A mulitmodal approach to treating canine osteoarthritis beyond NSAIDs (Sponsored by Nestlé Purina)

A mulitmodal approach to treating canine osteoarthritis beyond NSAIDs (Sponsored by Nestlé Purina)

Part of the 2009 Nestlé Purina Veterinary Symposium publication
Jun 01, 2009

Osteoarthritis, the most common orthopedic disease we see in dogs today, is an insidiously progressive disease of diarthrodial joints that can profoundly impact a dog's quality of life. It has been reported that one in five adult dogs experience osteoarthritis.1

The disease is characterized clinically by pain, limitation of movement, effusion, and variable degrees of inflammation of the affected joints. Clinical signs may initially be limited to occasional stiffness, difficulty rising, or reluctance to exercise, but as osteoarthritis progresses, the clinical signs of stiffness, lameness, loss of range of motion, and muscle atrophy in the region of the affected joint(s) become easily identifiable. Osteoarthritis causes pain and discomfort to the dog and can be an emotional and financial burden to the owner.

Because there is no cure for osteoarthritis, managing it is crucial and should involve a multimodal process in which practitioners seek to manage pain; maintain or improve range of motion of affected joints; maintain or improve muscle mass; return working and performance dogs to their previous levels; and control the progression of the disease process.

Several factors can complicate the successful management of osteoarthritis and assessment of treatment, including:
  • owner compliance
  • affordability of treatment plans
  • recognition of the location of the affected joints and cause of lameness
  • method of assessing success (subjective vs. objective measurements)
  • owner perceptions and expectations for the pet.

The initial treatment plan needs to be safe, noninvasive, easy for the owner to manage, and produce visible results. Fortunately, most osteoarthritis patients can be managed with one or more of the following: weight management, physical activity, disease-modifying osteoarthritis drugs (DMOADs), and nonsteroidal anti-inflammatory drugs (NSAIDs). Physical therapy, a developing modality in veterinary medicine, can also be beneficial. This multimodal approach to the osteoarthritis patient will ideally increase pain-free movement, decrease inflammation, decrease stress on joints, and have some chondroprotective attributes.

The normal joint

To understand the effects of osteoarthritis on a pet's mobility and well-being, it is helpful to review the anatomy of a normal joint. Diarthrodial joints are composed of a joint capsule, synovial fluid, articular cartilage, and subchondral bone. The synovial joint has two functions—to facilitate predictable, energy efficient, and pain-free movement, and to support the musculoskeletal system and transmit load. Synovial fluid is an ultrafiltrate of plasma containing the glycosaminoglycan (GAG) hyaluronic acid. The fluid serves as lubrication, has viscoelastic properties, and provides nutrients to the cartilage, as well as removing metabolic waste products from cartilage.

Chondrocytes are the cellular component of articular cartilage and are responsible for the synthesis and maintenance of the extracellular matrix (ECM). Chondrocytes are imbedded in the ECM, which is a hydrated proteoglycan gel and fibrous collagen framework. The ECM is composed of primarily type II collagen and proteoglycans with a small percentage of other glycoproteins.2,3

Proteoglycans consist of a central protein core to which one or more GAG side chains are attached. Proteoglycans provide the articular cartilage with selective permeability and compressive stiffness, while collagen fibers provide tensile strength. Destruction of proteoglycans or collagen framework inhibits the stress-absorbing capacity of the articular cartilage and contributes to inflammation and further damage of the cartilage.2


Understanding the pathophysiology of osteoarthritis is important for selecting appropriate treatment regimes. Osteoarthritis affects not only the cartilage, but also the entire joint structure, including the synovial membrane, subchondral bone, ligaments, and periarticular muscles. In osteoarthritis, the synovium undergoes inflammatory changes that include synovial hypertrophy and hyperplasia with an increased number of lining cells, and also an infiltration of the sublining tissue with a mixed population of inflammatory cells.4 Most specialists agree that the synovial inflammation frequently associated with osteoarthritis is secondary to the destruction of cartilage and the release of cartilage breakdown products into the synovial fluid.4