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Osteoarthritis in Small Animals
Steven A. Martinez, DVM, MS, DACVS, DACVSMR

Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA, USA

Osteoarthritis (OA, syn. osteoarthrosis, degenerative chondral bone resulting in secondary degeneration of
joint disease, DJD) is a syndrome that affects synovial or articular cartilage, primary degeneration of articular car-
diarthrodial joints and may manifest its presence by tilage, the synovium, or another tissue or combination of
causing pain in association with degeneration of articu- degeneration of tissues yet to be determined.
lar cartilage (loss of extracellular cell matrix and chon- Secondary OA is due to an underlying or secondary
drocytes, inflammatory response of synovium, and cause for the development of the disease. Joint instability,
critical changes in proteoglycan ratios within matrix and direct joint trauma, infection, toxins, immune‐ mediated
synovial fluid) and changes in periarticular soft tissues. disease, and developmental/congenital disease are some
Since typically a low‐grade inflammatory process is asso- of the known etiologies for the development of second-
ciated with the development and maintenance of the ary OA and others may include infectious (e.g., septic
degenerative process of articular cartilage, the underly- arthritis) or noninfectious (e.g., immune mediated,
ing subchondral bone response (e.g., sclerosis), intra‐ trauma, developmental/congenital) environment devel-
and periarticular response (e.g., synovial hypertrophy, opment within the joint. The hyaline cartilage matrix
periarticular fibrosis), the term osteoarthritis describes (type 2 collagen, proteoglycan molecules and chondro-
the disease process of the diarthrodial joint better than cytes) is directly damaged which results in chondrocyte
the older term degenerative joint disease. Typically, OA is death. Synoviocytes are then stimulated to produce myr-
an insidiously progressive, degenerative condition that iad cytokins and inflammatory mediators (e.g., interleu-
targets high‐motion synovial joints. Osteoarthritis can kins, inducible encosinoids, nitrous oxide, tumor necrosis
occur in two forms: primary and secondary, with sec- factor‐alpha, etc.). These synoviocyte‐based products
ondary OA being the more common form presenting then in turn stimulate surviving chondrocytes to pro-
clinically in veterinary medicine. duce many of the same cytokines and inflammatory
mediators which result in the production of chondro-
cyte‐based matrix metalloproteinases which catalytically
Etiology/Pathophysiology digest more cartilage matrix (increased aggrecans con-
tent of matrix and synovial fluid drawing more water into
Primary OA is considered a “wear and tear” phenome- matrix and synovium) and reduces the matrix’s ability to
non of joint degeneration occurring in older patients. biomechanically manage normal load and shear forces at
Although primary OA may be more common in cats the cartilage surface (resulting in more matrix loss and
than previously appreciated, it appears to be rare in dogs debris as well as fracturing of the supporting subchon-
compared to clinical presentations for secondary OA dral bone deep to the cartilage matrix). In addition, the
issues. Causes of this form of OA in humans have been chondrocyte‐based cytokines and inflammatory media-
linked to obesity, the hormone leptin, and the develop- tors directly result in chondrocyte apoptosis. The carti-
ment of OA. The target or targeted effected tissues that lage matrix is now in a continuous metabolic state of
initiate the development of primary OA are unknown catabolism which will drive the progression of osteoar-
but could involve the initial degeneration of the sub- thritis in the affected joint (Figure 173.1).

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical