Joint disease is a common problem, affecting up to 20% of dogs.1 Osteoarthritis (OA) is a progressive degenerative condition that affects synovial joints and has an insidious onset. Patients
with OA have restricted activity, limited ability to perform, muscle atrophy, pain and discomfort, decreased range of motion,
and decreased quality of life. As animals reduce their activity level, a vicious cycle of decreased flexibility, joint stiffness,
and loss of strength occurs.
Traditional management of dogs with OA has incorporated anti-inflammatory and analgesic drugs, changes in lifestyle, and surgical
management. Advances in the management of human OA include weight loss, exercise programs, and physical modalities to reduce
the severity of symptoms and to control pain and discomfort. Some of the benefits of a complete program include increasing
muscle strength and endurance, increasing joint range of motion, decreasing edema, decreasing muscle spasm and pain, and improving
performance, speed, quality of movement, and function. OA is cytologically categorized as a noninflammatory condition, but
many inflammatory mediators are involved, including metalloproteinases and interleukins, with a progressive cascade of mechanical
and biochemical events, resulting in cartilage destruction, subchondral bony sclerosis, synovial membrane inflammation (synovitis),
and the development of periarticular osteophytes. Much of the pain associated with OA has been attributed to synovitis. The
goals of treatment are to reduce the severity of clinical signs, maintain an acceptable quality of life, control pain and
discomfort, slow the progression of the disease, and promote repair of damaged tissue when possible.
Management of OA
Medical treatment of OA is multifaceted and includes physical modalities, controlled exercise, weight reduction, slow-acting
disease-modifying osteoarthritic agents, alteration of the environment, and anti-inflammatory medications. Veterinarians must
impress on owners that the management of chronic OA is a lifelong commitment, and it is hard work. It is critical to evaluate patients on a regular basis and provide feedback and encouragement to owners.
Management of the arthritic patient should be approached in a logical, stepwise progression.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most popular analgesic drugs used in small-animal veterinary practice
to manage pain from OA. NSAIDs function, in part, by inhibiting cyclooxygenase (COX) isozymes to different degrees. COX isozymes
play an important role in converting arachidonic acid to prostaglandins, associated with normal functions and with inflammation.
Typically, traditional NSAIDs (tNSAIDs) — such as aspirin, carprofen, etodolac and meloxicam — inhibit both COX-1 and COX-2
to varying degrees when administered at labeled doses, although there are exceptions. It is believed, based on in vitro and
ex vivo studies, that when coxib-class NSAIDs are given at labeled doses, these drugs inhibit COX-2 activity with relative
sparing of COX-1 activity (COX-2 selective NSAIDs). It is also believed that coxib-class NSAIDs (deracoxib and firocoxib)
offer analgesic and anti-inflammatory effects that are at least comparable to those of tNSAIDs without interfering with the
homeostatic functions of prostaglandins in the gastrointestinal tract and platelets. The clinical relevance of the laboratory
data on which these beliefs are based is not known, although coxib-class NSAIDs appear to result in fewer gastrointestinal
Comparative efficacy of NSAIDs
So which NSAID is the best? Many different parameters might influence the answer, including patient history, patient medical
condition, the veterinarian's experiences, owner preference, product efficacy and safety, concurrent medications, patient
response, and cost. Ground reaction force has also been used as an objective differentiator between an NSAID and a nutraceutical.
Moreau et al measured ground reaction force response in 71 arthritic dogs (elbow, stifle, or hips) after 30 and 60 days of administration
of either placebo, carprofen, meloxicam, or a combination nutraceutical (chondroitin sulfate, glucosamine, and manganese ascorbate).2 Although ground reaction force significantly improved in both the meloxicam and carprofen groups, only meloxicam-treated
dogs returned to normal ground reaction force values for some situations. Performance of the meloxicam group was superior
to the carprofen group, and no improvement was seen in the combination nutraceutical group. One case of hepatotoxicosis was
reported in the carprofen group.
In another study,3 experimentally induced acute synovitis in beagles was used to compare the analgesic and anti-inflammatory effect of single
doses of carprofen, etodolac, meloxicam, and butorphanol to a placebo. Compared with control dogs, treated dogs had significantly
different vertical ground reaction forces and weight-bearing scores. Etodolac had the fastest onset of action, but the greatest
improvement in lameness was observed in carprofen-treated dogs. Both carprofen and etodolac were associated with significantly
lower pain scores.
One study4 investigated the effectiveness of several NSAIDs further, examining aspirin, acetaminophen, carprofen, deracoxib, etodolac,
meloxicam, tepoxalin, and firocoxib in comparison to a placebo. The study was a 3x3 crossover study of nine mixed-breed hounds,
weighing 40 to 60 lb. The dogs had mild to moderate OA resulting from cranial cruciate ligament transection with immediate
stifle stabilization, and each had measureable differences in peak vertical force in the rear limbs. Results from this study
showed that each dog responded to at least one NSAID, but not every dog responded to each. As determined by peak vertical
force, deracoxib gave the greatest response; dogs responded equally to etodolac, firocoxib, and aspirin; and acetaminophen
was not effective. Dogs receiving meloxicam, carprofen, and tepoxalin had results intermediate between the placebo and the