Biomedical Engineering Reference
In-Depth Information
After a few days, the proliferation phase begins, marked by active fibroblast matrix
synthesis [
3
]. The newly formed ECM exists as a disorganized network; collagen type
III formation peaks during this phase andwater and glycosaminoglycan concentrations
remain high [
53
]. It is believed that these changes help optimize collagen synthesis and
the gradual conversion from collagen type III to collagen type I [
42
,
54
]. The healing
tissue can remain in the proliferation stage for up to 6 weeks [
52
].
The last phase, remodeling, is characterized as having decreased fibroblast size
and slowed matrix synthesis. The collagen fibers align themselves along the long
axis of the tendon. Collagen type I content and crosslinking increases, and glycos-
aminoglycan, water, and DNA content have returned to levels of a normal tissue.
The healing tissue can take up to a year to develop the functional strength of the
uninjured tissue [
54
,
55
].
15.3.3 Current Reconstruction Techniques
The standard treatment for tissue replacement uses autografts [
56
-
58
]. This procedure
has shown to improve cell proliferation, promote new tissue growth, and initially
exhibit sufficient mechanical strength for normal function [
4
,
23
,
59
]. However, over
time, an anterior cruciate ligament (ACL) autograft is not capable of providing
complete stabilization to the knee under torsion loads [
28
]. This failure may be caused
by the lack of revascularization at the injury site, which is necessary for long-term
success of the surgical graft. Lastly, there is a scarce availability of tissue because this
procedure takes tissue from the injured patient, creating the limitation of donor site
morbidity [
4
,
27
,
59
-
61
] Another procedure for tissue replacement uses allografts [
27
,
60
]. Tissues are often taken from cadaver patellar tendon, hamstring tendon, or Achilles
tendon [
4
,
60
]. Although this procedure eliminates the limitation of donor site morbid-
ity, it carries the risk for disease transmission and is subject to limited availability
[
60
-
62
]. Additionally, sterilization of allografts to prevent an immune response alters
the mechanical properties of the tissue [
4
,
60
]. Furthermore, graft surgeries do not
address replacement of the tendon or ligament to bone interface [
63
,
64
].
15.4 Tissue Engineering of Fibrous Tissues
In response to the aforementioned limitations of tissue grafts, a myriad of means to
engineer tendons and ligaments has been developed over the past 15 years. Ideally,
tissue engineering methods will regenerate injured tissue to sufficient mechanical
strength to restore function and promote cell growth [
27
]. Approaches examined to
date include using varied cell types seeded on both natural and synthetic bio-
materials. Additionally, such constructs may be further stimulated with biological
and/or mechanical signals. Each of these key aspects in tendon and ligament tissue
engineering is discussed in depth in this section.
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