Chapter 3 Musculoskeletal Structure and Physiology 65cells. Type B synoviocytes are fibroblastic cells
with a slightly flattened morphology and are
primarily responsible for production of
hyaluronic acid, proteoglycans, surfactants,
and matrix metalloproteinases. Type A synovi
ocytes are intimal macrophages that form
within the bone marrow and traffic to the joint.
They are responsible for immune surveillance
within the joint, and phagocytosis of intra‐
articular debris. Both cell types communicate
continuously with chondrocytes through the
elaboration into the synovial fluid of cytokines,
growth factors, and other mediators that reach
the chondrocytes by diffusion through the
matrix. The synovial lining lacks a basal lam
ina. The synovium is therefore an inefficient
barrier, and the trafficking of cells and media
tors between the subintimal vasculature and
the synovial fluid, or between periarticular tis
sues and the joint space, is relatively uncon
strained. Hence, periarticular tissues are often
affected by primary joint pathology, and like
wise, periarticular lesions can cause significant
bystander‐type joint injury.
The subintima is a richly vascularized and
innervated tissue that forms the fibrous
component of joint capsules. Normal subintima
is a highly flexible tissue that helps guide and
constrain joint motion and that may merge with
adjacent ligaments. It often forms extensive villi
and areolar folds that project the synovium
deep into the joint space in close proximity with
the surface of the articular cartilage. The
margins of diarthrodial joints are delineated by
the enthesial attachments of fibrous capsules
to adjacent bone.
Synovial joint degeneration
Osteoarthritis (OA) is the most prevalent mus
culoskeletal disease in dogs, and is a significant
cause of decreased performance in canine ath
letes. OA is often considered to be primarily a
disease of articular cartilage. However, current
thinking recognizes the diarthrodial joint as an
organ, and describes progressive joint
degeneration as a form of organ failure (Loeser
et al., 2012). Thus, while mechanical failure of
articular cartilage is a defining element of OA,
the trajectory of cartilage loss is affected by
concurrent maladaptive changes involving
both synovium and subchondral bone.
Cartilage damage may occur in normal joints
as a result of either traumatic injury or chronic
overuse. Cartilage injury may also occur when
physiological loads are placed upon a joint that
suffers from inherent anatomic incongruity,
such that the applied force is concentrated upon
a small contact area. The latter scenario occurs
in dogs with developmental joint disease such
as elbow incongruity or hip dysplasia. Cartilage
overloading can lead to death of chondrocytes
and rupture of the collagen network of the
matrix. This can result in loss of proteoglycans
by diffusion into the synovial fluid and matrix
collapse. Once the mechanical properties of the
matrix are compromised, cartilage becomes less
capable of withstanding load, and even
physiological stresses can cause further
structural matrix damage. At the histological
level, this is manifest as irregularity and
fissuring of the articular surface, cartilage
thinning, mineralization of the intermediate
zones, and ultimately complete cartilage loss
and exposure of the subchondral bone (eburna
tion) (Figure 3.18).
Chondrocytes are sensitive to the mechanical
properties of the matrix, and changes in matrix
structure are detected by chondrocytes as
altered patterns of force. Chondrocytes initially
respond to matrix disruption by upregulating
anabolic activities and increasing biosynthesis
of collagen and proteoglycans. This represents
a reparative response; however, the regenerative
capabilities of cartilage are limited, andFigure 3.18 Gross appearance of end‐stage synovial
joint degeneration showing severe capsular fibrosis
(white arrow) and subchondral bone eburnation and
sclerosis (black arrow).