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Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
Labrador Retriever
Cranial Cruciate Ligament Rupture
Related terms: cranial cruciate rupture; cranial cruciate disease; cruciate disease
Outline: Labrador retrievers are predisposed to degeneration and rupture of the cranial cruciate ligament – one of the ligaments of the knee. It causes pain and lameness, which may be mild or severe depending on the stage of the disease and other factors, and which tends to progress as chronic arthritis develops. They are 2-5 times more likely to develop this disease than other breeds of dog.
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Summary of Information
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1. Brief description
Rupture of the cranial cruciate ligament (CCL) is one of the commonest orthopaedic conditions affecting the stifle joint (the knee) in large breeds of dog (Corr 2009). It is a leading cause of lameness in these breeds (Wilke et al 2006a).
The cranial cruciate ligament helps to stabilise the knee joint. Some sudden, complete ruptures of this ligament occur due to trauma (injury), particularly in active young dogs; however, recently it has been recognised that probably over 75% of cases of rupture are due to a degenerative condition developing in the stifle joint. This leads to inflammation, with partial or full rupture of the ligament occurring as the disease progresses (Harasen 2007). This degenerative condition is likely to be due to multiple factors and there is a significant inherited component to its occurrence in Labrador retrievers (Comerford 2008, Corr 2009).
The acute form of the disease causes sudden non weight-bearing lameness in affected animals whilst the degenerative disease tends to cause more chronic (long term) intermittent lameness which rapidly worsens if the ligament completely ruptures. If left untreated (and also often with treatment) joint inflammation and instability lead to arthritic changes and permanent pain, lameness and disability. In many cases both knees become affected – occasionally at the same time and often within a year of each other.
Surgical treatment of this condition is thought to be necessary in larger breeds of dogs, such as Labrador retrievers, in order to restore acceptable function in the joint. There are various surgical options depending on the circumstances. Recovery takes time and arthritic changes may develop after surgery.
2. Intensity of welfare impact
Cranial cruciate ligament disease and rupture causes varying levels of pain and disability. If left untreated, osteoarthritis develops causing permanent pain and disability affecting quality of life. Even with surgery full joint function may not return.
Veterinary diagnosis, surgery and physiotherapy can all cause significant stress and discomfort for the dogs, and pain-relieving medication can have significant side effects.
3. Duration of welfare impact
CCL rupture can occur at any age, but Whitehair et al (1993) - in a study that looked at many breeds of dogs - found a peak in incidence at between 7 to 10 years. This peak tended to occur earlier in dogs of heavier breeds such as the Labrador retriever. Typically, affected Labradors develop the disease in their other back leg five to six months after their first CCL rupture (Buote et al 2009).
In cases where there is sudden and dramatic onset of the disease, it is often diagnosed rapidly but when signs develop more slowly, the affected dogs may suffer weeks to months of lameness and pain prior to diagnosis and treatment. For dogs of more than 20kg body weight, surgical treatment is considered to be essential for the restoration of an acceptable level of function (Harasen 2007). Even with treatment, the joint may develop some degree of osteoarthritis but, without it, joint instability will result in more severe osteoarthritis leading to life-long disability, pain and the on-going need for pain-relieving medication.
4. Number of animals affected
In a study in the USA, it was found that just under 20% of all dogs examined for lameness at university hospitals had CCL rupture (Johnson et al 1994). Labrador retrievers are predisposed to CCL rupture and to develop the condition at an early age and in both hind legs (Whitehair et al 1993, Duval et al 1999, Harasen 2003, Buote et al 2009). It is suggested that Labradors are two to five times more likely to suffer from CCL rupture than the average dog (Whitehair et al 1993, Duval et al 1999).
5. Diagnosis
Rupture of the cranial cruciate ligament (CCL) may be suspected in any Labrador retriever with hind limb lameness because of the prevalence of the disease in this breed (Harasen 2007). Diagnosis is often confirmed through orthopaedic examination and manipulation of the joint, and, in some cases, by radiography, examination of joint fluid, arthroscopy and CT or MRI scans.
