DEFINITION
Degenerative joint disease (DJD), or osteoarthritis, is a noninflammatory, noninfectious degeneration of articular cartilage accompanied by bone formation at the synovial margins
and by fibrosis of periarticular soft tissue. Although classified as noninflammatory, a low-grade, ongoing inflammatory process
is associated with this condition.
GENERAL CONSIDERATIONS AND CLINICALLY RELEVANT PATHOPHYSIOLOGY
DJD may be classified as primary or secondary, depending on the cause. Primary osteoarthritis is a disorder of aging in which cartilage degeneration occurs for unknown reasons. Secondary osteoarthritis occurs in response to abnormalities that cause joint instability (e.g., CCL rupture) or abnormal loading of articular cartilage
(i.e., developmental or anatomic abnormalities, such as hip dysplasia), or in response to other recognizable joint disease
(e.g., infection and immune-mediated inflammation). Secondary osteoarthritis is more common than primary osteoarthritis in
dogs and cats (see Box 33-1). Abnormal joint motion increases the physiologic loads placed on some portions of normal articular
cartilage, initiating molecular changes that lead to osteoarthritis. Normal stress on abnormal cartilage (i.e., injured by
genetic or metabolic cartilage disorders, inflammation, or immune responses) initiates identical changes. Initially, fibrillation
of the superficial cartilage layer results in roughening of the articular surface, with fissures eventually extending to subchondral
bone. Free cartilage fragments can initiate an inflammatory response from synovium with production of inflammatory mediators
(i.e., cytokines and prostaglandins). Cartilage degradation results from altered chondrocytes, depletion of matrix proteoglycans,
and damage to the collagen fibril network. Collagen breakdown is induced by cytokines (i.e., interleukin 1 [IL-1] and tumor
necrosis factor [TNF]) and by up-regulation of the release of destructive enzymes (i.e., matrix metalloproteinases [MMPs]
and aggrecanase) from chondrocytes, synoviocytes, and inflammatory cells. Affected cartilage is more susceptible to breakdown
from the loads of weight bearing. The result is a vicious cycle of inflammation and cartilage destruction. Thus articular
fibrillation, cartilage loss, subchondral bone sclerosis, osteophyte formation, periarticular soft tissue fibrosis, and synovial
membrane inflammation cause pain and loss of function in osteoarthritis. DIAGNOSIS
Clinical Presentation
Signalment. Osteoarthritis may affect any age or breed of dog or cat. Dysplastic diseases leading to osteoarthritis are often breed specific;
however, osteoarthritis caused by trauma is not specific for age or breed.
History. The most common clinical sign of osteoarthritis is lameness, which may be acute or chronic and persistent or intermittent.
Most animals have a history of exercise intolerance, particularly when multiple joints are affected (e.g., hip dysplasia).
There may be a previous history of joint fractures, osteochondritis dissecans (OCD), congenital or chronic joint luxations,
inflammatory joint disease, septic arthritis, and/or neuropathies. Other causes in the forelimbs include fragmented coronoid
processes (FCP) (see p. 1197), ununited anconeal processes (UAP) (see p. 1209), and premature physeal closure (see p. 1218).
In the rear limbs, hip dysplasia, aseptic necrosis of the femoral head, patellar luxation, and cruciate ligament rupture may
also cause osteoarthritis.
Physical Examination Findings
Unilateral lameness usually is evident when affected animals stand or ambulate. Bilateral conditions (e.g., hip dysplasia)
often appear as unilateral lameness if one joint is more severely affected than another. Acutely affected joints may be swollen
because of joint effusion, but swelling is more commonly caused by periarticular fibrosis in chronic disease. Reduced range
of motion, palpable crepitus during motion, and joint instability are common. Joint palpation may elicit pain.
Featuring Information from:
