Biomedical Engineering Reference
In-Depth Information
10
◦
[
45
,
68
-
70
]. These values are higher than the equilibrium modulus
due to the transitory nature of the loading, which is normal for viscoelastic materials.
with the loss angle being
∼
1.1.3.4 Friction
Friction is a measure of the resistive force that exists when two contacting surfaces move laterally rela-
tive to each other. Several different mechanisms have been proposed to explain the low friction values
between cartilage surfaces; these include squeeze film lubrication [
71
,
72
], elasto-hydrodynamic lu-
brication [
73
,
74
], boundary lubrication [
75
-
77
], and fluid pressurization [
78
-
81
]. Current findings
indicate the latter is the most influential mechanism. Experiments focusing on interstitial fluid pres-
surization show that as pressure decreases ten-fold, the coefficient of friction, which represents the
ratio of the tangential frictional force to the compressive force, increases 250-fold. However, normal
loading does not allow for interstitial pressures to drop this dramatically, so friction at the cartilage
interface remains minimal. The coefficient of friction for a cartilage on cartilage interface (
∼
0.005)
is lower than any other known bearing [
82
].
1.2 ARTICULAR CHONDROCYTES
When compared to other tissues in the body, articular cartilage is sparsely populated by cells. The
chondrocyte, as the sole cell type resident within hyaline cartilage, is pivotal for the maintenance of
the tissue. All chondrocytes within articular cartilage share common traits with respect to gene and
protein expressions, surface markers, and cell metabolism. However, some differences do exist in the
genetic, synthetic, and mechanical characteristics of cells with respect to their zone of origin in the
tissue [
83
-
86
].
The chondrocyte is the basic metabolic unit of cartilage, and is responsible for limited matrix
remodeling [
3
]. Since articular cartilage is avascular, chondrocytes obtain nutrients by diffusion from
the synovial fluid, facilitated during joint movement [
87
]. Though chondrocytes have been catego-
rized as all belonging to the same phenotype, transient metabolic differences among chondrocytes
of different sizes [
88
] and zonal affiliations [
83
,
87
,
89
-
91
] have been observed
in vitro
. For instance,
superficial zone chondrocytes were found to attach to tissue culture plastic slower than those from
the deeper zones [
90
]. Deep zone cells displayed a higher label for vimentin [
92
], which has been
hypothesized to resist compression of the cell [
93
,
94
]. Keratin sulfate synthesis has been observed
to gradually increase through cartilage depth [
83
,
87
,
89
-
91
].
The characteristic gene and protein expressions of chondrocytes are closely associated with the
matrix constituents of articular cartilage. Maintenance of the surrounding matrix requires synthesis
of proteoglycans and collagens (described in a previous section) as well as other small molecules.
Disease and injury can alter cartilage physiology as well as tissue turnover, which can progressively
accelerate tissue breakdown. Compounding the problem is the sparse cell population's inability to
repair the cartilage to any extent [
95
].
Articular chondrocytes from the superficial, middle, and deep zones have morphologies and
expression profiles specific to their regions within the tissue. Cell diameters range from 10-13
μ
m,