6. Genetics
A strong breed predisposition to this disease in Labradors has long been noted (Harasen 2003, Powers et al 2005, Griffon 2010). The suspected pathology and the frequency of disease in both of the hind legs are further evidence of an important genetic role. A gene associated with CCL rupture in Newfoundlands has been found (Wilke et al 2009) and inheritance has been shown in two breeds - Newfoundlands (Wilke et al 2006a) and Boxers (Nielen et al 2003) - but has not yet been demonstrated in Labradors.
7. How do you know if an animal is a carrier or likely to become affected?
Although carriers (animals which are unaffected themselves but which can pass the disease on to their offspring) may well exist, currently it is not possible to identify these or animals that are at risk of developing the condition. Puppies of which one or both parents have had CCL rupture have a high risk of developing the condition, but having healthy parents does not guarantee freedom from the condition.
8. Methods and prospects for elimination of the problem
The genes that cause the disease have yet to be identified. Research into this is underway at Iowa State University, USA, with the aim of developing a genetic test for the condition (Wilke et al 2006a). Such a test would greatly assist in tackling the problem. It is currently difficult to select against the disease as it often does not show until after breeding age and some unaffected individuals carry and pass on the mutant gene to their offspring.
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
Rupture of the cranial cruciate ligament (CCL) is one of the commonest orthopaedic conditions affecting the stifle joint (the knee) in large breeds of dog (Corr 2009). It is a leading cause of lameness in these breeds (Wilke et al 2006a).
The stifle (knee) is the complex joint between the lower end of the femur (thigh bone) and the upper end of the tibia (shin bone). The patella (knee cap bone) is in the tendon of the quadriceps muscle that passes over the front of the joint. At the rear of the joint, there are several other small bones - the pea-sized fabellae. Located within the joint, and sandwiched between the ends of the femur and tibia, are two discs of cartilage called the menisci. These act as shock-absorbers
The joint is stabilized both by tendons, including the patella tendon, which attaches to the tibial tuberosity (a prominence on the front of the tibia), and by several ligaments. On either side of the stifle, there are collateral ligaments, running from the femur to the tibia (and fibula laterally); inside the joint are the two cruciate ligaments, so called because they cross over each other. The caudal cruciate ligament attaches the cranial (front) surface of the femur to the caudal (back) surface of the tibia, and the cranial cruciate ligament attaches the caudal femur to the cranial tibia. The canine stifle joint is somewhat flexed (bent) when weight bearing and the cranial cruciate ligament is designed to stop the tibia slipping forward relative to the femur, and to prevent excessive internal rotation of the tibia and hyperextension (over straightening) of the joint (Miller 1996). It consists of two main bands of tissue – a craniomedial band, which is taut at all times ie in flexion and extension, and a caudolateral band which is larger and taut only in extension (Miller 1996).
Some sudden (acute), complete ruptures of the cranial cruciate ligament (CCL) occur due to trauma (injury), particularly in active young dogs. However, recently it has been recognised that probably over 75% of cases of rupture are due to a degenerative condition in the stifle joint. This leads to inflammation with partial or full rupture of the CCL as the disease progresses (Harasen 2007). This degenerative process is called cruciate disease by some authors e.g. Harasen (2007).
The underlying disease process is not fully understood despite extensive studies. It has been suggested that various factors may play a role in it, including breed, genetics, gender, joint conformation, altered biomechanics, altered ligament blood supply, gait, activity levels, age, immune-mediated disease and alterations to the extracellular structure of the ligament (Harasen 2007, Comerford 2008). There is evidence that the ligaments are weaker in Labrador retrievers than in other dogs (Comerford et al 2005). In another breed, Wilke et al (2006a) suggested that a mutant gene predisposes the ligament to degeneration and rupture and this is likely to be the case in other predisposed breeds such as the Labrador retriever. The angle made between the top of the tibia and the long axis of the femur is considered to be a significant factor in rupturesby some but not others (Morris & Lipowitz 2001, Wilke et al 2002, Ragetly et al 2011). Neutered animals may be more at risk than entire ones (Duval et al 1999). Obesity may make the condition more likely (Lund 2006). Comerford (2008) and Corr (2009) listed various factors that have been implicated in cruciate disease, but which are unsubstantiated, including rheumatoid arthritis, conformational deformities, narrow intercondylar notch width (the shape of the distal end of the femur – the part furthest from the body), inactivity in puppyhood, and repetitive chronic trauma. Further testament to the importance of conformation of the hind legs has come from Mostafa et al (2009) and Ragetly et al (2011).
