IMPACT OF THE SUPERFICIAL TANGENTIAL ZONE IN CARTILAGE ON TISSUE ENGINEERING EFFORTS
*Owen, JR; +*Wayne, JS
+*Orthopaedic Research Laboratory, Departments of Orthopaedic Surgery and Biomedical Engineering
Virginia Commonwealth University, Richmond, Virginia
jswayne@vcu.edu
transplanted material with a quality STZ may provide an improved
mechanical environment for appropriate mechanotransduction signals in
the entire repairing region, even for repair tissue with inferior
mechanical properties. A viable STZ may be critical in achieving the
long-term survival of repairing cartilage.
ISOTI
REP
2
Negative
Flow rate
REPTI
2.5 E-02 µm/sec
1, 3
0
Figure 1: Radial effective fluid velocity after 30 sec of loading.
Deformation scale factor = 1. Only a 6mm radius is shown.
REP
REPT I
0.12
8%
0.1
6%
0.08
0.06
4%
2%
MPa
ISOT I
10%
Percent Compression
INTRODUCTION: Much effort is being devoted to create replacement
tissue for repair of defects in articular surfaces. While some success has
been realized, the normal zonal characteristics of articular cartilage
throughout its thickness, particularly the superficial tangential zone
(STZ), and normal material properties have not been reproduced in vitro
in scaffolds nor in vivo in repairing defects. Without sufficient quality,
the fate of such transplanted scaffolds in vivo may be doomed
mechanically from the outset. Removal of the STZ from normal
cartilage has been shown to negatively affect the remaining cartilage’s
ability to support axial loads and retain fluids [1-3]. Previous studies
have modeled excessive axial deformation of repair cartilage [4-5].
Other studies have shown that modeling the STZ of normal cartilage as
transversely isotropic provides better agreement with indentation
experimental results than isotropic models [6-9]. This finite element
study examines the role of transverse isotropy on the behavior of a
normal and repaired articular surfaces under contact loading.
METHODS: Using ABAQUS® (version 6.4) finite element analysis
software, a 2D axi-symmetric model (2760 quadratic quadrilateral pore
fluid/stress elements, 8808 nodes) was developed to represent a cartilage
surface 12mm radius and 1mm thick. The model was divided into
regions simulating naturally occurring zones (e.g. STZ=20%, middle
and deep=80%). A 3mm radius region was created in the center to allow
simulation of a repair cartilage plug for specific repair models. Mesh
was refined in areas expected to have large gradients. Material
properties comparable to those found in the literature [9] were assigned
to the regions as dictated by the scenarios (Table 1). A 5N load was
applied in ramp fashion over 0.5 sec to a 400mm radius impermeable
rigid sphere (E=200GPa, ν=0.3), which transferred load to the center of
the model’s articular surface. The load was then held constant for 30 sec
to evaluate short-term creep. Zero axial fluid flow was prescribed in the
contact region, while zero pore pressure was maintained on the articular
surface outside of the contact area and along the outer radial surfaces to
ensure unrestricted fluid flow. Three scenarios were investigated:
ISOTI: Normal isotropic cartilage in the middle and deep zones.
Normal transversely isotropic cartilage was modeled for the STZ. The
plane of isotropy was parallel to the articular surface with a higher
modulus in the radial direction.
REP: Repair isotropic cartilage in a central 3mm radius region
through the middle, deep, and STZ zones. Normal isotropic cartilage
in the middle and deep zones outside of the repair area. Normal
transversely isotropic cartilage in the STZ outside of the repair area.
REPTI: Repair cartilage in a central 3mm radius region going only
through the middle and deep zones. Normal isotropic cartilage in the
middle and deep zones outside of the repair area. Normal transversely
isotropic cartilage in the STZ, covering the entire geometry.
RESULTS: Abnormal radial flow occurred in the repair region of REP.
At the interface between normal and repair, negative radial flow
occurred. The presence of a normal STZ in REPTI restored outward
radial flow in the repair (Fig 1). Compared to ISOTI, REP (without
STZ) resulted in a 32% increase in full axial compression, in more than
doubling of compression in its’ STZ region (top 20%), in large
reductions in von Mises stress on the center of the articular surface and
immediately beneath the STZ region (64% and 87%, respectively), and a
26% reduction in fluid pressure at the bottom center of the model (Fig
2). As compared to REP, placing an STZ over the repair in REPTI
improved surface and underlying stresses by a factor of 2.5 and 2.3,
respectively. Fluid pressure improved by 21%, axial and STZ
compressions were reduced by 20% and 69%, respectively.
DISCUSSION: This analysis predicts a reduction in axial deformation,
in von Mises stress on the articular surface and in underlying repair
tissue, and an increase in repair pore pressure when a transversely
isotropic STZ is in place over the region of repair. Previous studies that
have emphasized the importance of the STZ in normal cartilage [1-3]
support these findings. Prescribing unrestricted axial flow has indicated
that strain-dependent permeability in the STZ is an important factor in
protecting underlying tissues [10]. In-vivo conditions likely allow some
axial flow out of the tissue. This study strongly suggests that
0.04
0.02
0%
0
Full
ST Z Surface Repair Fluid
Figure 2: Full thickness and STZ axial compression; von Mises stress
on the articular surface and in the repair beneath the STZ; fluid pressure
at the bottom of the repair region after 30 sec of creep.
Material
Normal
Repair
Normal
Material Property
Iso
Iso
Trans-Iso
0.46
0.1
5.8
E1 and E3 (MPa)
0.46
0.1
0.46
E2 (MPa)
0
0
0
νp (in-plane)
0
0
0
νtp (transverse)
N/A
N/A
2.9
Gp (MPa)
N/A
N/A
0.37
Gt (MPa)
5.1
10
5.1
k (x10-15m4/N-s)
4
4
4
Initial Void Ratio
νp=ν13=ν31; νtp=ν21=ν23; νpt=ν12=ν32; Gp=G13; Gt=G12=G23
Table 1: Material properties assigned to respective regions.
(Iso ≡ isotropic; Trans-Iso ≡ transversely isotropic)
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[2] Torzilli, P, et al, Med Biol Eng Comput. Jul; 31 Suppl:S93-8, 1993.
[3] Torzilli, P, et al, J. Biomech, 16(3):169-79, 1983.
[4] Smith, C, et al, 47th Ann Mtg ORS, 2001.
[5] Wayne, J, et al, Proc Inst Mech Eng, 205(3):155-62,1992.
[6] Korhonen, R, et al, Med Eng Phys, 24, 99-108, 2002.
[7] Mow, V, et al, 46th Ann Mtg ORS, 2000.
[8] Gardner, T, et al, ASME Bioengr. Div. 2003 Summer Conf.
[9] Cohen, B, 39th Ann Mtg ORS, 1993.
[10] Owen, J and Wayne, J, ASME Bioengr. Div. 2005 Summer Conf.
52nd Annual Meeting of the Orthopaedic Research Society
Paper No: 1436