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.
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.
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.
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
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
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,