Degenerative joint disease (DJD), or osteoarthritis (OA), is among the most prevalent chronic pain conditions in dogs. Studies suggest it affects up to 20% of dogs over one year of age and the majority of dogs over 8 years, making it a major welfare challenge across the canine population.
OA involves progressive degradation of articular cartilage, subchondral bone remodelling, synovial inflammation, and periarticular soft tissue changes. Cartilage has no nerve supply and poor repair capacity — once lost, it does not regenerate. The disease is typically insidious, with years of subclinical change before clinical signs become apparent. Pain arises from bone-on-bone contact, synovial inflammation, stretching of joint capsule, and periarticular muscle tension.
Developmental orthopaedic diseases (hip dysplasia, elbow dysplasia, osteochondrosis) are the primary cause in large and giant breed dogs. Previous injury including fractures involving joint surfaces, cruciate ligament disease, and luxating patella all accelerate joint degeneration. Obesity dramatically increases OA risk and severity — adipose tissue produces pro-inflammatory cytokines that directly promote cartilage degradation, independent of mechanical loading effects. Age-related 'wear and tear' OA affects most geriatric dogs in multiple joints.
Chronic pain is profoundly welfare-compromising. Dogs with OA experience persistent low-grade to moderate pain with episodic exacerbations. Behavioural signs are often subtle and frequently missed by owners: reluctance to exercise, stiffness after rest, reluctance to use stairs, altered posture, reduced play activity, changes in sleep pattern, and withdrawal from social interaction. Only a minority of owners correctly identify their dog as being in pain — many attribute signs to 'slowing down with age' and do not seek treatment.
Physical examination — gait analysis, limb palpation, joint manipulation — identifies affected joints and assesses pain severity. Radiography demonstrates classic OA changes: osteophyte formation, subchondral sclerosis, joint space narrowing, and soft tissue swelling. However, radiographic severity correlates poorly with clinical pain — some dogs with severe radiographic changes appear less affected than dogs with mild changes. Advanced imaging provides additional detail. Force plate gait analysis objectively quantifies weight bearing and treatment response.
NSAIDs: Non-steroidal anti-inflammatory drugs (meloxicam, carprofen, grapiprant) are the cornerstone of pharmacological OA management. Regular dosing provides better pain control than intermittent dosing. Monitoring for side effects (gastrointestinal, renal, hepatic) with baseline and periodic blood tests is essential.
Adjunct analgesics: Gabapentin, amantadine, and paracetamol (not at all doses used in humans — dogs require specific veterinary dosing) provide additional pain control for poorly controlled cases.
Anti-NGF therapy: Monoclonal antibodies targeting nerve growth factor (bedinvetmab) represent a significant advance in canine OA management. Monthly subcutaneous injections provide sustained pain control with a different mechanism to NSAIDs.
Physiotherapy and hydrotherapy: Therapeutic exercise maintains muscle mass, joint range of motion, and proprioception. Hydrotherapy is particularly beneficial — buoyancy reduces joint loading while maintaining cardiovascular fitness. Evidence supports significant improvement in objective gait measures with regular hydrotherapy.
Weight management: Even modest weight reduction (6.7% body weight) dramatically reduces lameness severity in obese OA dogs. Weight management should be a treatment priority in every overweight OA patient.
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