PATHOGENESIS OF

OSTEOARTHRlTIS
Dr.H.Djumadi Achmad, SpPA(K)

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Osteoarthritis is a slowly progressive
destruction of the articular cartilage that
is manifested in the weight-bearing joints
and fingers of older persons or the joints
of yonger persons subjected to trauma

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Primary osteoarthritis (degenerative joint
disease)
Unknown etiology
The destruction of the joints is believed to
result from an intrinsic defect of the joint
cartilage

OSTEOARTHRlTIS
Progressive degradation of articular cartilage
leads to :
- joint narrowing
- subchondral bone thickening
- eventually a nonfunctioning, painful joint

OSTEOARTHRlTIS
Pathogenesis
1. Increased unit load on the chondrocyte
2. Decreased resilience of the articular

cartilage
3. Increased stiffness of the coarse
cancellous bone of the epiphysis
4. Genetic influences

OSTEOARTHRlTIS
INCREASED UNIT LOAD :
Abnormal force on the cartilage may result
from a number of factors. For example, in
congenital hip dysplasia, the socket of the
acetabulum is shallow, covering only 30%,
to 40%, of the femoral head (normal,
50'%)

OSTEOARTHRlTIS
INCREASED UNIT LOAD :
Other factors include excessive body
weight, muscular weakness of the
extremities. When the critical unit load is
exceeded, the death of chondrocytes
leads to degradation of the articular
cartilage

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RESILIENCE OF THE ARTICULAR
CARTILAGE :
Articular cartilage binds extensive
amounts of water, and normally has a
swelling pressure of at least 3
atmospheres. A disruption in the water
bonding leads directly to decreased
resilience.

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STIFFNESS OF THE SUBCHONDRAL
COARSE CANCELLOUS BONE :
The mechanical forces are not transferred
to articular cartilage by normal stress, but
rather are dissipated by microfractures of
the coarse cancellous bone. Damage to
the coarse cancellous bone results in an
increased unit load on the cartilage.

OSTEOARTHRlTIS
STIFFNESS OF THE SUBCHONDRAL
COARSE CANCELLOUS BONE :
Furthermore, the increased pressure also
interferes with the lubricating function of
the articular cartilage, which normally
reduces friction to less than one third of
that created when two blocks of ice slide
across each other.

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BIOCHEMICAL ABNORMALITIES :
There is a decrease in proteoglycan
content and aggregation, as well as a
reduction in the chain length of the
glycosaminoglycans. Keratan sulfate is
decreased, and chondroitin sulfate is
increased. There is also a decline in the
glucosamine concentration.

OSTEOARTHRlTIS
BIOCHEMICAL ABNORMALITIES :
The collagen fibers are thicker than
normal, and the water content of
osteoarthritic cartilage is increased. It is
thought that the reduction in proteoglycans
allows more water to be bound to the
collagen fibers.

OSTEOARTHRlTIS
BIOCHEMICAL ABNORMALITIES :
Although the synthesis of matrix by
chondrocytes is augmented in the early
stages of osteoarthritis, protein synthesis
eventually tends to decrease, suggesting
that the cells reach a point at which they
fail to respond to reparative stimuli.

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GENETIC FACTORS :
Genetic analysis of patients with a type of
familial, early-onset osteoarthritis has
disclosed a variety of mutations in the
gene for type II collagen (COL2A1), the
major collagen species of articular
cartilage.

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The joints commonly affected by
osteoarthritis :
1. The proximal and distal interphalangeal
joints of the upper extremity
2. Knees
3. Hips
4. The cervical and lumbar spine

OSTEOARTHRlTIS
Radiology
(1) narrowing of the joint space, which
(2)
(3)
(4)

represents the loss of articular cartilage

increased thickness of the subchondral
bone
subchondral bone cysts
large peripheral growths of bone and
cartilage called osteophytes

OSTEOARTHRlTIS
Pathology
1. In the earliest stage : loss of
protcoglycans from the surface of the
articular cartilage. At the same time, empty
lacunae in the articular cartilage indicate
the death of chondrocvtes. Osteoarthritis
may arrest at this stage for many years
before it proceed to the next stage

OSTEOARTHRlTIS
Pathology
2. The next stage is characterized by
fibrillation (i.e., the development of surface
cracks parallel to the long axis of the
articular surface). These fibrillations also
may persist for many years before further
progression occurs.

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Pathology
3. As fibrillations propagate, synovial fluid
begins to flow into the defects. The cracks
are progressively oriented more vertically,
tending to parallel the long axis of the
collagen fibrils. Svnovial fluid works its
way deeper into the articular cartilage
along the cracks.

OSTEOARTHRlTIS
Pathology
3. Eventually, pieces of articular cartilage
break off and inducing inflammation and a
foreign-body giant cell reaction. The result
is a hyperemic and hypertrophied
synovium.

OSTEOARTHRlTIS
Pathology
4.As the crack extends down toward the tide
mark and eventually crosses it,
neovascularization from the epiphyseal
and subchondral bone extends into the
area of the crack, inducing subchondral
osteoclastic bone resorbtion.

OSTEOARTHRlTIS
Pathology
4. Adjacent osteoblastic activitv also occurs,
and the result is thickening of the
subchondral bone plate in the area of tile
crack. Neovascularization progressively
extends into the area of the crack