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Vol.18, No. 8August 1996
Pathophysiology,Diagnosis, andTreatment of CanineHip Dysplasia
University of Missouri
 James L. Cook, DVM James L. Tomlinson, DVM, MVScGheorghe M. Constantinescu, DVM, PhD, Drhc
C
anine hip dysplasia (CHD) is a common developmental disease of thecoxofemoral joint of dogs.
1–6
The disease affects 1.8% to 48.1% of dogsof a given breed.
4
Heritability indexes (which measure the percentageof phenotypic variation attributable to genetics) also vary greatly amongbreeds. Canine hip dysplasia is most frequently reported in large and giant ca-nine breeds but can affect any breed. The disease most commonly occurs bilat-erally; unilateral disease reportedly ranges from 3% to 30%, depending on thebreed.
4
 Although many causes have been proposed, a definitive cause has not beenestablished. A genetic predisposition involving a polygenic mode of inheritancehas been reported.
1–5
 Affected dogs are predisposed to developing a biomechan-ical imbalance between muscle mass and skeletal stresses on the hip joint.
2,5
The imbalance leads to laxity, subluxation, and degenerative joint disease(DJD). Nutrition and rapid growth rate are important factors that contributeto the disparity between muscle mass and skeletal stresses.
1–3
Other proposedcausal factors include hormonal influences; collagen, muscle fiber, ligamentand nerve abnormalities; and abnormal synoviocyte ratios.
1–3,6
These factors areprobable components of the polygenic basis of the disease.The multifactorial nature of CHD can confuse client education and manage-ment of the disease. The basic concept involved is the biomechanical imbalancebetween the forces on the coxofemoral joint and the associated muscle mass; theresult is joint laxity in young, growing dogs. This laxity leads to incongruity; theeventual result is DJD. This article considers the pathophysiology and treat-ment options for patients with CHD and provides a framework for decisionmaking and prognosis for various categories of patients with the disease.
Continuing Education Article
FOCAL POINTKEY FACTS
I
Dogs that are affected withhip dysplasia are geneticallypredisposed to developinga biomechanical imbalancebetween muscle mass andskeletal stresses on the hip joint.
I
The disparity between soft tissuestrength and biomechanicalforces during skeletal growthcauses a loss of congruitybetween the articular surfaces ofthe acetabulum and the femoralhead.
I
A comprehensive evaluationincludes signalment, history,general physical examination,orthopedic examination,neurologic examination, andradiography.
I
The goals of treatment are toalleviate pain, to arrest secondarydegenerative changes, and tomaximize joint function.
#
Accurate diagnosis, treatment,and prognosis of patients withcanine hip dysplasia depends oncomprehensive evaluation ofaffected dogs.
 
PATHOPHYSIOLOGY
The coxofemoral joint is normalat birth and begins as a congruentunit.
2,5
Genetically susceptible dogsbecome dysplastic when the primary muscle mass that supports the jointfails to mature at the same rate as theskeletal structures.
2,5,7,8
The resultantdisparity between soft tissue strengthand biomechanical forces duringskeletal growth is manifested as a lossof congruity between the articularsurfaces of the acetabulum and thefemoral head.
2,5
This incongruity re-sults in the instability that leads toDJD.The most important time in thedevelopment of the canine coxo-femoral joint is the first 60 days of life, when the periarticular soft tis-sues are immature.
2
During this peri-od, the muscles and nerves are func-tionally limited. If the stresses on thehip from weight bearing and activity exceed the strength of the supportingsoft tissue, the articular surfaces areforced apart. If the elastic limit of thesoft tissue is exceeded, the laxity re-sults in irreversible incongruity.
2
Theincongruity in the joint results inabnormal joint motion (instability).The abnormal motion produces re-modeling of the joint and joint effu-sion, both of which result in furtherincongruity and laxity due to articu-lar cartilage changes and loss of hy-drostatic pressure.
2,9–17
Overloading of the hip can begin assoon as a puppy begins to push itself to nurse and can continue into the lat-er developmental stages, when addi-tional stresses exacerbate the incon-gruity and lead to further remodeling.
2
The dysplastic changes evident inCHD apparently correlate with theseverity and duration of the biome-chanical overloading.
