The original meaning of arthritis is inflammation of a synovial (containing joint fluid) joint. Since any abnormality of a synovial joint can produce inflammation to a greater or lesser extent, the term ‘arthritis’ has therefore become a rather unspecific umbrella term for all manner of joint conditions.
Osteoarthritis (OA) or degenerative joint disease is the most common form of arthritis in the dog. Osteoarthritis is not a disease in itself but rather a process caused by another initiating factor. The underlying process of this condition is the gradual loss of articular cartilage. Articular cartilage is an active, dynamic tissue which is capable of both repair and breakdown activities. In OA the tendency is for the balance between synthesis and degradation to swing towards degradation. The sequence and timing of these processes can vary depending on the joint affected and the inciting cause.
Osteoarthritis is estimated to affect 20% of dogs over 1 year of age, and growing evidence suggests that feline OA is much more common than previously thought. Estimates purport that 30-50% of cats and dogs will be affected by OA at some point in their lives. Unlike humans, where OA is usually related to ageing and “wear and tear” of joints, OA in pets usually has a specific underlying cause and is therefore often seen earlier in life.
The causes of OA are wide ranging but typically relate to an underlying disease process. These may include joint laxity or instability, previous trauma to the joint, immune-mediated arthropathy of the joint, articular (joint) fracture, osteochondrosis, septic arthritis and angular limb deformities. All of these conditions and many more have the potential to initiate inflammation within the joint which in turn can lead to the production of cartilage-damaging enzymes such as matrix metalloproteinases.
In dogs, the main signs of OA are stiffness, lameness and varying degrees of pain. Stiffness and lameness are often seen following a period of rest, especially if this is preceded by a period of activity. The patient tends to “walk off” the stiffness after a few strides. Joint pain is seen usually via increased vocalisation, restlessness at rest or during sleep, licking of affected areas, and altered behaviour (including aggression).
In cats, a reluctance to jump as high as usual (or at all), decreased play activity, reduced or over-grooming and exercise are all indicators of OA, although are not specific to OA alone.
Diagnosis of OA is via physical examination with the demonstration of restricted range of motion of joint and a decrease of palpable muscle mass secondary to reduced use. Radiography is the most common method of diagnosis confirmation, as it aids exclusion of other causes of joint pain such as dysplasia (abnormal development), fracture, dislocation or infection. Occasionally, further imaging such as CT, MRI or ultrasound scans are needed to investigate OA. Arthroscopy (keyhole surgery) enables direct assessment of the joint using a rigid endoscope and camera and is sometimes indicated for OA. Collection and analysis of joint fluid can be important to exclude infection and rheumatoid-like conditions.
OA is a lifelong condition that cannot be cured. Treatment is aimed at managing the signs and slowing the progression of the disease using a combination of therapies. Treatment type depends upon whether OA is actively causing pain and lameness, or silent (causing stiffness, but no pain/lameness). Some patients may have silent OA for long periods of time, with occasional bouts of the active form. No one treatment is most successful, and a multi-modal approach of the following is often advocated:
In humans there is a strong link between OA and obesity. From research we know obesity accelerates the development of OA. Weight reduction alone can be very effective for some animals in reducing pain from osteoarthritis.
There is a variety of special weight reduction diets available which help provide a ‘full feeling’ but at a reduced calorie load. It is important to adhere to the recommended daily allowance given on the pack and avoid any other treats, snacks and scraps. Regularly visiting your vet for weigh-ins will help keep you updated on your pet’s progress while offering an opportunity to seek further advice and support.
A combination of reducing exercise at periods of pain and lameness and slowly building it back up to a level that does not cause over-exertion and OA flare-ups for the patient.
The aim of exercise therapy is to find a balance between excessively stressing the osteoarthritic joint and limiting the stiffness which often accompanies prolonged inactivity.
Generally controlled (lead) walks are recommended, with little and often being a good policy. Short walks regularly often do more to alleviate signs of stiffness than more irregular long walks that can cause unnecessary pressure on the joint.
The potential benefits of physiotherapy and hydrotherapy are two fold as they encourage weight reduction through gentle, controlled exercise and also aid joint motion to decrease stiffness and improve circulation. In humans, physiotherapy has been shown to have functional and pain relieving benefits.
Canine hydrotherapy and swimming have gained increased popularity in recent times and may result in greater range of motion of affected joints. Research suggests improved joint comfort after physiotherapy and hydrotherapy but further research is required to determine the exact role of swimming/hydrotherapy in dogs with OA.
Acupuncture is a growing area of research in OA but reports are as of yet limited, although anecdotally improvements are reported.
Non-steroidal anti-inflammatory drugs (NSAIDs) are the mainstay in pain control for pets with OA. These reduce inflammation but are also an effective pain killer. Your pet may require repeated, long courses (weeks to months) of these drugs since OA is a condition which is managed but not cured. Monitor for side effects such as vomiting and diarrhoea, which should be immediately reported to the vet.
Other drugs may be used to control discomfort such as other types of pain-killers and other drugs that target joint pathology specifically in order to directly reduce pain.
Some dietary supplements (those containing omega-3 fatty acids, green-lipped mussel, chondroitin, glucosamine) are proposed to decrease rate of OA progression.
Increased omega-3 fatty acid dietary supplementation has been advocated as an adjunctive therapy to degenerative and inflammatory arthritic conditions. Supplementing omega-3 fatty acids in the diet changes the composition of cell membranes and ultimately leads to a decrease in inflammatory products. There is evidence in the veterinary literature that these products have a drug sparing effect in dogs with OA i.e. dogs with Omega 3 fatty acids in their diet required less NSAIDs (anti-inflammatory drugs) to make them comfortable.
Chondroitin sulfate is a ‘building block’ in articular cartilage whereas glucosamine is a ‘building block’ in synovial fluid. Numerous formulations of glucosamine and chondroitin sulfate are available. Although anecdotal data suggests a positive effect, there is little evidence for using these preparations.
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