Front Matter

66 Canine Sports Medicine and Rehabilitation

abnormal loading ultimately shifts the chon­
drocyte toward a catabolic phenotype
(Goldring, 2006). This involves elaboration of a
cadre of proinflammatory mediators and matrix
metalloproteinases. Proinflammatory media­
tors can feed back in an autocrine or paracrine
manner to further augment catabolic activity of
chondrocytes. They may also be released into
the synovial fluid where they can activate the
synovium. Enzymatic digestion of collagen and
proteoglycan components of the matrix by met­
alloproteinases leads to further mechanical
compromise, and can lead to a progressive cas­
cade of matrix collapse (Kurz et al., 2005).
The ability of articular cartilage to withstand
physiological loading is dependent upon the
compliance of the subchondral bone (Goldring,
2006). Primary diseases or remodeling pro­
cesses of bone that affect the stiffness of sub­
chondral bone can lead to stress concentration
within overlying cartilage and can render the
matrix susceptible to injury even under physi­
ological conditions. Conversely, as cartilage
matrix is lost, altered patterns of loading are
experienced by the subchondral bone itself,
which can lead to secondary maladaptive
remodeling and loss of underlying trabeculae.
This interplay between cartilage and subchon­
dral bone can establish an independent self‐
perpetuating cascade of joint degeneration.
The synovium is highly responsive to
changes in the cartilage and may affect cartilage
degeneration at several levels (Sellam &
Berenbaum, 2010). Inflammatory diseases of
the joint involve rapid activation of the
synovium and typically lead to joint effusion
and intra‐articular recruitment of leukocytes.
Matrix metalloproteinases released by
leukocytes and synovial cells may initiate a
cascade of cartilage degradation by direct
attack upon matrix components. Release of
proinflammatory cytokines by the synovium
may also enhance the catabolic activities of
chondrocytes. Degradation of cartilage matrix
causes the release into the synovial fluid of
small proteolytic fragments of many matrix
components, including collagen, fibronectin,
proteoglycan core and link proteins, and many
others. These fragments can function as potent
biological mediators. Matrix fragments (or
matrikines) bind to synovial cell surface
receptors and can alter patterns of synovial

fluid production, elicit the production of

proinflammatory mediators and growth

factors, and increase production of matrix met­

alloproteinases by the synovium.

The complex interplay that develops between

cartilage, synovium, and subchondral bone

leads to synovial hyperplasia and villous

hypertrophy, sustained decreases in the quality

of synovial fluid, sclerosis of subchondral bone,

and persistent capsular inflammation and

fibrosis. Alterations in the thickness and

compliance of the joint capsule lead to joint

stiffness and loss of range of motion (common

clinical manifestations of progressive OA) and

also may contribute to OA progression by

further altering patterns of cartilage loading.

Tendons, ligaments, and entheses

Tendons are bands of collagen‐rich tissue that

link muscle to bone and that transfer forces of

muscle contraction to the skeleton. Several

forms of tendon are recognized. Positional

tendons (e.g., the tendon of origin of the biceps

brachialis) are dense cord‐like structures with

discrete sites of osseous attachment and are

primarily involved in muscular control of joint

position. Positional tendons are frequently

contained within a fluid‐filled sheath that

provides for low‐friction sliding motion. Wrap‐

around tendons (e.g., digital extensor tendons)

are positional tendons that undergo a sharp

change of direction as they cross a joint. They

often pass through specialized bony grooves

that function as pulleys during joint motion.

The portion of a wrap‐around tendon that

traverses a joint is usually stabilized by a

fibrous retinaculum, and the tendon itself may

contain fibrocartilage that provides resistance

to the compressive stresses that concentrate at

the site of the pulley. Energy‐storing tendons

(tarsal extensors and carpal flexors) are adapted

to weight‐bearing and maintenance of posture,

and contain higher concentrations of elastin

than other tendon types. Aponeuroses are flat­

tened sheet‐like structures that often link mus­

cles to other fascial structures (e.g., insertional

aponeuroses of the abdominal wall muscles).

Ligaments are connective tissue bands with

osseous origins and insertions and that typically

cross a joint. Some ligaments (e.g., the transverse