Osteoarthritis (OA) is a common problem in small animal medicine. It is estimated to affect 20% of the United States' canine population, translating to over 10 million dogs. However, it remains widely underdiagnosed and misunderstood. Unlike in humans, canine osteoarthritis is rarely primary. It is virtually always secondary to other joint pathology. Its insidious onset, slow progression, and wide range of clinical signs make osteoarthritis a challenge to diagnose.

Terminology

The nomenclature surrounding the discussion of osteoarthritis and degenerative joint disease (DJD) can be confusing, as these terms are often interchanged. Further confusion arises when considering the term of an "itis, (i.e., inflammatory,) and sometimes an "osis", (i.e., degeneration without inflammation). While degenerative joint disease is the more technically more correct term, due to the literature and definitions promoted in humans it is easier to refer to the disease as osteoarthritis.

Osteoarthritis is characterized by articular cartilage degeneration and changes in the periarticular soft tissues (synovium and joint capsule) and subchondral bone. Specifically, the pathologic changes of osteoarthritis encompass articular cartilage degeneration, which includes matrix fibrillation, fissure appearance, gross ulceration, and full-thickness loss of the cartilage matrix. This pathology is accompanied by hypertrophic bone changes with osteophyte formation and subchondral bone plate thickening. Failure to repair the damage affecting the surface cartilage is a distinctive condition of OA. Failure of chondrocytes in injured articular cartilage to restore a functional matrix in spite of high metabolic activity remains a complex and challenging problem. Currently, there is no treatment regimen proven to arrest or reverse the cartilage degeneration.

Clinical Signs

Osteoarthritis is a syndrome affecting synovial joints that is characterized by pain and dysfunction, associated with degeneration of the articular cartilage and changes in the periarticular soft tissues. It occurs with varying degrees of severity, ranging from a mild, intermittent condition that causes mild discomfort and minimal disability, to a disease state characterized by constant pain along with severe functional disability. As such, it is often difficult to describe any single treatment that will cover the entire spectrum of change that may be present.

Treatment Goal

Current therapy is primarily palliative, aiming to reduce pain and inflammation and maintain or improve joint function without altering the pathologic process in the tissue. Remember, most OA in the dog and cat is secondary to some other pathologic state, and thus the underlying cause must be identified in an attempt to minimize the long-term effects. Certainly efforts are being made to provide treatments which may alter the course of the disease but these therapies are still to a large part unproven.

Treatment Plan

Management Components

1. Weight Reduction: Weight control is a must when dealing with OA. The vast majority of our patients seen with clinical manifestations of OA are obese. Owner education and proper dietary management must be considered in every case. In many cases, the implementation of weight reduction with rest and exercise modification diminishes or completely alleviates the clinical signs of OA.

2. Nutritional Support: The recent influx of diets on the market with a high N3:N6 fatty acid ratio is adding a whole new area of intervention. It is important to understand that there is an increase in N3 fatty acids in the diet and that specific N3 fatty acids are elevated (EPA and DHA).

3. Exercise modification/Physical Therapy: Protecting the osteoarthritic joint from excessive mechanical stress may limit clinical signs. Use of the joint in a manner that consistently results in discomfort is generally believed to lead to acceleration of cartilage destruction. Most patients with OA are comfortable with light to moderate exercise regimens that do not vary significantly. Enforced rest and exercise modification is different for each animal, but exercise extremes tend to exacerbate clinical signs. Swimming is a wonderful minimal load exercise, and in many parts of the country is available nearly year round to our patients.

4. Pharmacologic Management: Analgesic and antiinflammatory agents are the most common final component in the management of OA. However, these agents are not used without risk of side effects. The application of analgesic nonsteroidal antiinflammatory drugs (NSAIDs) reduces inflammation responsible for joint damage. It also reduces physiologic pain signals which limit activity, and thus can indirectly cause overuse. This is precisely why part of our whole treatment protocol specifically involves exercise modification.

Disease-modifying osteoarthritis drugs (DMOAD) or structure modifying osteoarthritis drugs (STMOAD) are an expanding area of interest in osteoarthritis management. These products are directed at preventing, reducing, or reversing the cartilaginous lesions of OA. Agents that have been previously called chondroprotective are now considered DMOADs or STMOADs. These drugs can have both effects on the inflammatory cascade and release of mediators and also direct effects on the target tissues (cartilage, bone, synovium).