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

NSAIDs

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 side effects.

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 other NSAIDs.