Biomedical Engineering Reference
In-Depth Information
the region between the deep layers of articular cartilage and the underlying
subchondral bone. In healthy joints, the osteochondral junction has a
complex structure; it comprises of deep layer of non-calcified cartilage,
tidemark, calcified cartilage, cement line and subchondral bone
(Figure 7.2).
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This junction is essential for providing both functional and
structural integration of cartilage into the underlying bone.
Osteoarthritis is a major cause of physical disability. It is a degenerative
joint disease characterized by structural, chemical and mechanical changes
at the osteochondral junction. These changes have been identified as loss of
integrity and plasticity at the osteochondral junction. With the disruption of
the integrity of osteochondral junction, its barrier action will be comprom-
ised. The subchondral bone becomes exposed to the endothelial growth
factors (VEGF) produced by articular chondrocytes and bone turnover in-
creases. Reciprocally, invasion of the articular cartilage by vascular channels
exposes
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n
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r
4
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g
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1
the chondrocytes
to differentiation factors produced from
Sclerostin
Cartilage (non calcified)
Chondrocyte
cluster
Chondrocyte
cluster
F
F
Tidemark
Subchondral
bone
SOX 9
TGF-
α
WISP-1
OPG/RANK/RANKL
Synovial fluid
Intermediate zone/Interface
(calcified cartilage)
MMP3
Joint capsule
.
Cartilage
HGF
Aggrecan
HGF
Aggrecan
Peri-vascular
nerve fiber
Peri-vascular
nerve fiber
VEGF
PDGF
NGF
VEGF
PDGF
NGF
Subchondral bone
Macroph
Chondroc
Macroph
Chondroc
Osteoblast
Osteoclast
Osteoblast
Osteoclast
Sclerostin
Figure 7.2 Molecular cross-talk (as indicated by dashed arrows; the direction of
each arrow shows the direction of cross-talk) between subchondral bone
and cartilage at the osteochondral interface. A vascular channel passing
from subchondral bone to non-calcified cartilage through the osteochon-
dral interface (calcified cartilage). This channel contains a blood vessel,
osteoblasts, osteoclasts and macrophages. These cells interact with each
other through cytokines, growth factors and other signals; local inter-
actions lead to stimulation of angiogenesis, nerve growth, and osteo-
blastic activity and new bone formation. In the case of osteoarthritis,
these interactions are enhanced by signals across the osteochondral
interface. With the disruption of tidemark, subchondral bone becomes
exposed to the endothelial growth factors (VEGFs) produced by articular
chondrocytes nearer the interface. Reciprocally, invasion of the articular
cartilage by vascular channels exposes the chondrocytes to differen-
tiation factors produced from subchondral bone, and both chondrocytes
hypertrophy and endochondral ossification occur.
Modified from Suri and Walsh.
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