While considered a very common problem in small animal medicine, osteoarthritis is very likely the most under diagnosed, and
misunderstood rheumatic disease in dogs and cats. Part of the problem veterinarians face with OA is that it is a slow, progressive
and often insidious problem. In the dog, primary OA is uncommon and OA development always occurs secondary to another joint
pathology. The wide range of clinical signs makes OA a commonly misdiagnosed condition. Osteoarthritis has been estimated
to affect 20% of the US canine population. This widely referenced estimate, in practical terms, translates to over 10 million
dogs. No realistic estimate has ever been made about the number of cats affected. Thus the identification and management of
the disease is of the utmost importance to the small animal clinician.
There is often confusion in the nomenclature during a discussion of osteoarthritis and degenerative joint disease (DJD). It
usually becomes unclear to many individuals whether these are the same disease process or different problems. Further confusion
arises when considering the term of an "itis, (i.e.,inflammatory,) and sometimes an "osis", (i.e., degeneration without inflammation).
Without an exhaustive explanation, it is easier to call the process osteoarthritis due to the literature and definitions promoted
in humans. Although, using the term degenerative joint disease is technically correct given ones point of view and is sometimes
interchanged with osteoarthritis.
The American Academy of Orthopaedic Surgeons proposed the following consensus definition: Osteoarthritic diseases are a result
of both mechanical and biologic events that destabilize the normal coupling of degradation and synthesis of articular cartilage
chondrocytes, extracellular matrix (primarily collagen and aggrecan), and subchondral bone. Although they may be initiated
by multiple factors, including genetic, developmental, metabolic, and traumatic factors, osteoarthritic diseases involve all
of the tissues of the diarthrodial joint. Ultimately, osteoarthritic diseases are manifested by morphologic, biochemical,
molecular, and biomechanical changes of both cells and matrix which lead to softening, fibrillation, ulceration, articular
cartilage loss, sclerosis and subchondral bone eburnation, and osteophyte production. When clinically evident, osteoarthritic
diseases are characterized by joint pain, tenderness, limitation of movement, crepitus, occasional effusion, and variable
degrees of inflammation without systemic effects.
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. What this says to the clinician at the present time is that 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
Management of OA should be thought of as a multi-step approach with four to five important components. While some clinicians
tend to reach for pharmacologic management alone, this is usually unsuccessful without concurrent management of exercise and
weight reduction. Thus, starting to treat a patient with OA requires a lengthy discussion of all aspects of management with
the client. Our discussion will follow the typical pattern we use in our practice. Remember, one must examine each case differently,
assessing the age, normal activity levels, and, most importantly, the owner's expectant activity levels of the animal. Success
largely depends on the accurate assessment of the client's expectations for the pet.