2,7,8
If congruity ismaintained until the soft tissue is ma-ture or is restored before irreversiblechange, nerve function and musclemass are sufficient to maintain con-gruity of the joint.
2
 When the patientis approximately 6 months of age (i.e.,
Small Animal
The Compendium 
August 1996
GENETIC SUSCEPTIBILITY
I
COXOFEMORAL JOINT
I
DYSPLASTIC CHANGES
Figure 3—
Schematic illustration of femoral head subluxation
(arrows) 
as the resultof a shallow acetabulum.
Figure 2—
Schematic illustration of normal
(left) 
and increased
(right) 
angles of an-teversion. Increased anteversion results in greater stress on the coxofemoral joint.
Figure 1—
Schematic illustration of normal, increased, and decreased angles
(from left to right) 
of inclination. An increased angle results in greater stress on the cox-ofemoral joint.
 
 when 90% of the ossification process is complete),changes in joint shape can only be accomplished by theproduction or resorption of bone.
2
BIOMECHANICS
Normal weight bearing through the coxofemoral joint is transmitted through the shaft of the femur, thefemoral neck and head, the acetabulum, the ilium, andthe sacrum. The load placed on the coxofemoral jointis determined by body weight, conformation, and ac-tivity.
6
 When a dog is standing, 30% to 40% of thebody weight is distributed to the pelvic limbs.
6,9
Duringactivity, however, the coxofemoral joint load may ap-proach three times body weight.
6
The amount of force placed on the joint is influ-enced by the femoral neck–shaft angle of inclination,the length of the femoral neck, the position of thegreater trochanter, and the distance of the femoral headfrom the body’s center of gravity.
6
Increased stress onthe joint occurs with an increased angle of inclination(Figure 1), an increased angle of anteversion (Figure 2),a relatively short femoral neck, and distal or medial dis-placement of the greater trochanter.
6
Increased stress onthe joint potentiates laxity, incongruity, and DJD. Inaddition, if the craniodorsal aspect of the acetabulumdoes not meet the force vector of the femoral head per-pendicularly (because of slanting orincomplete coverage), subluxationresults
6
(Figure 3).
DIAGNOSIS
Dogs that have clinical signs at-tributable to CHD are commonly presented to veterinary practitionersfor evaluation. Dysplastic dogs with-out clinically evident abnormalitiesmay be evaluated during routinephysical examinations. A compre-hensive evaluation is essential foraccurate diagnosis, treatment, andprognosis. Other causes of hindlimblameness (e.g., cruciate ligament rup-ture, patellar luxation, osteochondro-sis, and trauma) must be ruled out.Evaluation should include signal-ment, history, complete generalphysical examination, complete or-thopedic examination, neurologicexamination, and radiography.
1,3,7
Signalment and History
Two distinct groups of dogs withCHD have been clinically recog-nized.
2,10
Dogs 4 to 12 months of age often present with a sudden onset of clinical signs.
10
These dogs ex-hibit a sudden decrease in activity in conjunction withpain and/or lameness in the pelvic limbs.
10
The cause of the pain and lameness has been attributed to joint effu-sion, tearing or stretching of the round ligament, syn-ovitis, acetabular microfractures, and loss of articularcartilage.
10,18–49
Most of these patients have a positiveOrtolani sign in the affected joints and atrophy of theassociated pelvic muscle mass.
7,10
In older dogs, clinical signs result from degenerativechanges in the joint.
10
Signs are usually insidious butmay present suddenly as the result of acute trauma tothe abnormal tissue.
10
Older dogs with CHD are oftenbilaterally lame, especially after exercise; joint crepitus,restricted range of motion (especially extension), andmuscle atrophy of the hindlimbs may be present.
10
 A positive Ortolani sign is rare.
7,10
In both groups of dogs,clinical signs may include varying degrees of lameness,so-called bunny hopping, difficult rising, and abnormalstance or gait.
Palpation Techniques
Bardens’ method
11
of coxofemoral joint palpation inpuppiesat 6 to 8 weeks of age is reportedly accurate inpredicting CHD in commonly affected breeds.
12
The
The Compendium 
August 1996Small Animal
NORMAL WEIGHT BEARING
I
INCREASED JOINT STRESS
I
CREPITUS
Figure 4—
Schematic illustration of hand placement for eliciting of the Bardens’sign.
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