Pathophysiology and Diagnosis
Canine hip dysplasia (CHD) is an inherited developmental disorder of the coxofemoral joint commonly affecting many of the larger breeds of dogs. Patients with clinical signs referable to CHD are regularly presented for evaluation and treatment, and selection of the most appropriate medical or surgical therapy requires a comprehensive orthopedic evaluation of each individual. The purpose of this series of articles is to describe the pathophysiology of the disease and the techniques employed for its successful diagnosis as well as the indications for the multitude of surgical procedures utilized to treat the condition.
The cause and pathogenesis of canine hip dysplasia are still poorly understood; however, numerous studies over the last 15 years have indicated that CHD is a developmental disorder and that multiple factors can influence or modify the expression of the disease. No specific genetic pattern of inheritance has been demonstrated; however, the pattern of inheritance is multi-factorial. The spread of hip dysplasia is centered around the genetic transmission and heritability of a particular body size, type, confirmation, and growth pattern. The occurrence of hip dysplasia has been reduced by breeding dogs that have radiographically disease-free joints and by selecting dogs for breeding based on family performance and progeny selection. Unfortunately, many factors affect the choice of dogs used in breeding programs and breeding dogs for desirable traits (i.e., large size, temperament) may result in the inadvertent selection of dogs predisposed to CHD. Therefore, while CHD is a heritable disease, controlled breeding programs have only reduced the prevalence of hip dysplasia, but the disease has not been eliminated.
Dogs with the highest incident of hip dysplasia are large, rapidly growing and maturing breeds with a heavy body confirmation. It has been speculated that slow growth and late maturation favors the completion of ossification and development of the joint before the hips are subjected to possible injury from excessive extrinsic forces, especially excessive body weight. Rapid growth and early weight gain may result in disparities of tissue development triggering a series of events leading to subluxation, hip dysplasia, and degenerative joint disease. While the role of nutrition has been thoroughly investigated, diet has not affected the occurrence or course of CHD other than the mechanical effect of increased or decreased weight upon the hip.
Several hormones have been implicated as playing a role in causing CHD, including estrogen and relaxin. Based on the results of several studies, there is no evidence that hormonal influence (within the biologic range) is associated with the development of spontaneously developing hip dysplasia in the dog.
A causal relationship between pelvic muscle mass and/or muscle myopathies and hip dysplasia has also been advanced. The disparity between primary muscle mass and/or failure of the muscles to develop and reach maturity at the same rate as the pelvis may lead to alterations in the function of pelvic muscles and the development of CHD. There are substantial evidence that the consequence of hip joint laxity. Joint laxity is thought to precede hip joint remodeling and degenerative joint disease. The possibility that joint laxity may be associated with or influenced by pelvic muscle mass and/or maturation as well as by the anatomic structures important in maintaining hip stability (i.e., ligament of the head of the femur, joint capsule, joint confirmation) has been extensively explored. The available evidence, however, does not single out any one factor or variable, which would lead to increased joint laxity. In conclusion, the confirmation and stability of the hip is governed by a number of factors which influence the congruency of the articular surfaces between the femoral head and acetabulum, the integrity of the joint capsule and ligamentum teres, combined with the overall mass and strength of the associated pelvic musculature. The failure of one or more of the orthopedic or soft tissue supporting structures leads to joint laxity with stretching and confirmational change of the aforementioned structures, progressive subluxation, hip dysplasia, and resultant degenerative joint disease.
The clinical signs of hip dysplasia are many and varied, ranging from minimal to pronounced pain, lameness, and disability. Symptoms may be seen as early as four weeks of age, but are generally not detected until 4-6 months of age. Physical examination must include gait analysis, palpation, and precise radiography of the hip.
Observation of the gait may disclose a weight bearing lameness, which is more severe after exercise, a stilted or swaying rear limb gait, an audible “click” when walking, or walking with an arched back. There may also be pain and/or crepitation present upon manipulation of the hip and evidence of poorly developed musculature of the hind quarters.
Palpation of the hip has been utilized to determine the presence or absence of joint laxity and early CHD, especially in immature dogs. The ability to accurately quantitate hip joint laxity should provide key diagnostic and prognostic information for affected dogs. There are, however, a number of concerns, which must be addressed relating to the accuracy of palpation as a method of diagnosis. Palpation is at best a subjective evaluation and is influenced by practitioner experience, positioning of the dogs, amount of forced applied, and whether or not the dog is anesthetized. As of yet, an objective method of determining the amount of joint laxity of subluxation in dogs manifesting symptoms of CHD prior to the development of detectable radiographic changes. The two most common procedures employed are the Bardens’ method and the test for the Ortolani sign, both of which are described extremely well in the article authored by Chalman and Butler. The Bardens’ test detects movement of the femoral head in and out of the acetabulum as the femur is lifted horizontally. Elicitation of an Ortolani sign may be performed with the patient in either dorsal or lateral recumbancy. During testing, the application of pressure along the femoral shaft will subluxate the femoral head dorsally. As the limb is abducted, the femoral head will reseat within the acetablulum. The resulting sound and vibrations or “clicks” produced by this reseating is a positive Ortolani sign. The degree of grading residence of “click” gives an appreciation of the severity of the existing pathology. Dogs with extensive pathology, however, may have a negative Ortolani sign because distortion of the acetabular rim combined with a thickened joint capsule and osteophyte production may lead to an extremely limited range of motion. In these cases, however, radiographic evidence of joint distortion exists and diagnosis should be straightforward.
Although observation of the gait and palpation of the hip can indicate the possibility of CHD, radiographic examination is used to establish the diagnosis in the majority of cases. Historically, radiographic evaluation consists of a symmetric ventrodorsal radiograph of the pelvis and femors with the hind limbs extended and parallel to each other. Lateral pelvic views contribute minimally in the assessment of possible CHD. A major deficiency in this standard radiographic view is the failure to adequately delineate the weight bearing portion of the acetabulum. In addition, this hip extended position may mask the true potential hip joint laxity because in this position, the joint capsule tightens and may act to drive the femoral head into the acetabulum. The dorsal acetabular rim radiographic view has been recommended to evaluate the dorsal rim of the acetabulum for damage and secondary changes to show acetabular filling and congruency of the hip and to correlate palpation of joint laxity and crepitation with radiographic appearance.
The primary radiographic signs of CHD are a shallow acetabulum and a small flattened femoral head. The dorsal acetabular rim recedes and becomes less concave, and increased joint space and subluxation or luxation of the femoral head is observed. As dysplasia progresses, joint instability, synovitis, and cartilage degeneration increase as evidenced by radiographic indication of osteoarthritic changes including femoral neck and acetabular osteophyte development, sclerosis of subchondral bone, subcondral cysts of the femoral head, and ossification of the joint capsule.
While one study reports excellent success in obtaining pelvic radiographs of dogs for hip dysplasia without sedation or anesthesia, chemical restraint is usually employed to achieve proper positioning. Once again, while anesthesia allows for proper positioning, the effects of anesthesia on the relaxation of tissues in the hip joint region and how this may affect the radiographic diagnosis of CHD needs to be taken into consideration.
In conclusion, CHD is a developmental disorder, the expression of which is influenced by a multitude of factors. Gait analysis, palpation, and radiography are indicated to establish a correct diagnosis, but the incipient disease may be difficult to identify because interpretation of the aforementioned diagnostic procedures can be subjective and requires a great deal of skill and expertise for accuracy.
In the next article, we will discuss the treatment of the young growing dog with hip dysplasia. The third article will address the treatment of the mature dog with secondary osteoarthritic changes and degenerative joint disease.