Canine Osteoarthritis: Understanding the etiology, clinical presentation, and diagnosis


Canine Osteoarthritis: Understanding the etiology, clinical presentation, and diagnosis

Osteoarthritis is the most common rheumatic disease encountered in small animal practice. No longer is osteoarthritis regarded as a simple consequence of aging and cartilage degeneration, but rather, the pathologic changes of osteoarthritis may result from active biochemical and biomechanical processes partly due to disturbances of the homeostatic mechanisms of anabolic and catabolic pathways. As to the cause of osteoarthritis, there is no one etiology and its cause may be multifactorial. While there are many initiating causes, osteoarthritis is an irreversible process that often results in an end-stage clinical syndrome of the joint. Osteoarthritis exhibits varying degrees of severity, ranging from a mild, intermittent condition that causes mild discomfort and minimal disability, to a clinical state characterized by constant pain and severe disability. Clinically, osteoarthritis can be a challenging diagnosis to make. The disease is typically a slowly progressive problem. Because of the wide range of presenting signs, osteoarthritis is likely one of the most underdiagnosed syndromes in dogs and, especially, in cats.1,2 It afflicts at least 20% of the canine population at any time.1,3 This translates to roughly 10 to 12 million dogs in the United States. There are no accurate estimates of the number of cats with osteoarthritis.

A single definition of osteoarthritis remains elusive. At a 1995 workshop, the American Academy of Orthopaedic Surgeons proposed the following consensus definition: Osteoarthritic diseases are a result of both mechanical and biologic events that destabilize the normal coupling of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix, and subchondral bone. Although they may be initiated by multiple factors, including genetic, developmental, metabolic, and traumatic factors, osteoarthritic diseases involve all of the tissues of the diarthrodial joint. Ultimately, osteoarthritic diseases are manifested through morphologic, biochemical, molecular, and biomechanical changes in both cells and matrix that lead to softening, fibrillation, ulceration, articular cartilage loss, sclerosis and subchondral bone eburnation, and osteophyte production. When clinically evident, osteoarthritic diseases are characterized by joint pain, tenderness, movement limitation, crepitus, occasional effusion, and variable degrees of inflammation without systemic effects.4

Pathophysiology of osteoarthritis

For simplicity, think of osteoarthritis progression in three broad stages.5 Stage one is the proteolytic breakdown of cartilage matrix. Stage two involves fibrillation and erosion of the cartilage surface, accompanied by breakdown product release into the synovial fluid. Finally, during stage three, synovial inflammation begins when synovial cells ingest a breakdown product through phagocytosis and produce proteases and proinflammatory cytokines. However, these stages don't progress in a specific order. Morphologically, osteoarthritis is characterized by articular cartilage degeneration and changes in the periarticular soft tissues (synovium and joint capsule) and subchondral bone. Specifically, the pathologic changes of osteoarthritis involve articular cartilage degeneration, which includes matrix fibrillation, fissure appearance, gross ulceration, and full-thickness loss of the cartilage matrix. This pathology is accompanied by hypertrophic bone changes with osteophyte formation and subchondral bone plate thickening. Research also has shown some continuity between bone and cartilage changes in osteoarthritis, suggesting an interaction between these tissues.6

Normal articular cartilage is primarily composed of water (70% by weight in mature, healthy cartilage), a collagen fibril network, extracellular matrix, and chondrocytes. During normal weight bearing, several events occur in the joint. The different matrix components must share loads applied to the articular surface. Collagen fibrils dominate the tensile behavior of cartilage, while the osmotic properties of the proteoglycans provide resistance to volumetric compression. Two very desirable events occur during cartilage loading: cartilage deformation and increased joint conformity. Cartilage deformation increases overall contact area, which reduces tissue stress levels. And increased joint conformity provides additional joint stability. Furthermore, the ability to change the shape of the loaded cartilage may help form and retain a thin gel of concentrated lubricant between the articular surfaces; fluid is distributed away from the compressed regions of cartilage. These properties are controlled primarily by the cartilage's ability to maintain hydration under pressure, which is achieved through the low hydraulic permeability and the high osmotic pressure of the constituent proteoglycans.

An early event in osteoarthritis development is the increasing volume (swelling) of the collagen. This can only occur if the collagen network's tensile properties are altered. The level of aggrecan (a proteoglycan) also changes in the tissue early in osteoarthritis development.

Cytokines and growth factors appear to play a critical role in the induction and progression of osteoarthritis. Proinflammatory cytokines, including interleukin-1α and β and tumor necrosis factor α, induce articular cartilage depletion by increasing the synthesis of matrix-degrading enzymes and decreasing matrix protein synthesis in vitro.