Biomedical Engineering Reference
In-Depth Information
after two weeks, these cells differentiate into hypertrophic chondrocytes
that deposit type X collagen. afterwards, this matrix is partially mineralized,
resorbed and replaced by a matrix formed predominantly of type i collagen.
To prepare the matrix for calcification, the chondrocytes release two types
of enzymes, phosphatases and proteases.
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phosphatases provide phosphate
ions that precipitate with the calcium delivered from the mitochondria to
form calcified cartilage. Proteases degrade the proteoglycans that inhibit
mineralization, allowing the chondrocytes to control the rate and physical
chemistry of the mineralization process. After four or five weeks, the
callus is mostly composed of calcified cartilage (hypertrophic chondrocyte
mineralization of the matrix). this tissue becomes a target for chondroclasts,
multinucleated cells that degrade the calcified cartilage matrix and, in doing
so, send a signal that enables blood vessels to penetrate the tissue and bring
perivascular mesenchymal stem cells that differentiate into osteoprogenitor
cells and then into osteoblasts. Matrix
metalloproteinase-expressing cells,
including endothelial cells, facilitate vascular invasion, as
well as removal
of cartilaginous septa and any remnants
of chondrocytes.
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Tissues derived from intramembranous and endochondral ossification grow
in size until they unite
.
after about six to seven weeks, there is a combination
of calcified cartilage and newly formed woven bone. The transition from
cartilage to bone involves a highly programmed series of events for cell
removal and matrix modification. During endochondral fracture healing,
chondrocytes undergo a process of programmed cell death (apoptosis).
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Calcification of cartilage starts at the interface between the maturing cartilage
and newly formed woven bone. once the cartilage component of
the callus
has been resorbed, there are two new surfaces of
bone: an inner surface
that has grown over the original cortex
and an outer thinner layer that has
encapsulated the callus
and forms the new interface with the periosteum.
thus, a trabecular
structure is seen bridging these surfaces in the space that
was previously occupied by cartilage.
Since the outer shell is located
far from the geometric center of the bone,
it will be responsible
for the majority of weight bearing.
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this outer shell
is connected to the original cortex via trabecular-like
structures that provide
sufficient support in order to stabilize
the fracture. This represents an efficient
mechanism, using
minimal material, to restore rapidly biomechanical stiffness
and strength and allow for remodeling on internal surfaces. the exact role of
osteoclasts in fracture
repair is still uncertain,
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even though they probably
contribute to vascular invasion and
early endochondral ossification. Lamellar
bone starts forming soon after the collagen matrix of either tissue becomes
mineralized. at this point, vascular channels with accompanying osteogenic
precursors penetrate the mineralized matrix and osteoblasts form new lamellar
bone upon the recently exposed surface of the mineralized matrix.