Cranial cruciate ligament disease can appear in two distinct ways, as outlined below:
- The first is acute lameness due to complete sudden rupture of the CCL caused by trauma. In these cases, the dogs are usually completely non weight-bearing on the affected hind limb. With time, rest and pain-relieving medication they may improve and start to bear weight in 7 to 10 days (Corr 2009). The diagnosis is usually straightforward and may be made after veterinary examination and manipulation of the joint (Corr 2009). Affected dogs will suffer pain due to the damaged ligament, the instability (excessive movement) of the joint, and from resulting inflammation.
- The second form is due to chronic, gradual degeneration of the ligament. In these cases, which are harder to diagnose, pain and inflammation may start within the joint, as the ligament degenerates, before it ruptures. This pain and inflammation result in intermittent, chronic lameness in affected animals, which tends to be of a lower grade and in which the dog still weight-bears to some extent (Corr 2009). This lameness often responds to rest but reoccurs once exercise is reintroduced (Corr 2009). It is thought that the degenerative process in the ligament initiates painful inflammation within the joint before any instability of the joint occurs (Harasen 2007). However, it is not known whether the joint inflammation or the ligament degeneration occurs first.
As the ligament degenerates it may partially or fully rupture, leading to an acute worsening of signs as the joint becomes unstable. Many affected dogs have concurrent damage to the caudal cruciate ligament and severe joint inflammation (synovitis). The apparently greater intensity of inflammation seen in these animals is thought to provide some evidence that this plays a part in subsequent ligament degeneration (Sumner et al 2010).
About 50% of affected dogs also have damage to the meniscal cartilages and this may contribute to the pain and lameness suffered (Harasen 2007). In some cases both legs are affected at the same time. Such dogs are severely disabled. It has been found that 30-40% of dogs with CCL rupture will, at some time, suffer rupture of the CCL in the other stifle, often within weeks to months (Harasen 2007, Corr 2009).
Because of the inflammation and/or instability, osteoarthritis (degenerative joint disease) develops within the affected joints. In osteoarthritis there are progressive changes to the cartilage of the joint and varying levels of inflammation and ongoing damage to other joint structures - the joint capsule, the synovial fluid of the joint and the surrounding bone – that are irreversible.
Surgical treatment of rupture of the CCL is considered to be necessary in dogs of over 20kg bodyweight, such as Labrador retrievers, in order to restore acceptable function in the leg (Harasen 2007). Several surgical interventions have been used, these include extracapsular (staying outside the joint) stabilization methods, intracapsular stabilization methods, and more invasive methods such as tibial plateau levelling osteotomy and tibial tuberosity advancement, all of which have advantages and disadvantages. Which is the most appropriate depends on individual circumstances. Corr (2009) suggested that tibial plateau levelling osteotomy (TPLO) procedures - in which the bone of the joint is levelled off to stabilize it -may result in the quickest recoveries for dogs of large and giant breeds such as the Labrador retriever but this is disputed. Harasen (2007) suggests these procedures, though at risk of more complications, seem to be associated with better results in dogs of large breeds and less post-operative osteoarthritis. In a study of 438 cases treated with TPLO less than 10% of cases had radiographical signs of osteoarthritis in the joints two years after surgery (Jandi et al 2006).
It is known that cranial cruciate rupture often affects both back legs. A study by Buote et al (2009) found that around 10% of affected Labradors had a rupture in the CCL of both legs when seen and that, of those with a single rupture, 48% developed a rupture in the other stifle in the future; the median time for this being between five and six months. Cabrera et al (2008) showed that dogs with bilateral CCL rupture tended to be much younger than dogs with a single rupture.
2. Intensity of welfare impact
In most dogs, CCL rupture causes chronic, intermittent low-grade pain and disability until diagnosis and treatment. A few suffer more severe, acute pain and disability. If left untreated, permanent disabling osteoarthritis is very likely to develop causing constant pain and affecting quality of life permanently.
