Introduction

The canine hip joint is a diarthrodial (ball and socket joint) with the acetabulum of the pelvis and head of the femur being closely matched by their radius of curvature maintaining a highly congruent and mobile joint. Whilst traumatic damage to the joint does occur, the anatomy of the joint and the robust pelvic musculature are somewhat protective to the joint making the forces required to cause traumatic damage significant. The most commonly seen non-traumatic diseases of the canine hip joint are hip dysplasia and secondary osteoarthritis and avascular necrosis of the femoral head (Legg-Calvé-Perthes disease). Slipped capital femoral epiphysis is reported in dogs although it is more common in cats and non-traumatic spontaneous coxofemoral luxation has been reported in dogs with marked joint laxity usually secondary to hip dysplasia. Von Willebrand's heterotopic osteochondrofibrosis is an uncommon cause of lameness localisable to the hip mainly seen in Dobermans but also identified in the German Shepherd Dog and in the St. Bernard.

Hip Dysplasia

Hip dysplasia is an inherited developmental disease of the hip joint that leads to the development of hip laxity and secondary osteoarthritis. It is one of the most common orthopaedic conditions of the dog, affecting mainly large and giant breeds and is often bilateral.

At birth, the hips of affected dogs are normal but a lack of congruity between the acetabulum and femoral head develops as they age.¹ In the early stages, stretching of the teres ligament, increased synovial fluid volume, subluxation of the femoral head and loss of the dorsal acetabular rim contribute to joint laxity.¹ The laxity causes stretching of the joint capsule that in turn causes pain. Due to the laxity, microfractures develop in the dorsal acetabular rim exposing subchondral bone contributing to the discomfort. Affected dogs have poor limb use and muscle atrophy develops further reducing the stability of the joint. Over time, remodelling of the hip joint begins; the femoral head flattens, the neck thickens and the acetabulum fills in. These changes and a concurrent thickening of the joint capsule stabilise the joint reducing the discomfort seen. The reduced discomfort allows dogs to become more mobile, encouraging muscle build up that further stabilises the joint. By the time the dog reaches skeletal maturity (12–18 months old), the hip is usually stable allowing adequate return of limb function. From this point on, osteoarthritis continues to progress slowly.¹

There is a bimodal presentation seen in cases with hip dysplasia. Young dogs (<1 year) tend to present with signs relating to hip laxity and synovitis whilst older dogs present with osteoarthritis. Radiography is still the gold standard method of diagnosis. Three view hip radiographs are required under heavy sedation or GA. If less than 50% of the femoral head is covered by the acetabulum in the young dog, the hip is dysplastic. Secondary radiographic changes seen will depend on the severity of the condition.

Early diagnosis of the condition is ideal because there is a high correlation with hip laxity and the development of secondary osteoarthritic changes.² Use of the Penn-Hip screening method identifies those dogs that have hip laxity and who may benefit from early surgical intervention to prevent further disease development.²

The aim of any treatment for hip dysplasia is to alleviate pain, maintain limb function and reduce progression of osteoarthritis. Conservative treatment involves a multimodal approach including analgesia, exercise modulation/rehabilitation and dietary management.

Surgical procedures may be preventative, palliative or salvage. In young dogs, juvenile pubic symphysiodesis and pelvic osteotomy may be performed to alter the angle of the acetabulum, increasing coverage of the femoral head and improving congruity of the joint.

Palliative surgeries include denervation of the hip joint capsule by disruption of the innervation of the cranial gluteal, sciatic, obturator and femoral nerve components. Salvage procedures include femoral head and neck ostectomy (FHNO) and total hip arthroplasty (THA).

Coxofemoral Luxation

Coxofemoral luxation is usually seen following significant trauma, however in dogs with hip dysplasia and joint laxity, spontaneous luxation may occur.³ As with traumatic luxations, diagnosis is made on physical examination and radiographs. Treatment depends on the stability of the joint once reduced however if the joint is already severely lax as is normally the case with atraumatic luxation, salvage procedures (FHNO, THA) may be indicated.

Avascular Necrosis of the Femoral Head (Legg-Calvé-Perthes)

Avascular necrosis of the femoral head is a non- inflammatory local ischaemia leading to necrosis of and subsequent changes to the anatomy of the femoral head and neck. The condition is most commonly seen in small-breed dogs with toy breeds and terriers being predisposed⁴ and 12–16.5% of cases are bilateral⁵.

Most dogs present between 4–7 months old with pelvic limb lameness and pain localised to the hip joint. The aetiology of the condition is unknown although a vascular origin is likely. A hereditary component has been identified in Manchester terriers.⁴

The ischaemia and subsequent necrosis of the trabeculae within the femoral head leads to collapse of the subchondral bone and crack formation in the articular cartilage. During the process of reossification and healing, revascularization of the epiphysis and metaphysis occurs and new bone is formed causing deformation of the femoral head and neck and irreversible joint incongruity and instability. Degenerative change of the joint leads to severe osteoarthritis.

