Introduction

• Characterized by abnormal development (dysplasia) of hip joint. Mismatch between skeletal and soft tissue growths.
• Cause: genetically mediated and influenced by environmental factors, eg breed, rate of growth, type of feeding, other co-existing skeletal disorders, eg lumbosacral deformities, spinal disease, trauma, bone or joint disorders of forelimbs.
• Signs: pelvic limb stiffness, difficulty rising, swaying gait in young dog. Degenerative joint disease secondary to laxity may cause pain/lameness in the older dog.
• Diagnosis: clinical signs, radiography, palpation of instability.
  There is no correlation between radiographic appearance of hip joints and degree of lameness or disability.
• Due to inherited nature of hip dysplasia (HD), a number of control schemes exist in many countries based on examination and evaluation of radiographs of hip joints by specialists, eg BVA/KC Hip Dysplasia Scheme BVA / Kennel Club hip dysplasia scoring scheme in the UK and the PennHip® Scheme for hip dysplasia PennHIP® scheme for hip dysplasia Hip dysplasia OFA certification scheme.
• Treatment: surgical - denervation, femoral head and neck ostectomy, corrective osteotomy (of acetabulum or femur) or total hip replacement, conservative - anti-inflammatory drugs, glycosaminoglycans.
• Prognosis: guarded, although corrective osteotomy may eliminate joint instability in certain cases.
  Print off the owner factsheet Hip dysplasia Hip dysplasia to give to your client.

Use the interactive tool from ROYAL CANIN® UK  to explain dog anatomy and disease conditions to your client. Visit ROYAL CANIN Natom Explorer to find out more.​

Pathogenesis

Etiology

• Inherited condition influenced by environmental factors such as:
  • Size and breed.
  • Growth rate.
  • Type of feeding.
  • Type and duration of exercise.
  • Co-existing skeletal disorders.

Pathophysiology

• Laxity/instability of hip joint developing early in life, which is largely genetically mediated but influenced by environmental factors.

• Inflammatory joint disease/synovitis develops secondary to joint laxity, causing pain/lameness initially.
• Increase in joint fluid contributes to joint laxity.
• Thickening of joint capsule leads to joint stabilization.
• Progressive remodelling of hip results from erosion of dorsal and cranial borders of acetabulum, infilling of acetabular fossa, and new bone formation along joint margin and acetabular border.
• Teres ligament may become stretched or ruptured allowing further joint subluxation/luxation.
• Joint mice may develop from fragments of articular cartilage (not common).
• Muscle development delayed in early months because of pain/disuse resulting in poor soft tissue support of joint.
• Femoral head and neck become deformed by stress-induced remodelling: flattened femoral head, new bone production around femoral neck.
• Once skeletal maturity is reached, joint has become stable and no longer luxates, but range of movement restricted. (May enable adequate hip function in non-working dogs.)
• Changes after maturity progress slowly dependent upon weight of dog, type and duration of activity.
• May be gradual joint deterioration: erosion of articular cartilage, narrowing of joint space, progressive increase in new bone formation.
• Dogs with advanced secondary remodelling at 1 year of age may not go on to develop clinical signs of lameness during adult life. In adults no correlation has been found between radiographic appearance of hip joints and degree of lameness/disability.

Timecourse

• Months to years.

Diagnosis

Treatment

Prevention

Outcomes