Diagnosis and Management of Osteoarthritis (OA)
WSAVA 2002 Congress
Rick Read, BVSc, PhD, FACVSc
Division of Veterinary and Biomedical Sciences, Murdoch University
Perth, Western Australia

What is arthritis?

There are two basic types of joint disease which affect humans and animals-degenerative joint disease and inflammatory joint disease. The most commonly recognized and diagnosed type of arthritis is degenerative joint disease (DJD) but it is more commonly referred to today as Osteoarthritis (OA). Inflammatory joint disease refers to those diseases of joints in which inflammation is a primary and central feature in the process (pathogenesis) of the disease and the pathological appearance of the joint. Rheumatoid arthritis (although not very common) is an example of one of the many types of inflammatory joint disease that affect dogs and cats. In OA, inflammation may very well be present but it is not a central feature of the disease and tends to come and go as the condition goes through cycles of remission and exacerbation. This explains why we commonly prescribe anti-inflammatory drugs for OA but also why they are not always fully effective.

The clinical signs of OA and inflammatory arthritis may be very similar and yet the course of progression of and subsequent prognosis for individual cases and types of arthritis may be very different. Therefore it is very important that veterinarians are aware of both types of arthritis and their distinguishing features. This will be the focus of this symposium.

THE PATHOPHYSIOLOGY OF ARTHRITIC DISEASES

1. Osteoarthritis (OA)

There are many different causes of OA and this is an important concept to grasp because once we accept this as a governing factor, it is much easier to see why so many different treatments have been shown to be useful in the treatment of individual cases of OA. OA is becoming recognized as a significant cause of lost productivity in the human population. As we are faced with a gradually ageing population, the importance of this disease in man is likely to increase. OA is a progressive condition in which the articular cartilage is slowly degraded and the surrounding bone reacts by producing osteophytes which thicken the joint and frequently result in restriction of the range of movement of the joint.

The cause (etiology) of OA can be classified as primary or secondary. The term secondary osteoarthritis refers to the situation in which the underlying or initiating cause is known (e.g., hip dysplasia). In primary osteoarthritis however, the cause is unknown. In some cases, it has been suggested that overloading a previously normal joint may trigger changes. Situations in which this may be applicable include the elbows of baseball pitchers or pneumatic drill operators.

2. Inflammatory arthritis

The inflammatory processes which initiate joint disease fall into two distinct categories-infective and non-infective. As the names suggest, in the infective group the inflammation is associated with a septic process and therefore this group of inflammatory joint disease has also been referred to as septic arthritis. The other basic inflammatory process that is associated with joint inflammation is that associated with the development of immune complexes in the joint tissues, principally the synovial membrane, and this group is usually referred to as immune-mediated or non-septic arthritis.

Inflamed synovial joints suffer an influx of plasma through an increasingly permeable synovial membrane. This dilutes the synovial fluid and increases its protein content. The presence of proteins such as fibrinogen increases the tendency for synovial fluid aspirated from inflamed joints to clot. Dilution results in a decrease in the HA concentration and the molecular weight of HA may also fall in inflammatory conditions. Since the viscosity of HA solutions is highly dependent on concentration and molecular weight, any such changes will result in a decreased ability of the synovial fluid to lubricate the joint. Inflammatory cells may migrate into the synovial fluid releasing cytokines and hence exacerbating the inflammatory process. Synovial fluid aspirated from osteoarthritic joints also contains products of cartilage degradation.

Diagnosis of arthritic conditions

Joints affected by arthritic diseases have a limited range of ways that they can express the presence of disease in the form of physical signs. These include:

1.  Pain on local manipulation or pressure

2.  Thickening of joint capsule/osteophyte production

3.  Increased synovial fluid production (effusion)

4.  Change in range of movement

5.  Crepitus on manipulation

6.  Heat

These physical signs may or may not be associated with clinical presenting signs and again the joint is somewhat limited here to lameness or weakness. Because of these limitations, the various different joint diseases (OA, inflammatory joint diseases etc) can be very difficult to differentiate on physical signs alone. The problems association with making a specific diagnosis of the type of arthritis that is present will be discussed here.

