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.
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.