Managing osteoarthritis (Proceedings)


Managing osteoarthritis (Proceedings)

Apr 01, 2010

Osteoarthritis can result from direct trauma to the joint or cartilage, injury to ligaments or soft tissues resulting in joint instability, obesity or developmental disease. The effect of osteoarthritis varies, with a wide range of severity and associated radiographic and clinical signs; however, resultant discomfort and activity restrictions can have a profound effect on quality of life. Because osteoarthritis progresses slowly, and veterinary patients are often able to compensate and mask clinical signs, the diagnosis and clinical significance is often overlooked.

Clinical signs

Osteoarthritis (OA) is diagnosed by means of historical behavior changes, clinical signs, physical examination and radiographic evaluation. Arthrotomy and arthroscopy can also be used to determine the severity of damage to the articular cartilage. Behavioral changes often associated with OA include; sore when touched or reluctant/avoiding being touched in certain areas, reluctance to walk, run, climb stairs, jump or play, difficulty rising from rest or slow to sit, crying, cowering, or whimpering, changes in temperament, aggressiveness, stiffness, especially early in the day. The clinical signs of OA include; discomfort, lameness and abnormal posture (hunched back, abnormal tail carriage, etc), decreased joint range of motion, loss of muscle mass and tone, joint thickening, crepitus and decreased overall limb use.

Additionally, chronic discomfort and nociceptive input can lead to modulation of the central nervous system, referred to as "spinal windup" amplifying the primary disease and systemic response while impairing the response to therapy. Though OA is considered a chronic progressive disease, the clinical picture may be quite dynamic with intermittent periods of acute signs or "flare ups" with periods of clinical quiescence. In addition, there also appears to be variation in the clinical impact between individual dogs.

Though radiographs are the simplest least invasive way to confirm the diagnosis of OA, because of the individual nature of the disease, radiographic changes correlate poorly with the severity of clinical signs. Owner assessment of behavior and activity and physical examination are the best estimators of disease severity and response to treatment.

The objectives for the management of OA are to minimize signs associated with OA, maintain or improve limb use and quality of life, and if possible, slow the progression of disease. A multimodal approach provides treatment aimed at different aspects of the disease process working synergistically and non-competitively for a more effective response in the treatment of OA. This allows for the administration of collectively lower doses of medication, decreasing the potential side effects of any one treatment prescribed. There is no specific recipe for the management of OA. In addition to Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), multimodal therapy for the treatment of OA also incorporates weight loss, exercise modification and rehabilitation, and diet changes. Additionally, adjunctive analgesics, chondromodulating agents, nutraceuticals and other dietary supplements may be utilized.

Nonsteroidal Anti-inflammatory Medications (NSAIDs). NSAIDs are the most commonly prescribed class of medications to alleviate the clinical signs of OA. NSAIDs reduce the formation of inflammatory prostaglandins and thromboxane production by inhibiting cyclo-oxygenase (COX) enzymes in the arachadonic acid pathway decreasing synovitis and limiting cartilage matrix degradation associated with OA. With the inhibition of COX isoenzymes, NSAIDs have a local effect at the site of injury as well as a central effect minimizing spinal nociception and central sensitization. There are many NSAIDs available on the veterinary market. The selection of an NSAID is primarily based on individual response (analgesic and adverse), veterinarian and owner preference, availability, cost, and ease of administration. Despite similar efficacies between different NSAIDs, there can be a dramatic difference in individual response. It is common to try different NSAIDs until an acceptable response is achieved or the patient experiences an adverse reaction. Similar to humans, an individual may become refractory to chronic administration to a certain NSAID at which point another should be selected. Interestingly this lack of response to a certain NSAID does not last indefinitely and may be used again, effectively, in the future. Presently there is extensive debate regarding the length of washout between different NSAIDs. This only appears to be an issue when switching from aspirin and the formation of a protective aspirin triggered lipoxin (ATL) to a COX-2 selective or COX-1 sparing NSAID, which will block those gastric mucosa protective lipoxins. This is also a concern since COX-2 selective NSAIDs have been shown to impede gastric healing once ulceration is present.