PROBLEMS IN DIAGNOSIS

Problem 1. Variation in severity of clinical/physical signs

Although the range of clinical and physical signs is limited, the variation in severity of these signs can create problems with diagnosis. In particular, many severely arthritic joints may exhibit marked physical signs such as thickening and reduced range of motion, but the correlation with clinical lameness is very poor. This can be summed up by acknowledging the presence of a significant level of subclinical arthritic disease. The differentiation between clinically significant arthritis and subclinical disease must be done through careful and thorough physical examination and analysis of gait and stance.

Problem 2. Variation in presenting syndrome

Arthritic diseases can present with the following range of primary clinical problems or complaints: pain, lameness, weakness, or systemic signs. More than one of these may be present in an individual case. Weakness and systemic signs (fever, lassitude, anorexia) are very non-specific and if the local physical signs of joint disease are subtle accurate diagnosis may be missed or delayed. Again an accurate and thorough physical examination and case workup using a problem solving approach provides the best chance of early and accurate diagnosis.

Problem 3. Variation in severity of radiographic changes

Radiography is an important diagnostic tool in clinical orthopaedics and in particular in arthrology. However, it must be remembered that radiographs best demonstrate bony changes and that changes in the cartilage and synovial membrane (two very important joint components that are crucial to the development of arthritis) cannot be accurately demonstrated on plain radiographs. However, even the ability to detect and quantify the degree of bony changes (osteophyte development, subchondral sclerosis, change in congruity of articular surfaces) is of questionable importance when assessing the clinical significance of the pathology in a particular joint because the correlation between these changes and the level of physical dysfunction is very poor. Radiology should always be regarded as merely an aid to diagnosis, and radiographic data needs to be taken back to the patient and correlated with physical signs before any significant decisions regarding diagnosis and treatment are concerned.

Problem 4. Multiple causes of pain

Pain is a prominent clinical feature of OA. However the cause of pain is sometimes hard to determine. Cartilage itself is devoid of nerve endings so cartilage erosion per se should not be painful. However there are numerous nerve endings in the joint capsule, ligaments and bone and these can be stimulated by a number of types of mechanisms.

The role of joint fluid analysis in diagnosis

Although degenerative joint disease (osteoarthritis) is the most common form of arthritis in dogs, inflammatory joint disease is also a significant cause of joint pain and lameness. Although some types of inflammatory joint disease cause very obvious signs of joint effusion, local pain, joint thickening and obvious radiographic signs, other types can result in much more subtle changes in the joint. These changes may be either overlooked completely or misinterpreted as osteoarthritis. Since the treatment of inflammatory joint disease is different from that used for osteoarthritis, failure to accurately diagnose the condition can result in prolonged discomfort and disability for the patient.

The single most important differentiating factor in distinguishing between OA and inflammatory joint disease is synovial fluid analysis. Routine tests include cytology (total white cell count and differential), protein analysis and mucin clot test.

The most important parameters to be assessed by synovial fluid analysis are nucleated cell count and differential and protein. Significant increases in the percentage of neutrophils (>12%) is conclusive evidence of inflammatory joint disease. Septic and immune-mediated disease can usually be separated by the detection of toxic neutrophils in septic disease, with the additional assistance of culture of the fluid.

