Osteoarthritis, or degenerative joint disease, is the most prevalent joint disorder in dogs. Mild osteoarthritis may cause subtle gait changes or intermittent lameness. As osteoarthritis severity progresses, the dog may become less active, show visible lameness, experience difficulty rising or lying down, express pain, or experience difficulty posturing to urinate or defecate.
Osteoarthritis, or degenerative joint disease, is the most prevalent joint disorder in dogs. Mild osteoarthritis may cause subtle gait changes or intermittent lameness. As osteoarthritis severity progresses, the dog may become less active, show visible lameness, experience difficulty rising or lying down, express pain, or experience difficulty posturing to urinate or defecate. As many as 20% of adult dogs are affected with osteoarthritis and may suffer pain and disability. Dr. Steven Budsberg discusses the clinical aspects of this important condition.
Selecting appropriate treatment for a canine patient with osteoarthritis depends not only on understanding the clinical and gross pathologic changes associated with osteoarthritis, but also understanding the cellular and metabolic pathways involved. Recently, considerable advances have been made in understanding these pathways, as Drs. Middleton and Hannah discuss.
Normal articular cartilage is composed of chondrocytes imbedded in a hydrated proteoglycan gel and a fibrous collagen framework, collectively referred to as the extracellular matrix. Proteoglycans provide the articular cartilage with selective permeability properties and compressive stiffness, while the collagen fibers provide tensile strength. Proteoglycans have a great affinity for water; in fact, they can absorb 50 times their weight in water. However, the collagen framework in normal cartilage constrains the proteoglycans and limits their ability to expand to about 20% of their potential. This swelling pressure keeps the cartilage turgid, helping to resist deformation when a compressive load is applied. This dynamic tissue can tolerate both compressive and shearing forces without damage, transmitting and distributing the forces to the underlying subchondral bone, which aids in shock absorption. Destruction of the proteoglycans or collagen framework inhibits the stress-absorbing capacity of articular cartilage and can contribute to inflammation and further damage. Damage to these tissues is an important aspect of osteoarthritis.
Although osteoarthritis has been classified as a noninflammatory arthropathy, low-grade, nonpurulent inflammation is common in affected dogs. Several inflammatory mediators increase in osteoarthritis, including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and prostaglandin E2 (PGE2). Among other actions, these inflammatory mediators stimulate an increase in matrix metalloproteinases (MMPs).
MMPs are enzymes that break down various proteins in cartilage. In healthy joints, they function in normal tissue turnover and repair as their catabolic activity is kept in balance by tissue inhibitors of metalloproteinases (TIMPs). In osteoarthritis, MMPs degrade glucosaminoglycans and collagen, thus damaging or destroying articular cartilage. They also reduce hyaluronic acid concentrations in the synovial fluid, leading to less viscous synovial fluid and impairing joint lubrication.
Prostaglandins, including PGE2, are synthesized from arachidonic acid by the cyclooxygenase (COX) enzymes. Under physiologic conditions, the COX-1 enzyme converts arachidonic acid to PGE2. However, COX-2 is stimulated by inflammation, which greatly increases the amount of PGE2 produced: osteoarthritic cartilage spontaneously releases 50 times more PGE2 than normal cartilage. Using nonsteroidal anti-inflammatory drugs (NSAIDs) to inhibit the COX-2 enzyme responsible for PGE2 production is one way to provide relief for osteoarthritis patients. Dietary omega-3 (n-3) polyunsaturated fatty acids also can decrease PGE2 production. The long-chain n-3 polyunsaturated fatty acids, especially eicosapentaenoic acid, compete nutritionally with arachidonic acid as substrates for the COX and lipooxygenase enzymes, decreasing production of the proinflammatory eicosanoids PGE2, leukotriene B2, and others. Dr. Mark Waldron addresses this further. Dietary n-3 polyunsaturated fatty acids also suppress the proinflammatory mediators IL-1β, IL-2, and TNF-α in cartilage tissue.
Osteoarthritis management is focused on controlling pain, improving joint function, and slowing the degenerative process within the joint. Therapy usually involves weight management, controlled exercise, and anti-inflammatory and analgesic medications. As Dr. Gail Smith describes, maintaining ideal body condition through controlled feeding is important in the management of canine osteoarthritis. Inhibition of prostaglandins and MMPs, or stimulation of TIMP activity, may be beneficial in the management of osteoarthritis. Nutritional management, discussed, also may help reduce inflammatory mediator production, promote chondrocyte health, and reduce oxidative stress.
Osteoarthritis is a complex, inflammatory condition that may respond to nutritional, as well as pharmaceutical, management. These articles have been organized to offer a deeper understanding of osteoarthritis.