C h a p t e r 4 4
Disorders of the Skeletal System: Metabolic and Rheumatic Disorders
1129
the mechanical stress.
3
Thus, the subchondral bone pro-
tects the overlying articular cartilage, providing it with
a pliable bed and absorbing the energy of the force (Fig.
44-10). Articular cartilage has two major components:
an extracellular matrix, which is rich in proteoglycan
and collagen fibers, and a limited number of chondro-
cytes, which produce the matrix.
Popularly known as
wear-and-tear
arthritis, OA is
characterized by significant changes in both the com-
position and mechanical properties of cartilage.
3,4
The articular cartilage injury is thought to result from
chondrocyte injury and release of cytokines such as
interleukin (IL)-1 and TNF (Fig. 44-11). These chemi-
cal messengers stimulate the production and release of
proteases (enzymes) that are destructive to joint struc-
tures. The resulting damage predisposes the chondro-
cytes to additional injury and impairs their ability to
maintain cartilage synthesis and repair the damage. The
combined effects of inadequate repair mechanisms and
imbalances between the proteases and their inhibitors
contribute further to disease progression.
The earliest structural changes in OA include
enlargement and reorganization of the chondrocytes in
the superficial part of the articular cartilage.
3,4
This is
accompanied by edematous changes in the cartilaginous
matrix, principally the intermediate layer. The cartilage
loses its smooth aspect and surface cracks or micro-
fractures occur, allowing synovial fluid to enter and
widen the crack. As the crack deepens, vertical clefts
form and eventually extend through the full thickness
of the articular surface and into the subchondral bone.
Portions of the articular cartilage eventually become
completely eroded and the exposed surface of the sub-
chondral bone becomes thickened and polished to an
ivory-like consistency (eburnation). Fragments of car-
tilage and bone often become dislodged, creating free-
floating osteocartilaginous bodies (“joint mice”) that
enter the joint cavity. Synovial fluid may leak though the
defects in the residual cartilage to form cysts within the
bone (Fig. 44-12). As the disease progresses, the under-
lying subchondral bone becomes sclerotic and thickened
in response to increased pressure on the surface of the
joint, rendering it less effective as a shock absorber.
Sclerosis, or formation of new bone and cysts, usually
occurs at the joint margins, forming abnormal bony out-
growths called
osteophytes,
or
spurs
(see Fig. 44-12). As
the joint begins to lose its integrity, there is trauma to the
synovial membrane, which results in nonspecific inflam-
mation. Compared with RA, however, the inflammatory
A
B
FIGURE 44-10.
(A)
A joint normally undergoes deformation of
the articular cartilage and the subchondral bone when carrying
a load.This maximizes the contact area and spreads the force
of the load.
(B)
If the joint does not deform with a load, the
stresses are concentrated and the joint breaks down.
Aging Mechanical
stress
Chondrocyte response
Release of
cytokines
(e.g., TNF, IL-1)
Production, release
of protease enzymes
Loss of smooth
cartilage surface
Development of
surface cracks
Destruction of
subchondral bone
Osteophyte
formation
Destruction of
joint structures
FIGURE 44-11.
Disease process in osteoarthritis.
Osteophyte
Bone
cysts
Erosion of
cartilage and
bone
Joint space
narrows
FIGURE 44-12.
Joint changes in osteoarthritis.The left
side denotes early changes and joint space narrowing with
cartilage breakdown.The right side shows more severe disease
progression with lost cartilage and osteophyte formation.