Medical management of osteoarthritis (OA)

Osteoarthritis remains a disease that we can at best hope to control rather than cure. Articular cartilage has very limited potential to heal defects in its substance (in this instance, healing refers to replacement of damaged matrix with new matrix with complete restoration of structure and function). At best, articular cartilage is able to undergo a limited repair process which usually results in the laying down of fibrocartilage matrix which is inferior to normal hyaline cartilage matrix both in structure and its ability to withstand normal weight bearing loads. The following groups of medications are all used in management of OA:

1. Non-steroidal anti-inflammatory drugs (NSAIDs)

NSAIDs belong to a group of drugs which act predominantly by blocking the inflammatory effects of prostaglandins through inhibition of the breakdown of arachidonic acid by cyclo-oxygenase (and in some cases lipoxygenase). Recent research has shown that two forms of cyclo-oxygenase (COX) exist-an endogenous form known as COX-1 and an inducible form known as COX-2. The endogenous form is responsible for the production of protective prostaglandins which help to maintain the integrity of the gastric mucosa and vascular endothelium. The COX-2 form of the enzyme is produced as part of the inflammatory response and is responsible for the production of the inflammatory prostaglandins. The recognition of these two distinct forms of COX explains the occurrence of side effects such as gastrointestinal bleeding and renal failure associated with NSAID use in all species. Many commonly used NSAIDs significantly block COX-1 rather than COX-2, leading to a higher incidence of side effects.

NSAIDs remain the first line of approach for many veterinarians treating dogs with OA. Historically, the choice of drug has been very much a matter of personal preference with aspirin, phenylbutazone and ibuprofen all being used extensively. The incidence of side effects such as gastrointestinal bleeding is variable and occurs mainly in dogs on higher than normal dose rates. Some NSAIDs have the potential to exacerbate OA through inhibition of proteoglycan synthesis in cartilage. In addition, by relieving pain, they may permit greater use of the joint and therefore increase wear and tear.

2. Disease modifying osteoarthritic drugs (DMOADs)

The theories on the etiopathogenesis of OA all concur that the abnormal loading of articular cartilage (through a variety of postulated mechanisms) is a crucial step in the development of OA. The fact that a net loss of cartilage proteoglycan occurs reflects the fact that the ability of the chondrocytes to manufacture new matrix components is unable to keep pace with the rate at which the matrix is being degraded. This is despite the fact that some of the chondrocytes are metabolically hyperactive especially in the early stages of OA.

It has been suggested therefore that a rational approach to drug therapy in OA is to perfuse cartilage with molecules that slow down the degradative processes and support the biosynthetic functions of the chondrocyte. In addition, the therapeutic agent should promote the synthesis of macromolecular hyaluronic acid, decrease synovial inflammation (if present) and relieve pain. Such an agent would be acting to preserve the cartilage and therefore could be termed "chondroprotective." However, such agents have been shown to have the potential to affect the joint in other ways, such as improving synovial fluid quality and blood supply to the joint, so the term DMOADs is deemed to be more appropriate.

Examples of such therapeutic agents are pentosan polysulphate and the large number of products which are registered mainly as food additives and contain various combinations of glucosamine, chondroitin sulphate and other nutritional supplements.

3. Corticosteroids

Corticosteroids tend not to be commonly used in pet practice although they are favored by some greyhound practitioners to help extend the racing life of a dog.

Physical therapy in the management of OA

Physical therapy is a very significant part of the management of OA in humans. Veterinarians have probably neglected this aspect of the management of joint diseases in our animal patients, justifying this neglect by claiming poor patient and owner cooperation. While there is some validity in this excuse, many arthritic patients can be greatly helped by dietary management, weight loss, controlled exercise, heat and massage therapy and passive joint manipulation. These aspects of patient management should be discussed with every client with encouragement to use these modalities in addition to the medical and surgical methods described above.

Surgery in the management of OA

Surgical treatment of OA is indicated in the later stages of the disease when medical therapy and physical therapy are not providing sufficient relief from discomfort or the function is poor. The procedures involved are almost all salvage procedures such as excision arthroplasty, arthrodesis or total joint replacement.

Speaker Information
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Richard Read, BVSc, PhD FACVSc
Division of Veterinary and Biomedical Sciences
Murdoch University
Perth, Western Australia


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