Pathogenesis of canine hip dysplasia Flashcards
The combination of what factors likely predisposes a patient to development of hip dysplasia?
Combination of genetically predisposed animals exposed to environmental factors that enhance the expression of genetic weakness.
What are some changes that can be seen in dysplastic hips as early as 30 days of age?
Edematous ligament of the head of the femur with torn fibers and hemorrhage, increased volume of the ligament, and increased synovial fluid volume.
How does muscular pull on the canine hip joint potentially impact the development of hip dysplasia in dogs with hip joint laxity?
When the hip is in the swing phase of the gait, subluxation of the hip joint is thought to occur secondary to parallel pull of the rectus femoris, cranial sartorius and iliopsoas muscles. During the stance phase of the gait the gluteal and adductor muscles exert large forces across the hip joint causing traumatic reduction and damage to the articular cartilage.
In a lax hip joint the adductor and gluteal muscles also have to increase their force of contraction to maintain reduction of the joint, and the forces are acting over a smaller area (the dorsal labrum of the acetabulum).
When is hip joint laxity at its maximum?
When the joint is in a neutral weight bearing position (pulling the pelvic limbs into extension causes wind-up of the joint capsule and limits lateral movement of the femoral head).
What are three radiographic measures of hip joint laxity?
1) Norberg angle.
2) Distraction index.
3) Femoral head coverage.
What formed the basis of the PennHip testing?
The understanding that displacement of the femoral head from the acetabulum is maximized in the neutral position and is largely independent of the distraction force (above a minimum force). That is, above a certain force (30N), distraction of the hip joint should be fairly uniform based on degree of laxity.
What is a normal Norberg angle?
> 105 degrees.
What is the primary risk factor for development of hip dysplasia?
Hip joint laxity.
What is the issue with the genetic tissue for hip dysplasia as developed for use by IDEXX in Labradors?
Testing was performed in animals with a mean age of 21-64 months, and doesn’t therefore account for animals that may develop hip dysplasia later in life.
The risk for development of osteoarthritis increases beyond what distraction index score?
> 0.30
What are some proposed causes of joint laxity in dogs with hip dysplasia?
- Joint fluid: higher volumes of synovial fluid, thickened ligament of the head of the femur. Unclear whether these are primary or secondary changes.
- Pelvic muscle mass: may be decreased in dogs with hip dysplasia.
- Hormonal factors: high levels of relaxin might contribute to development of hip dysplasia. Gonadal hormones also appear to have an effect (non-neutered Golden retrievers half as likely to develop hip dysplasia as compared to dogs neutered before 12-months of age).
- Weight and growth: early closure of the acetabular growth plates in rapidly growing dogs may cause dysplastic joints. Body weight is unlikely to cause dysplasia but may exacerbate phenotype through increasing pressure on the joints.
- Nutrition: excess calcium and vitamin D might contribute to the development of disease through disturbances/delays of endochondral ossification.
- Environmental: food restriction in juvenile patients may reduce the severity of dysplasia development, weekly intramuscular polysulfated glycosaminoglycans was shown to reduce incidence in one study.
None of these factors fully explains the development of hip dysplasia.
How is increased joint fluid volume proposed to impact the pathophysiology of hip dysplasia?
With increased joint fluid volume there is loss of passive intracapsular pressure and delayed mechanoreceptor activation during subluxation of the hip joint during the swing phase of the gait. This results in delayed activation of the periarticular muscles and traumatic reduction of the hip joint during the stance phase of the gait.
What are the two forms of hip dysplasia?
Juvenile or severe form: patients present between 5-12 months of age. Clinical signs are thought to be related to extreme joint laxity with stretching and tearing of the joint capsule, ligaments and muscles, along with microfracture of the dorsal acetabular rim. As dogs age the clinical signs may resolve due to periarticular fibrosis, before recurring later in life with severe DJD.
Chronic form: variable onset in older patients associated with progressive DJD of the joint.
What clinical signs might be observed in dogs with hip dysplasia?
Initially a wide based stance to try and prevent hip luxation. Once this fails, a narrow stance may be adopted to try and prevent pain associated with hip reduction.
Swaying of the hips, bunny-hopping gait, shifting of the weight to the thoracic limbs with hyperextension of the tarsi and stifles is also common.
What are some tests that can be used to assess hip joint laxity in the puppy?
- Bardens: laterally directed pressure on the femur (lifting of the femur from the medial aspect). Any movement greater than 1/2 inch is suggestive of hip joint laxity.
- Barlow: first part of the Ortolani procedure (prior to reduction).
- Ortolani: subluxation and reduction of the hip. Some surgeons use the angle of subluxation and reduction to determine the minimum and maximum angles required for TPO.