Diagnosis is based on signalment, history, orthopaedic examination and diagnostic imaging. A flexed ventrodorsal view is most likely to allow identification of the defect.

Conservative management consists of analgesia, rest, limited exercise and nutritional support; however, reports suggest that lameness resolves in less than 25% patients.⁵ Surgical treatment of the condition involves either FHNO or THA. In small-breed dogs, FHNO is reported to be adequate for management of the condition although recent work questions the functional outcome following this procedure.⁶ THA provides better functional outcome and shorter recovery and rehabilitation times.⁷ Surgery is reported to relieve the lameness and discomfort in between 84–100% cases.^5,8

Slipped Capital Femoral Epiphysis

Slipped capital femoral epiphysis is a slow but progressive detachment of the proximal femoral metaphysis from the capital femoral epiphysis through the growth plate. It can be traumatic or non-traumatic in origin, is seen more commonly in cats than dogs and is often bilateral.⁹

Once again, the aetiology of the condition is unclear. There appears to be some evidence that osteochondrosis plays a role leading to a widened growth plate and the potential for torsion or shear forces to cause the growth plate to slip.⁹ Delayed growth plate closure due to neutering in combination with excessive body weight is a risk factor for cats although this has not been confirmed in dogs.

Affected animals usually have evidence of intermittent lameness with reduced willingness to exercise and jump, although acute onset lameness without trauma has also been reported.⁹ The diagnosis is made radiographically. Initially the widened growth plate may be difficult to appreciate but at later stages of disease the proximal femoral metaphysis is displaced and associated sclerosis and absorption of the femoral neck may be evident.

In early stages of the disease, internal fixation of the slipped epiphysis may be achieved however resorption of the femoral neck may necessitate FHNO. If the femoral neck remains intact THR is also an option. The prognosis for patients following surgical treatment is excellent.⁹

Von Willebrand's Heterotopic Osteochondrofibrosis

This is an uncommon cause of pelvic limb lameness, predominantly described in Doberman dogs.¹⁰ Traumatic and spontaneous aetiologies of the condition have been reported. Dogs with the condition present with a chronic, progressive lameness of insidious onset and often, pelvic muscle atrophy. Pain on hip manipulation and reduced range of motion of the joint are identified on physical examination.

The condition is thought to be due to a focal myopathy within the muscles caudal to the hip joint (gemelli, internal and external obturator muscles) and a soft tissue mass is palpable in this region. Over time chondro-osseous tissue is deposited within the muscle mass to replace the fibrous tissue and mineralisation becomes evident radiographically. Affected animals will test positive for von Willebrand's disease. Conservative treatment with rest and analgesia may lead to resolution of the signs although surgical excision of the mass may be required.¹⁰

References

1.  Riser WH. Growth and development of the normal canine pelvis. J Am Vet Rad Soc. 1973;14:24–34.

2.  Smith GK, Gregor TP, Rhodes H, Biery DN. Coxofemoral joint laxity from distraction radiography and its contemporaneous and prospective correlation with laxity, subjective score and evidence of degenerative joint disease from conventional hip-extended radiography in dogs. Am J Vet Res. 1993;54:1021–1042.

3.  Trostel CD, Peck JN, deHaan JJ. Spontaneous bilateral coxofemoral luxation in four dogs. J Am Anim Hosp Assoc. 2000;36:268–276

4.  LaFond E, Breur GJ, Austin CC. Breed susceptibility for developmental orthopaedic diseases in dogs. J Am Anim Hosp Assoc. 2002;38:467–477.

5.  Lee R, Fry PD. Some observations on the occurrence of Legg-Calvé-Perthes disease (Coxoplana) in the dog, and an evaluation of excision arthroplasty as a method of treatment. J Small Anim Pract. 1969;10:3–317.

6.  Off W, Matis U. Excision arthroplasty of the hip joint in dogs and cats - clinical, radiographic and gait analysis findings from the Department of Surgery, Veterinary Faculty of the Ludwig-Maximilians-University of Munich, Germany. Vet Comp Orthop Traumatol. 2010;23:297–305.

7.  Liska WD. Micro total hip replacement for dogs and cats: surgical technique and outcomes. Vet Surg. 2010;39:797–810.

8.  Warren DV, Dingwall JS. Legg-Perthes disease in the dog - a review. Can Vet J. 1972;13:135–137.

9.  Moores AP, Owen MR, Fews D, Coe RJ, Brown PJ, Butterworth SJ. Slipped capital femoral epiphysis in dogs. J Small Anim Pract. 2004;45:602–608.

10. Dueland RT, Wagner SD, Parker RB. von Willebrand heterotopic osteochondrofibrosis in Doberman pinschers: five cases (1980–1987). J Am Vet Med Assoc. 1990;197:383–388.