Osteoarthritis (OA) is a chronic, non-infectious, progressive disorder of any synovial joint. OA is characterized by deterioration
of the articular cartilage, synovitis, with secondary bony changes. Osteoarthritis is classified as being primary or secondary
in nature. Primary arthritis (age-related) results from abnormalities within the cartilage (abnormal quality) and is considered
an intrinsic problem with the cartilage homeostasis associated with aging. In this form of OA, normal joint forces impact
abnormal cartilage. The affected cartilage has limited ability to regenerate and maintain itself in the face of the cumulative
effects of ongoing trauma and/or inflammation. Primary osteoarthritis has a slow progressive course, generally involves one
or more joints, and is most common in geriatric patients.
Secondary arthritis is a more common cause of clinical lameness in the younger dog. It is the consequence of some external event or
force affecting the articular cartilage adversely. In this form there are abnormal forces affecting normal cartilage. Examples
would include overt trauma, joint incongruity (instability), and joint malalignment. Secondary arthritis can be seen in any
age animal and usually involves a single joint. In order to prevent, halt or minimize the degeneration process, the underlying
joint incongruity must be eliminated.
The pathophysiology of primary arthritis involves a series of steps that eventually becomes a progressive self-perpetuating
process. The mediators of the inflammation, pain, and joint destruction include prostaglandins, cytokines, leukotriens, and
kinnins. The variation in clinical response of the each pharmacological agent used in treating OA reflects the specific effect
on each of these specific inflammatory mediators or pathways. Articular cartilage is a very complex and dynamic structure.
The cartilage matrix is composed of proteogycan macromolecules (hyaluronic acid and GAGs), type 1 collagen, and 80% water.
The matrix is synthesized and maintained primarily by the chondrocytes. In primary arthritis, there is a shift in the cartilage
homeostasis towards catabolism. Initially there is decreased production of proteogycan by the chondrocytes, a loss of chondroitin
sulfates and water from the matrix. The resultant articular cartilage is less elastic with less shock absorption. Any minor
trauma produces cartilage fissures and chondrocytes damage. Surface cracks produce "flaking" exposing the collagen fibers
to wear and tear. Some cracks extend into the deeper layers and bone produce fibrillation. Degrading enzymes are released
which further break down cartilage matrix and collagen. These enzymes include serines, collagenase, cathepsins, metalloproteinase's,
hyaluronidases, stromelysins, plus the cartilage breakdown products, initiate a mild synovitis The resulting inflamed synovial
membrane releases primary inflammatory mediators IL 1, IL 6, tissue necrosis factor, proteases, and prostaglandins that further
increasing cartilage destruction and inhibiting new matrix production. The further decreased resiliency of the cartilage results
in sclerosis of the subchondral bone and osteophyte development in the periarticular margins in advanced cases.
The clinical signs of osteoarthritis are similar regardless of whether the disorder is primary or secondary. The onset is
often insidious but progressive. Early in the course of the disease, the animal may sporadically be reluctant to perform previous
tasks or activities, i.e., jumping into the car. In the next stage, a lameness or stiffness occurs following periods of excess
activity or overexertion. These signs often disappear after several days of rest. As the degeneration progresses, the stiffness
and lameness may be most pronounced following periods of rest. The pet typically "warms out" of the signs with activity. Any
cold or damp weather will increase the severity and duration of the symptoms. Continuous stiffness, lameness and chronic pain
typify the final stage producing an irritable, reclusive and restless pet. In a recent study, 90% cats > 12 years had radiographic
evidence of osteoarthritis (Hardie, E., JAVMA 2002). The most common location in cats was the spine followed by the elbow
and the hip. Common feline symptoms include grooming difficulties, inappropriate eliminations, less jumping, aggressive when
handled, and lameness.
There is no cure for arthritis, only control. The goals in the treatment should be to alleviate patient discomfort, minimize
further degenerative changes, and to restore the affected joints to as near normal and pain-free as function possible. The
management of arthritis involves the following strategies and should be tailored to best meet the patient and clients needs;
1. Client education on the progressive nature of the disease is critical; 2. Set realistic outcome goals (expectations); 3.
Adequate rest periods; 4. Sensible exercise program; 5. Weight assessment and reduction if necessary; 6.Analgesics and anti-inflammatory
therapy for rapid results; and/or 6. Chondroprotective agents; 7.Anti-oxidant nutritional therapy (dietary); 8. Complementary
therapies, i.e. message therapy, physical therapy, acupuncture, chiropractic, etc.