Disabling osteoarthritis develops despite surgery in some cases and the treatments can also have a significant welfare impact due to the stress and discomfort of recurrent veterinary visits, interventions, manipulations, physiotherapy and surgery. Commonly used pain-relieving, anti-arthritis medication can have significant side-effects such as kidney damage, and gastrointestinal ulcerations (Ramsey 2011).
3. Duration of welfare impact
CCL rupture can occur at any age, but Whitehair et al (1993) - in a study that looked at many breeds of dogs - found a peak in incidence at between 7 to 10 years. This peak tended to occur earlier in dogs of heavier breeds such as the Labrador retriever. Typically, affected Labradors develop the disease in their other back leg five to six months after their first CCL rupture (Buote et al 2009).
In cases where there is sudden and dramatic onset of the disease, it is often diagnosed rapidly but where signs develop more slowly the affected dogs may suffer weeks to months of lameness and pain prior to diagnosis and treatment. For dogs of over 20kg body weight, surgical treatment is considered to be essential for the restoration of an acceptable level of function (Harasen 2007). Even with treatment, the joint may develop some degree of osteoarthritis but, without it, joint instability will result in more severe osteoarthritis leading to life-long disability, pain and the need for on-going pain-relieving medication.
4. Number of animals affected
In a study in the USA, it was found that just under 20% of all dogs examined for lameness at university hospitals had CCL rupture (Johnson et al 1994). Labrador retrievers are predisposed to CCL rupture and to develop the condition at an early age and in both legs (Whitehair et al 1993, Duval et al 1999, Harasen 2003, Buote et al 2009). It is suggested that Labradors are two to five times more likely to suffer from CCL rupture than the average dog (Whitehair et al 1993, Duval et al 1999).
5. Diagnosis
CCL rupture may often be suspected in a Labrador retriever with hindlimb lameness because of the known high prevalence in the breed (particularly in young to middle-age dogs) but confirming the diagnosis is sometimes difficult (Harasen 2007, Corr 2009). Definitive diagnosis usually involves thorough orthopaedic examination and palpation of the joint, often performed under sedation or anaesthesia. On palpation, atrophy of the quadriceps muscle (loss of muscle mass at the front of the thigh) may be detected, as may stifle joint effusion (swelling) - evident as a less distinct patella ligament. Thickening of the medial aspect of the joint (called a medial buttress) can often be felt in dogs that have been affected for a few weeks or more (Corr 2009). Two joint manipulation tests may help in diagnosis: the cranial drawer test, and the test for cranial tibial thrust. The cranial drawer test can be difficult to perform and is painful in conscious animals so may be carried out under sedation or anaesthesia. Although many cases are diagnosed by examination and palpation alone (Harasen 2007), additional diagnostics are sometimes necessary. Radiography (x-rays) of the joint may give some indications of joint swelling and inflammation and aspiration and examination of joint fluid may also be useful for detection of inflammation within the joint. Arthroscopy (visual examination of the inside of the joint using a keyhole incision and endoscope to view the joint) can reveal damaged ligaments. Contrast CT (computer tomography) arthrography can be useful and MRI (magnetic resonance imaging) is the best diagnostic test in humans with CCL rupture, but can be prohibitively expensive in dogs (Corr 2009).
6. Genetics
A strong breed predisposition to the disease in Labradors has long been noted (Harasen 2003, Powers et al 2005, Griffin 2010). The suspected pathology and the frequency of the disease in both hind legs are further evidence of an important genetic role. A gene associated with CCL rupture in Newfoundlands has been found (Wilke et al 2006b, 2009) and inheritance has been shown in two breeds – Newfoundlands (Wilke et al, 2006a) and boxers (Nielen et al 2003) - but not yet in Labradors.
The presence of a significant recessive gene or genes is suspected. Dogs with two recessive mutant genes (one from each parent) could develop the condition but, as penetrance of the gene has been found to be 51%, only about half of these do. The other 49%, with the homozygous recessive genotype (2 recessive genes), do not develop CCL disease. Dogs with just one recessive gene are also unlikely to develop CCL disease, but are carrier animals that have the potential to pass on the mutant gene to their offspring.
