Front Matter

64 Canine Sports Medicine and Rehabilitation

joint trauma or surgery. Compressive loads
applied to articular cartilage are distributed
among the different components of the matrix.
The osmotic properties of the highly hydrated
aggregating PGs establish a relatively incom­
pressible fluid compartment that resists volu­
metric compression. Collagen fibrils resist
tensile stresses, and tether the PGs within the
matrix. In healthy cartilage, the hydraulic
swelling pressure of the aggregating PGs is
finely balanced by the tensile resistance of the
collagen network. Swelling pressure varies
with the density and distribution of the charged
GAG side chains of the PGs. The magnitude of
the resisting tensile counterforce depends in
turn on the stiffness and strength of the colla­
gen network. Imbalance between the osmotic
and tensile components of the cartilage matrix
leads to compromises in the mechanical integ­
rity of the cartilage and results in cartilage
degeneration, osteoarthritis, and decreased
joint function (Lai et al., 1991).
Fibrocartilage is made up of chondrocytes
suspended in an ECM that is denser than that
of articular cartilage. The ECM of fibrocartilage
is rich in type I collagen and contains smaller
quantities of PGs. Like articular cartilage,

fibrocartilage contains appreciable quantities of

elastin. Fibrocartilage is a tough and flexible

tissue with a rubbery consistency. The collagen

fibrils in fibrocartilage have a variable orienta­

tion that is specifically suited to an individual

tissue. For example, the circumferential orienta­

tion of fibrils in the peripheral regions of

menisci is adapted to accommodate the hoop

stresses that concentrate in these tissues in

response to compressive loads (Masouros et al.,

2008). Likewise, fibrocartilage develops within

the pulley regions of certain tendons where

compressive stresses become concentrated

within the ECM (Benjamin et  al., 2008).

Disorganized fibrocartilage develops readily as

a sequel to the degeneration or healing of many

musculoskeletal tissues, including bone, ten­

don, and ligament. It also forms following

vascularization of naturally occurring or iatro­

genic articular cartilage defects that communi­

cate with the trabecular bone subjacent to the

subchondral bone plate.

Synovium

The synoviae form the capsular enclosures of

diarthrodial joints, as well as tendon sheaths

and the walls of bursae (Figure 3.17). All syno­

vial membranes share a common histologic

structure and consist of a thin lining of intimal

synovial cells supported by a vascular fibroe­

lastic subintima. The synovial lining is a

discontinuous layer of two types of synovial

Unloading

Loading

Chondrocyte

Collagen

Proteoglycan

Water

Figure 3.16 Loading of articular cartilage causes
displacement of water from highly anionic aggregating
proteoglycans. Upon release of load, the hygroscopic
proteoglycans draw water into the matrix. Load‐induced
bulk flow of water through the matrix is a major
mechanism by which nutrients are delivered to
chondrocytes.

Figure 3.17 Histological appearance of normal synovial

membrane. The synovial cells (white arrow) overlie a

richly vascularized and innervated fibroelastic subintima

(black arrow).