuals with a single recessive gene would be carriers. The onset of the condition is always before breeding age (Gambarella 1993).
8. Methods and prospects for elimination of the problem
The genetic contributions to this condition are currently unknown and there are no means of detecting carriers at present. However, affected animals and parents that have already produced affected offspring should not be used for breeding (Shell 2007, Bell 2010). If there is a high likelihood of an individual being a carrier – based on the numbers of relatives being affected, then it is better to replace this individual in a breeding program with another individual thought to be genetically healthier – ie that does not have any close relatives with the disease. This process is greatly aided when a breed has a known average breeding value and when the breeding value of any potential breeding dog is known (Sampson 2006). Breeding value takes into account genetic information and the presence/absence of disease both in the individual being evaluated and its relatives.
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. World Small Animal Veterinary Association World Congress Proceedings
Boss JH and Misselevich I (2003) Osteonecrosis of the Femoral Head of Laboratory Animals: The Lessons Learned from a Comparative Study of Osteonecrosis in Man and Experimental Animals. Veterinary Pathology 40: 345
Brenig B, Leeb T, Jansen S and Kopp T (1999) Analysis of Blood Clotting Factor Activities in Canine Legg-Calvé-Perthes' Disease. Journal of Veterinary Internal Medicine 13: 570–573
Demko J and McLaughlin R (2005) Developmental Orthopedic Disease. Veterinary Clinics of North America Small Animal Practice 35: 1111-1135
Gambardella PC (1993) Legg-Calve-Perthes disease in dogs. In: Disease mechanisms in small animal surgery. Lea and Febiger edited by MJBojrab, DD Smeak and MS Bloomberg, Philadelphia pp 804
LaFond E, Breur GJ and Austin CC (2002) Breed susceptibility for developmental orthopaedic diseases in dogs. Journal of the American Animal Hospital Association 38: 467-477
Lee R (1970) A study of the radiographic and histological changes occurring in Legg-Calve-Perthes disease (LCP) in the dog. Journal of Small Animal Practice 11: 621-638
Lee R and Fry PD (1969) Some observations on the occurrence of Legg-Calve-Perthes disease (coxa plana) in the dog, and an evaluation of excision arthroplasty as a method of treatment. Journal of Small Animal Practice 10: 309
Ljunggren GL (1966) Conservative vs surgical treatment of Legg-Perthes disease. Animal Hospital 2: 6
Pidduck H and Webbon PM (1978) The genetic control of Perthes’ disease in toy poodles - a working hypothesis. Journal of Small Animal Practice 19: 729-733
Piek CJ, Hazewinkel HAW, Wolvekamp WTC, Nap RC and Mey BP (1996) Long term follow-up of avascular necrosis of the femoral head in the dog. Journal of Small Animal Practice 37: 12-18
Robinson R (1992) Legg-Calve-Pethes disease in dogs: Genetic aetioiogy. Journal of Small Animal Practice 33: 275-276
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
Shell L (2007) Aseptic Necrosis of the Femoral Head. VIN Associates accessed 7th January 2011
Vasseur PB, Foley P, Stevenson S and Heitter D (1989) Mode of inheritance of Perthes’ disease in Manchester terriers. Clinical Orthopaedics and Related Research 244: 281–292
© UFAW 2011
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