7. How do you know if an animal is a carrier or likely to become affected?
At present, as far as we are aware, there is no way to identify carrier animals (animals that have the potential to pass on the disease to their offspring but are themselves unaffected) or to identify animals that have the potential to develop CCL disease. It is recommended that only puppies with healthy parents (and other relatives) are purchased. Unfortunately this does not guarantee that the puppies will remain free of cruciate disease as it is thought that healthy carrier animals exist (see above). Also, the disease may not become apparent until after breeding age.
8. Methods and prospects for elimination of the problem
There is evidence that CCL rupture is becoming more common (de Rooster et al 2000) and it has been suggested that the incidence of cranial cruciate rupture has doubled in dogs over the last 30 years (Witsberger et al 2008). Efforts to use selective breeding to tackle this disease in Labrador retrieversare complicated by the suspected high prevalence of the mutant gene in the breed, by the fact that affected dogs can reach breeding age years before the disease develops, and because healthy carrier animals exist (Wilke et al 2006a). Affected animals should not be used for breeding (Harasen 2003). Breeding from animals from lines with low prevalence of the disease or out-crossing with unaffected dogs may help reduce the risk of the disease. Identification of the gene and development of a genetic test would greatly aid in tackling the problem.
Until that time, Inauen et al (2009) have suggested selective breeding based on the conformation of the tibial tuberosity – the protrusion on the front of the tibia to which tendons attach. They hypothesized that the smaller the width of the tibial tuberosity, the greater the cranial tibial thrust force acting on the joint, leading to increased rates of ligament degeneration and rupture. They concluded that only dogs with relative tibial tuberosity widths of greater than 0.9 should be used for breeding. This test is not yet being used as part of a breeding programme as far as we are aware.
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
Buote N, Fusco J and Radasch R (2009) Age, tibial plateau angle, sex, and weight as risk factors for contralateral rupture of the cranial cruciate ligament in Labradors. Veterinary Surgery 38: 481-9
Cabrera SY, Owen TJ, Mueller MG and Kass PH (2008) Comparison of tibial plateau angles in dogs with unilateral versus bilateral cranial cruciate ligament rupture: 150 cases (2000–2006). Journal of the American Veterinary Medical Association 232: 889-892
Comerford EJ, Tarlton JF, Innes JF, Johnson KA, Amis AA and Bailey AJ (2005) Metabolism and composition of the canine anterior cruciate ligament relate to differences in knee joint mechanics and predisposition to ligament rupture. Journal of Orthopaedic Research 23: 61–66
Comerford E (2008) What’s new in aetiopathogenesis of cranial cruciate ligament disease/rupture.British Veterinary Orthropaedic Association Autumn Scientific Meeting 21st-23rd October 2008, Liverpool http://www.bsava.org.uk/bvoa/proc_nov_08.pdf accessed 15.9.2011
Corr S (2009) Decision making in the management of cruciate disease in dogs. In Practice 31: 164-171
de Rooster H, Cox E and van Bree (2000) Prevalence and relevance of antibodies to type-I and -II collagen in synovial fluid of dogs with cranial cruciate ligament damage. American Journal of Veterinary Research 61: 1456-1461
Duval JM, Budsberg SC, Flo GL and Sammarco JL (1999) Breed, sex, and body weight as risk factors for rupture of the cranial cruciate ligament in young dogs. Journal of American Veterinary Medical Association 215: 811–814
Griffon DJ (2010) A Review of the Pathogenesis of Canine Cranial Cruciate Ligament Disease as a Basis for Future Preventive Strategies. Veterinary Surgery 39: 399–409
Harasen G (2003) Canine cranial cruciate ligament rupture in profile. Canadian Veterinary Journal 44: 845–846
Harasen G (2007) Cruciate Ligament Rupture. On-line VIN associate. http://www.vin.com/Members/Associate/Associate.plx?DiseaseId=453. Accessed 31.5.11
Inauen R, Koch D, Bass M and Haessig M (2009) Tibial tuberosity conformation as a risk factor for cranial cruciate ligament rupture in the dog. Veterinary and Comparative Orthopaedics and Traumatology 22: 16-20
Jandi AS, Kahlon SS and Schulman AJ (2006) Effect of tibial plateau leveling osteotomy on lameness, osteoarthritis, joint motion and post operative meniscal injury in dogs with ruptured cranial cruciate ligament: A 2 year prospective study of 438 cases (abstract). World Veterinary Orthopedic Congress 2006: 15
Johnson JA, Austin C and Breur GJ (1994) Incidence of canine appendicular musculoskeletal disorders in 16 veterinary teaching hospitals from 1980 through 1989. Veterinary and Comparative Orthopaedics and Traumatology 7: 56–69
Lund EM, Armstrong PJ, Kirk CA and Klausner JS (2006) Prevalence and Risk Factors for Obesity in Adult Dogs from Private US Veterinary Practices International Journal of Applied Research in Veterinary Medicine 4: 177-186
Miller A (1996) Decision making in the management of cranial cruciate ligament rupture. In Practice: 98-102
Morris E and Lipowitz AJ (2001) Comparison of tibial plateau angles in dogs with and without cranial cruciate ligament injuries. Journal of the American Veterinary Medical Association 218: 363-366
Mostafa AA, Griffon DJ, Thomas MW and Constable PD (2009) Morphometric characteristics of the pelvic limbs of Labrador Retrievers with and without cranial cruciate ligament deficiency. American Journal of Veterinary Research 70: 498-507
Nielen AL, Knol BW, van Hagen MA and van der Gaag I (2003) Genetic and epidemiological investigation of a birth cohort of boxers. Tijdschrift voor Diergeneeskunde 128: 586-90
Powers MY, Martinez SA, Lincoln JD, Temple CJ and Arnaiz A (2005) Prevalence of cranial cruciate ligament rupture in a population of dogs with lameness previously attributed to hip dysplasia: 369 cases (1994–2003). Journal of the American Veterinary Medical Association 227: 1109-1111
Ragetly CA, Evans R, Mostafa AA and Griffon DJ (2011) Multivariate Analysis of Morphometric Characteristics to Evaluate Risk Factors for Cranial Cruciate Ligament Deficiency in Labrador Retrievers. Veterinary Surgery 40: 327–333
Ramsey I (2011) Small Animal Formulary 7th Ed. BSAVA: Gloucester, UK
Sumner JP, Markel MD and Muir P (2010) Caudal Cruciate Ligament Damage in Dogs with Cranial Cruciate Ligament Rupture. Veterinary Surgery 39: 936-41
Whitehair JG, Vasseur PB and Willits NH (1993) Epidemiology of cranial cruciate ligament rupture in dogs. Journal of American Veterinary Medical Association 203: 1016–1019
Wilke VL, Conzemius MG, Besancon MF, Evans RB and Ritter M (2002) Comparison of tibial plateau angle between clinically normal Greyhounds and Labrador Retrievers with and without rupture of the cranial cruciate ligament. Journal of the American Veterinary Medical Association 221: 1426-1429
Wilke VL, Conzemius MG, Kinghorn BP, Macrossan PE, Weiguo C and Rothschild MF (2006a) Inheritance of rupture of the cranial cruciate ligament in Newfoundlands. Journal of American Veterinary Medical Association 228: 61–64
Wilke VL, Ruhe A, Conzemius MG and Rothschild MF (2006b) Predisposition to rupture of the cranial cruciate ligament in the dog is genetically associated with chromosome 3 (abstract). World Veterinary Orthopedic Congress 2006: 35
Wilke VL, Zhang S, Evans R, Conzemius MG and Rothschild MF (2009) Identification of chromosomal regions associated with cranial cruciate ligament rupture in a population of Newfoundlands. American Journal of Veterinary Research 70: 1013-7
Wingfield C, Amis AA, Stead AC and Law HT (2000) Comparison of the biomechanical properties of rottweiler and racing greyhound cranial cruciate ligaments. Journal of Small Animal Practice 41: 303-307
Witsberger TH, Villamil JA, Schultz LG, Hahn AW and Cook JL (2008) Prevalence of and risk factors for hip dysplasia and cranial cruciate ligament deficiency in dogs. Journal of the American Veterinary Medical Association 232: 1818:nyof
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